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"Not a scientist but it's to do with genetics. Coronavirus infects you by binding to the ACE2 receptors. We all have ACE2 receptors but the genetic coding is different in different people. If your ACE2 receptors are coded a certain way, coronavirus can't bind and therefore can't hurt you. " Interesting, i wonder if that is a different avenue of testing that could be developed then, a bit like how they test immediate family in some breast cancer cases to see if you have “the cancer gene” ... if you knew your receptors were coded this way then you would be immune and no need for vaccine or anything like that | |||
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"Question. How come some people can get covid 19 with little or no effects while others die? Especially healthy nurses and healthy bus drivers. I pondered this and came up with the following hypothesis. The common cold aka Rhino virus can be caught twice at the same time. Or " A cold on top of a cold." And inevitably your symptoms will be worse. This lends itself to the notion that covid can be the same. "Covid on top of covid." With the same result of worse symptoms. If this is correct. It would explain why there is such a dramatic variation of the severity of symptoms. Particularly to those who are likely to have repeated exposure to covid ie. Nurses and bus drivers. Is there anything in this or do I just have a great imagination? I'm not a scientist. But it seems logical. But like I said don't know shit because I'm not a scientist. Hence I'm asking the question? "As a scientist involved in infectious disease (bacterial not viral) there are a couple of assumptions you made which need correcting  The number of viruses which cause the common cold are in the 100s, including 4 coronaviruses. So if you do have cold on top of a cold, it's because they're different viruses. This isn't possible with COVID-19 as it's one virus, like you can't get HIV on top of HIV (which would be fucking awful if it were the case!).
The main variation is due to underlying co-morbitities, esp in the older patients. But this is a virus to which we've not had exposure before, and currently we don't quite know why some do better and others (without a co-morbitity) do worse. The specialists at my company are discussing that the virus may not be causing what's called ARDS but something else, esp in direct damage to the lungs (vascular injury).
Also if you want another overview to help, check Dr Mike Hansen on YouTube as he has a vid on why it kills some but not others. | |||
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"Not a scientist but it's to do with genetics. Coronavirus infects you by binding to the ACE2 receptors. We all have ACE2 receptors but the genetic coding is different in different people. If your ACE2 receptors are coded a certain way, coronavirus can't bind and therefore can't hurt you. Interesting, i wonder if that is a different avenue of testing that could be developed then, a bit like how they test immediate family in some breast cancer cases to see if you have “the cancer gene” ... if you knew your receptors were coded this way then you would be immune and no need for vaccine or anything like that " It's something that's being researched but still in the "too difficult" bucket at government level. But this is the kind of stuff they need to get on top of rather than hiding behind the line "it'll all be ok when we have a vaccine". It doesn't stop the spread, but there's a huge potential pay off. You could essentially eliminate deaths in front line workers. | |||
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In short in layman's terms. A cold on top of a cold is because you can catch 2 viruses at the same time which is a bitch. But not a double dose of 1 type of virus.
But you cannot catch 2 doses of the same virus at the same time. This makes perfectsense to me.
But so to the questions.
Firstly what are/ is ARDS?
Secondly one of the replies mentioned something about viral load. Could this be a factor? And what is a viral load?
Thanks | |||
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"Not a scientist but it's to do with genetics. Coronavirus infects you by binding to the ACE2 receptors. We all have ACE2 receptors but the genetic coding is different in different people. If your ACE2 receptors are coded a certain way, coronavirus can't bind and therefore can't hurt you. Interesting, i wonder if that is a different avenue of testing that could be developed then, a bit like how they test immediate family in some breast cancer cases to see if you have “the cancer gene” ... if you knew your receptors were coded this way then you would be immune and no need for vaccine or anything like that It's something that's being researched but still in the "too difficult" bucket at government level. But this is the kind of stuff they need to get on top of rather than hiding behind the line "it'll all be ok when we have a vaccine". It doesn't stop the spread, but there's a huge potential pay off. You could essentially eliminate deaths in front line workers." I would love to eliminate the whole damn bug. But alas all we can do is support those who are supporting us and eliminate ignorance. Which brings me nicely to my question which of course will lead to another question. What are ACE2 receptors and equally is there an ACE1 receptor? I am going to re- read your answer because I didn't understand it first time. Sometimes a re- read reveals something I missed. | |||
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"Not a scientist but it's to do with genetics. Coronavirus infects you by binding to the ACE2 receptors. We all have ACE2 receptors but the genetic coding is different in different people. If your ACE2 receptors are coded a certain way, coronavirus can't bind and therefore can't hurt you. " This, I believe | |||
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"Thank you for your imput. I think I get it. But naturally every answer raises questions. But yours seems to be the best answer so far.
In short in layman's terms. A cold on top of a cold is because you can catch 2 viruses at the same time which is a bitch. But not a double dose of 1 type of virus.
But you cannot catch 2 doses of the same virus at the same time. This makes perfectsense to me.
But so to the questions.
Firstly what are/ is ARDS?
Secondly one of the replies mentioned something about viral load. Could this be a factor? And what is a viral load?
Thanks "ARDS Acute respiratory distress syndrome (ARDS) is a type of respiratory failure characterized by rapid onset of widespread inflammation in the lungs. Symptoms include shortness of breath, rapid breathing, and bluish skin coloration. For those who survive, a decreased quality of life is common. | |||
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"Thank you for your imput. I think I get it. But naturally every answer raises questions. But yours seems to be the best answer so far.
In short in layman's terms. A cold on top of a cold is because you can catch 2 viruses at the same time which is a bitch. But not a double dose of 1 type of virus.
But you cannot catch 2 doses of the same virus at the same time. This makes perfectsense to me.
But so to the questions.
Firstly what are/ is ARDS?
Secondly one of the replies mentioned something about viral load. Could this be a factor? And what is a viral load?
Thanks "A detailed overview of ARDS can be found here https://www.mayoclinic.org/diseases-conditions/ards/symptoms-causes/syc-20355576 | |||
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"I’m not a scientist either and I await the microbiologist reply. I believe that it’s to do with viral load. If you touched a surface that had a small amount of the virus and then that got into your system, if you are otherwise healthy, then your immune system should be able to fight it off. If you are in a hospital and the virus is everywhere and when you do get exposed to it there is a chance that someone is sneezing on you then when you get it your viral load is a lot higher. It is then harder for your immune system to cope and therefore you are more likely to get more seriously ill. " You at precisely the point where I started. Just a different branch. Which is, is the over exposure to this virus making it more dangerous to the people exposed. So Ive asked our single sciencist your question and hope he replies. I've never come across the term viral load before | |||
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"Not a scientist but it's to do with genetics. Coronavirus infects you by binding to the ACE2 receptors. We all have ACE2 receptors but the genetic coding is different in different people. If your ACE2 receptors are coded a certain way, coronavirus can't bind and therefore can't hurt you. Interesting, i wonder if that is a different avenue of testing that could be developed then, a bit like how they test immediate family in some breast cancer cases to see if you have “the cancer gene” ... if you knew your receptors were coded this way then you would be immune and no need for vaccine or anything like that It's something that's being researched but still in the "too difficult" bucket at government level. But this is the kind of stuff they need to get on top of rather than hiding behind the line "it'll all be ok when we have a vaccine". It doesn't stop the spread, but there's a huge potential pay off. You could essentially eliminate deaths in front line workers. I would love to eliminate the whole damn bug. But alas all we can do is support those who are supporting us and eliminate ignorance. Which brings me nicely to my question which of course will lead to another question. What are ACE2 receptors and equally is there an ACE1 receptor? I am going to re- read your answer because I didn't understand it first time. Sometimes a re- read reveals something I missed. " I'm not an expert in this area. But there's ACE and ACE2. The "E" is for enzymes which is what they are. They are attached to your lungs and other organs. From what I understand, some people have a genetic coding that doesn't allow coronavirus to bind with the ACE2 receptors. There's also a line of research where people were given artificial ACE2 (hrsACE2) and so the coronavirus essentially wasted itself by binding to that, instead of their natural ACE2 receptors. That might link into the viral load discussions but at this point I'm really stretching my knowledge of the subject. | |||
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"Thank you for your imput. I think I get it. But naturally every answer raises questions. But yours seems to be the best answer so far.
In short in layman's terms. A cold on top of a cold is because you can catch 2 viruses at the same time which is a bitch. But not a double dose of 1 type of virus.
But you cannot catch 2 doses of the same virus at the same time. This makes perfectsense to me.
But so to the questions.
Firstly what are/ is ARDS?
Secondly one of the replies mentioned something about viral load. Could this be a factor? And what is a viral load?
Thanks "No worries. Regards contracting the virus and a double dose, of course you can come into contact with it multiple times. As to whether any of those times leads to an infection is another story - number of viral particles needed to cause infection is unknown for this one I think. So yes you can catch it multiple times in a very short period but as far as my knowledge goes on viruses it won't amplify the detrimental effects, but likely to increase chance of developing symptoms, sorry wasn't making myself clear However the virus has to get into the body first and then into the right system (lungs) to cause COVID-19 which is why hand washing is #1 preventative measure.
ARDS = Acute Respiratory Distress Syndrome. This is when mechanical ventilation is required, a type of respiratory failure.
Viral load simply refers to level of virus you have, if it's high you're considered more contagious. And usually if it's high you experience more severe symptoms...tho this may not be the case here.
Useless piece of info - if you take all the viruses in the world, they would weigh more than all other living matter put together. | |||
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"Sorry just catching back up on this. I've just f work and am having my tea. I'll read through what has been shared here later and try to formulate a reply, as best as I can. Sorry for the delay. " No probs we await a insight into this reached virus | |||
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"Sorry just catching back up on this. I've just f work and am having my tea. I'll read through what has been shared here later and try to formulate a reply, as best as I can. Sorry for the delay. " Thank you | |||
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" Useless piece of info - if you take all the viruses in the world, they would weigh more than all other living matter put together. " Mind. Blown. | |||
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" Useless piece of info - if you take all the viruses in the world, they would weigh more than all other living matter put together. Mind. Blown." There's more . . . How much does the Internet weigh. approximately 50 grams Given this information, and the fact that silicon logic runs at approximately 3 volts and a chip runs at a gigahertz, Seitz calculates that the entire weight of the internet is approximately 50 grams, the same as the weight of a large strawberry (VSauce, 2011). | |||
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" Useless piece of info - if you take all the viruses in the world, they would weigh more than all other living matter put together. Mind. Blown." But totally wrong, think about it totally impossible | |||
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" Useless piece of info - if you take all the viruses in the world, they would weigh more than all other living matter put together. Mind. Blown. But totally wrong, think about it totally impossible " Then the director of London School of Hygiene & Tropical Medicine is wrong. His quote, not mine. Happy to revise as it seems plants are king | |||
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" Useless piece of info - if you take all the viruses in the world, they would weigh more than all other living matter put together. Mind. Blown. But totally wrong, think about it totally impossible Then the director of London School of Hygiene & Tropical Medicine is wrong. His quote, not mine. Happy to revise as it seems plants are king "Think about it. How can the weight of all the virus matter in the world which is contained in all the living organisms in the world weigh more than those living organisms, | |||
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" Useless piece of info - if you take all the viruses in the world, they would weigh more than all other living matter put together. Mind. Blown. There's more . . . How much does the Internet weigh. approximately 50 grams Given this information, and the fact that silicon logic runs at approximately 3 volts and a chip runs at a gigahertz, Seitz calculates that the entire weight of the internet is approximately 50 grams, the same as the weight of a large strawberry (VSauce, 2011)." Is this true? My head just exploded | |||
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"There was a news story the other day stating that ace2 is more comman in men than woman with a higher concentration in your bollox which could explain the higher infection and mortality rate of men." I would take any report that talks like that with a pinch of salt (yes I know they wouldn't have said bollox). There are potential sex differences, but the easiest answer is women are more likely to raise concern and see a doctor than men and men's lifestyle habits. We don't know at this stage whether sex hormones or chromosomal differences play a part. Nor if there are racial differences but probably will once there is more data. More of concern is those with underlying issues and elderly, not whether you have a pair of balls  | |||
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" Useless piece of info - if you take all the viruses in the world, they would weigh more than all other living matter put together. Mind. Blown. There's more . . . How much does the Internet weigh. approximately 50 grams Given this information, and the fact that silicon logic runs at approximately 3 volts and a chip runs at a gigahertz, Seitz calculates that the entire weight of the internet is approximately 50 grams, the same as the weight of a large strawberry (VSauce, 2011). Is this true? My head just exploded" As far as I know - just search The Weight of the Internet it's been around quite a while. | |||
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"Thank you for your imput. I think I get it. But naturally every answer raises questions. But yours seems to be the best answer so far.
In short in layman's terms. A cold on top of a cold is because you can catch 2 viruses at the same time which is a bitch. But not a double dose of 1 type of virus.
But you cannot catch 2 doses of the same virus at the same time. This makes perfectsense to me.
But so to the questions.
Firstly what are/ is ARDS?
Secondly one of the replies mentioned something about viral load. Could this be a factor? And what is a viral load?
Thanks
No worries. Regards contracting the virus and a double dose, of course you can come into contact with it multiple times. As to whether any of those times leads to an infection is another story - number of viral particles needed to cause infection is unknown for this one I think. So yes you can catch it multiple times in a very short period but as far as my knowledge goes on viruses it won't amplify the detrimental effects, but likely to increase chance of developing symptoms, sorry wasn't making myself clear However the virus has to get into the body first and then into the right system (lungs) to cause COVID-19 which is why hand washing is #1 preventative measure.
ARDS = Acute Respiratory Distress Syndrome. This is when mechanical ventilation is required, a type of respiratory failure.
Viral load simply refers to level of virus you have, if it's high you're considered more contagious. And usually if it's high you experience more severe symptoms...tho this may not be the case here.
Useless piece of info - if you take all the viruses in the world, they would weigh more than all other living matter put together. "If there was a person who was exposed to coronavirus but it couldn't bind to their ACE2 receptors, would they show nothing or as asymptomatic on a test? There's a French Aircraft carrier which had an outbreak and just under half the crew got infected. It is a pretty big ship but I'm wondering if half didn't get infected or couldn't. | |||
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ACE stands for angiotensin-cleaving enzyme. Put simply, this is an enzyme found in the cell membranes of many human cells that is involved in the chopping (cleaving) of a hormone called angiotensin. Among many things, angiotensin is responsible for regulating blood pressure, through the constriction of the muscle within blood vessels. Higher active angiotensin = constriction of blood vessels; less active angiotensin = relaxation of blood vessels. ACE2 is the "opposite number" ACE. ACE2 causes the chopped angiotensin, that causes constriction of blood vessels, to be converted into a different form that is biologically inactive, therefore blood vessels dilate again. ACE2 was identified in the last SARS outbreak, in 2004, as the binding site for some coronaviruses, including SARS viruses and a couple of other coronaviruses. Viruses must enter into a host cell to reproduce themselves, as they do not contain the cellular machinery required to copy their own genetic information, so viruses effectively "trick" cells into allowing them to enter. This is a complex thing which I won't go into much, but suffice to say it is like a lock and key situation. The lock is the receptor (in this case, ACE2) and the key would usually be the biologically active form of angiotensin. All proteins have a specific 3D shape, but viral proteins on their surface mimic these "key" shapes, to facilitate entry to cells, a bit like a master key allowing access to any lock.
ACE and ACE2 are found in considerable levels in specific cells of the alveoli (the deepest parts of the lung, found at the end of the bronchioles); the small intestine and in smaller amounts in the kidney and other organs. This makes sense, because regulation of blood pressure is especially fundamental in organs that rely on specific pressures for normal function (OK, all organs rely on this, but the lungs require very specific blood pressures in order to efficiently exchange oxygen and carbon dioxide). The small intestine is exceptionally vascular, as this is the site of the absorption of the micronutrients from digestion, and absorption is directly into blood vessels. We require oxygen via the lungs, and glucose via the small intestine to perform aerobic respiration (the means by which we can convert the energy from nutrients into a form available for us to use for movement etc). The kidneys are the site of the majority of the fluid balancing via excretion of water and also considerably involve in regulation of ions, such as sodium and potassium. These ions are also involved in maintenance of normal blood pressure and so the presence of large concentrations of ACE and ACE2 make sense. I hope I did not digress too much.
We all have different genetic sequences (ish) that generate overall the same protein, so one (wo)man's ACE/ACE2 is not the same as another's. Plenty of research has gone into polymorphisms (the genetic variations found between people) and concluded that polymorphisms did not contribute to the difference in disease processes in the SARS outbreak in 2004. This SARS-CoV-2 is exceptionally similar to SARS, and so it is likely this is also the case this time: Info here, for example: https://academic.oup.com/clinchem/article/50/9/1683/5640134
- ACE2 is coded for on the human X-chromosome. As we probably know, human females have 2 X chromosomes, and human males have 1 X chromosome. There is a hypothesis that due to males only having the 1 copy of ACE2, that they might be more susceptible, but that would only hold water if having genetic variants of ACE2 was significant, which the research above from the SARS outbreak said was not. That doesn't mean 100% that it isn't and it's probably too early yet to have enough data from the SARS-CoV-2 outbreak to back that up. The increased severity/deaths in males might be related to males being more likely to have the co-morbidities that we know increase risk (heart conditions, diabetes, etc); because males are more likely to smoke and consume alcohol in excess; because males are less likely to seek medical advice early/visit doctors for routine health screening that might pick up underlying conditions. There are too many unknowns right now to fully explain that stat, but if you look at the ICU admission data above, the rate of admission of men vs women is pretty stark: 72.5% male for Covid-19 related admissions vs 54.3% males for non-Covid related pneumonias. However, note the data set of the non-Covid related pneumonias spans two calendar years (2017-19), so there will be varying pathogens circulating; both bacterial and viral, and the number of patients in the non-Covid data set is about double that of the Covid-19 dataset, so that allows smaller numbers to be seen more prominently in the overall percentages.
OK, that's enough science for now, and sorry for waffling on
N
BSc (Hons) Microbiology; lecturer of biology, physiology and medical health sciences in an institution somewhere in the vicinity of Manchester | |||
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"OK, here goes, and sorry if I miss any points raised by previous commentators: 1) Viral load theory (the theory that people are infected with more particles of SARS-Cov-2 are more likely to have more severe disease) - This works out for some diseases, but the evidence so far for SARS-CoV-2 is that this is not the case. Two studies (obviously not huge scale) have disproven this theory. One in Lombardy, the most affected part of Italy, and another in China, found no difference in viral load and severity of disease. What viral load will indicate is how infectious an individual might be, because viral load correlates to viral shedding. We don't yet know the infectious dose for SARS-CoV-2, but it is likely to be fairly low, given the ease at which is seems to pass from person to person. This New Scientist article deals with the viral load hypothesis in fairly easy to understand terms: https://www.newscientist.com/article/2238819-does-a-high-viral-load-or-infectious-dose-make-covid-19-worse/ 2) Why are apparently healthy medics, bus drivers etc succumbing to Covid-19? - A few things here. 1) Apparently healthy and actually healthy are two different things. People may walk around without any obvious signs/symptoms of an underlying medical condition for some considerable time, and it is often routine screening that uncovers issues before people show symptoms. An example would be that hypertension does not really cause any observable outward symptoms in the patient, but it easily identified with a blood pressure test and the patient is usually totally unaware they have it. For example, evidence from routine screening is that far more people have high blood pressure than realise it (e.g. when they do drop-in screening in shopping centres etc). Also, we don't know if any of the individuals smoked (smoking increases the risk of any respiratory disease being severe) or any other information about lifestyle, which might pre-dispose them to poorer outcomes. 2) Weight seems to be playing a huge factor in the severity of disease; quote: "Data from the first 2204 patients admitted to 286 NHS ICUs with COVID- 19 reveal that 72.7% of them were overweight or obese. We shouldn’t ignore the fact that 50-60% % of the 1.4 million NHS workforce are themselves overweight or obese too." Data for the ICU admissions here: https://www.icnarc.org/DataServices/Attachments/Download/c31dd38d-d77b-ea11-9124-00505601089b Evidence for the data on NHS workforce obesity/weight: https://bmjopen.bmj.com/content/7/12/e018498 It is also true that the chronic stress associated with working long shifts, including overnights and the general level of stress associated with healthcare roles causes chronic inflammation and this might also cause a more severe set of symptoms too. Bus/public transport drivers tend to work shifts too, especially in London, where it would seem a larger number of such workers have been affected. Up here in't North, for example, bus and train services have been severely curtailed since the lockdown began, with services starting later and ending earlier in the day than is usual. I believe TfL are still operating nightbuses etc; whereas we don't actually have nightbuses even on a "good" day here in Manchester anymore really. They were withdrawn a couple of years ago by TfGM. 3) ACE2 and its role in SARS-CoV-2 - OK, so this is where it might be harder to stay away from the complex science that I love so much
ACE stands for angiotensin-cleaving enzyme. Put simply, this is an enzyme found in the cell membranes of many human cells that is involved in the chopping (cleaving) of a hormone called angiotensin. Among many things, angiotensin is responsible for regulating blood pressure, through the constriction of the muscle within blood vessels. Higher active angiotensin = constriction of blood vessels; less active angiotensin = relaxation of blood vessels. ACE2 is the "opposite number" ACE. ACE2 causes the chopped angiotensin, that causes constriction of blood vessels, to be converted into a different form that is biologically inactive, therefore blood vessels dilate again. ACE2 was identified in the last SARS outbreak, in 2004, as the binding site for some coronaviruses, including SARS viruses and a couple of other coronaviruses. Viruses must enter into a host cell to reproduce themselves, as they do not contain the cellular machinery required to copy their own genetic information, so viruses effectively "trick" cells into allowing them to enter. This is a complex thing which I won't go into much, but suffice to say it is like a lock and key situation. The lock is the receptor (in this case, ACE2) and the key would usually be the biologically active form of angiotensin. All proteins have a specific 3D shape, but viral proteins on their surface mimic these "key" shapes, to facilitate entry to cells, a bit like a master key allowing access to any lock.
ACE and ACE2 are found in considerable levels in specific cells of the alveoli (the deepest parts of the lung, found at the end of the bronchioles); the small intestine and in smaller amounts in the kidney and other organs. This makes sense, because regulation of blood pressure is especially fundamental in organs that rely on specific pressures for normal function (OK, all organs rely on this, but the lungs require very specific blood pressures in order to efficiently exchange oxygen and carbon dioxide). The small intestine is exceptionally vascular, as this is the site of the absorption of the micronutrients from digestion, and absorption is directly into blood vessels. We require oxygen via the lungs, and glucose via the small intestine to perform aerobic respiration (the means by which we can convert the energy from nutrients into a form available for us to use for movement etc). The kidneys are the site of the majority of the fluid balancing via excretion of water and also considerably involve in regulation of ions, such as sodium and potassium. These ions are also involved in maintenance of normal blood pressure and so the presence of large concentrations of ACE and ACE2 make sense. I hope I did not digress too much.
We all have different genetic sequences (ish) that generate overall the same protein, so one (wo)man's ACE/ACE2 is not the same as another's. Plenty of research has gone into polymorphisms (the genetic variations found between people) and concluded that polymorphisms did not contribute to the difference in disease processes in the SARS outbreak in 2004. This SARS-CoV-2 is exceptionally similar to SARS, and so it is likely this is also the case this time: Info here, for example: https://academic.oup.com/clinchem/article/50/9/1683/5640134
- ACE2 is coded for on the human X-chromosome. As we probably know, human females have 2 X chromosomes, and human males have 1 X chromosome. There is a hypothesis that due to males only having the 1 copy of ACE2, that they might be more susceptible, but that would only hold water if having genetic variants of ACE2 was significant, which the research above from the SARS outbreak said was not. That doesn't mean 100% that it isn't and it's probably too early yet to have enough data from the SARS-CoV-2 outbreak to back that up. The increased severity/deaths in males might be related to males being more likely to have the co-morbidities that we know increase risk (heart conditions, diabetes, etc); because males are more likely to smoke and consume alcohol in excess; because males are less likely to seek medical advice early/visit doctors for routine health screening that might pick up underlying conditions. There are too many unknowns right now to fully explain that stat, but if you look at the ICU admission data above, the rate of admission of men vs women is pretty stark: 72.5% male for Covid-19 related admissions vs 54.3% males for non-Covid related pneumonias. However, note the data set of the non-Covid related pneumonias spans two calendar years (2017-19), so there will be varying pathogens circulating; both bacterial and viral, and the number of patients in the non-Covid data set is about double that of the Covid-19 dataset, so that allows smaller numbers to be seen more prominently in the overall percentages.
OK, that's enough science for now, and sorry for waffling on
N
BSc (Hons) Microbiology; lecturer of biology, physiology and medical health sciences in an institution somewhere in the vicinity of Manchester "Just wondering if you've seen this paper and if so, what your thoughts were: https://pubmed.ncbi.nlm.nih.gov/32142651/ | |||
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"OK, here goes, and sorry if I miss any points raised by previous commentators: 1) Viral load theory (the theory that people are infected with more particles of SARS-Cov-2 are more likely to have more severe disease) - This works out for some diseases, but the evidence so far for SARS-CoV-2 is that this is not the case. Two studies (obviously not huge scale) have disproven this theory. One in Lombardy, the most affected part of Italy, and another in China, found no difference in viral load and severity of disease. What viral load will indicate is how infectious an individual might be, because viral load correlates to viral shedding. We don't yet know the infectious dose for SARS-CoV-2, but it is likely to be fairly low, given the ease at which is seems to pass from person to person. This New Scientist article deals with the viral load hypothesis in fairly easy to understand terms: https://www.newscientist.com/article/2238819-does-a-high-viral-load-or-infectious-dose-make-covid-19-worse/ 2) Why are apparently healthy medics, bus drivers etc succumbing to Covid-19? - A few things here. 1) Apparently healthy and actually healthy are two different things. People may walk around without any obvious signs/symptoms of an underlying medical condition for some considerable time, and it is often routine screening that uncovers issues before people show symptoms. An example would be that hypertension does not really cause any observable outward symptoms in the patient, but it easily identified with a blood pressure test and the patient is usually totally unaware they have it. For example, evidence from routine screening is that far more people have high blood pressure than realise it (e.g. when they do drop-in screening in shopping centres etc). Also, we don't know if any of the individuals smoked (smoking increases the risk of any respiratory disease being severe) or any other information about lifestyle, which might pre-dispose them to poorer outcomes. 2) Weight seems to be playing a huge factor in the severity of disease; quote: "Data from the first 2204 patients admitted to 286 NHS ICUs with COVID- 19 reveal that 72.7% of them were overweight or obese. We shouldn’t ignore the fact that 50-60% % of the 1.4 million NHS workforce are themselves overweight or obese too." Data for the ICU admissions here: https://www.icnarc.org/DataServices/Attachments/Download/c31dd38d-d77b-ea11-9124-00505601089b Evidence for the data on NHS workforce obesity/weight: https://bmjopen.bmj.com/content/7/12/e018498 It is also true that the chronic stress associated with working long shifts, including overnights and the general level of stress associated with healthcare roles causes chronic inflammation and this might also cause a more severe set of symptoms too. Bus/public transport drivers tend to work shifts too, especially in London, where it would seem a larger number of such workers have been affected. Up here in't North, for example, bus and train services have been severely curtailed since the lockdown began, with services starting later and ending earlier in the day than is usual. I believe TfL are still operating nightbuses etc; whereas we don't actually have nightbuses even on a "good" day here in Manchester anymore really. They were withdrawn a couple of years ago by TfGM. 3) ACE2 and its role in SARS-CoV-2 - OK, so this is where it might be harder to stay away from the complex science that I love so much
ACE stands for angiotensin-cleaving enzyme. Put simply, this is an enzyme found in the cell membranes of many human cells that is involved in the chopping (cleaving) of a hormone called angiotensin. Among many things, angiotensin is responsible for regulating blood pressure, through the constriction of the muscle within blood vessels. Higher active angiotensin = constriction of blood vessels; less active angiotensin = relaxation of blood vessels. ACE2 is the "opposite number" ACE. ACE2 causes the chopped angiotensin, that causes constriction of blood vessels, to be converted into a different form that is biologically inactive, therefore blood vessels dilate again. ACE2 was identified in the last SARS outbreak, in 2004, as the binding site for some coronaviruses, including SARS viruses and a couple of other coronaviruses. Viruses must enter into a host cell to reproduce themselves, as they do not contain the cellular machinery required to copy their own genetic information, so viruses effectively "trick" cells into allowing them to enter. This is a complex thing which I won't go into much, but suffice to say it is like a lock and key situation. The lock is the receptor (in this case, ACE2) and the key would usually be the biologically active form of angiotensin. All proteins have a specific 3D shape, but viral proteins on their surface mimic these "key" shapes, to facilitate entry to cells, a bit like a master key allowing access to any lock.
ACE and ACE2 are found in considerable levels in specific cells of the alveoli (the deepest parts of the lung, found at the end of the bronchioles); the small intestine and in smaller amounts in the kidney and other organs. This makes sense, because regulation of blood pressure is especially fundamental in organs that rely on specific pressures for normal function (OK, all organs rely on this, but the lungs require very specific blood pressures in order to efficiently exchange oxygen and carbon dioxide). The small intestine is exceptionally vascular, as this is the site of the absorption of the micronutrients from digestion, and absorption is directly into blood vessels. We require oxygen via the lungs, and glucose via the small intestine to perform aerobic respiration (the means by which we can convert the energy from nutrients into a form available for us to use for movement etc). The kidneys are the site of the majority of the fluid balancing via excretion of water and also considerably involve in regulation of ions, such as sodium and potassium. These ions are also involved in maintenance of normal blood pressure and so the presence of large concentrations of ACE and ACE2 make sense. I hope I did not digress too much.
We all have different genetic sequences (ish) that generate overall the same protein, so one (wo)man's ACE/ACE2 is not the same as another's. Plenty of research has gone into polymorphisms (the genetic variations found between people) and concluded that polymorphisms did not contribute to the difference in disease processes in the SARS outbreak in 2004. This SARS-CoV-2 is exceptionally similar to SARS, and so it is likely this is also the case this time: Info here, for example: https://academic.oup.com/clinchem/article/50/9/1683/5640134
- ACE2 is coded for on the human X-chromosome. As we probably know, human females have 2 X chromosomes, and human males have 1 X chromosome. There is a hypothesis that due to males only having the 1 copy of ACE2, that they might be more susceptible, but that would only hold water if having genetic variants of ACE2 was significant, which the research above from the SARS outbreak said was not. That doesn't mean 100% that it isn't and it's probably too early yet to have enough data from the SARS-CoV-2 outbreak to back that up. The increased severity/deaths in males might be related to males being more likely to have the co-morbidities that we know increase risk (heart conditions, diabetes, etc); because males are more likely to smoke and consume alcohol in excess; because males are less likely to seek medical advice early/visit doctors for routine health screening that might pick up underlying conditions. There are too many unknowns right now to fully explain that stat, but if you look at the ICU admission data above, the rate of admission of men vs women is pretty stark: 72.5% male for Covid-19 related admissions vs 54.3% males for non-Covid related pneumonias. However, note the data set of the non-Covid related pneumonias spans two calendar years (2017-19), so there will be varying pathogens circulating; both bacterial and viral, and the number of patients in the non-Covid data set is about double that of the Covid-19 dataset, so that allows smaller numbers to be seen more prominently in the overall percentages.
OK, that's enough science for now, and sorry for waffling on
N
BSc (Hons) Microbiology; lecturer of biology, physiology and medical health sciences in an institution somewhere in the vicinity of Manchester "Thank you | |||
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"Question. How come some people can get covid 19 with little or no effects while others die? Especially healthy nurses and healthy bus drivers. I pondered this and came up with the following hypothesis. The common cold aka Rhino virus can be caught twice at the same time. Or " A cold on top of a cold." And inevitably your symptoms will be worse. This lends itself to the notion that covid can be the same. "Covid on top of covid." With the same result of worse symptoms. If this is correct. It would explain why there is such a dramatic variation of the severity of symptoms. Particularly to those who are likely to have repeated exposure to covid ie. Nurses and bus drivers. Is there anything in this or do I just have a great imagination? I'm not a scientist. But it seems logical. But like I said don't know shit because I'm not a scientist. Hence I'm asking the question? "Over exposure and incomparable immune system. | |||
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" Just wondering if you've seen this paper and if so, what your thoughts were: https://pubmed.ncbi.nlm.nih.gov/32142651/ " I'd read a bit about the drug, camostat, that has been suggested as being a possible option, which is partly what this paper from "Cell" discusses. A couple of things: 1) Camostat is already approved in Japan and Korea for pancreatitis. It does not follow that this drug would be able to target cells in the respiratory system at all or with the same efficacy as it targets pancreatic cells. That remains to be deduced. 2) The Danes are already trialling it (camostat) so there should be some data in the next few months. 3) The research was done in cell lines in-vitro, and with anything, again does not guarantee the same response in the whole organism (in-vivo). The Danes might be able to expand on that soon. 4) The cross efficacy of plasma from recovered SARS patients is interesting. We are trialling already the use of plasma from recovered Covid-19 patients, to see if that can reduce severity or to shorten the stays in critical care/ICU. Its worth noting that neither of the things above are cures and at best, would perhaps reduce severity, reduce duration of symptoms etc, if they work in the real life patient at all. To many unknowns again, unfortunately! | |||
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" Just wondering if you've seen this paper and if so, what your thoughts were: https://pubmed.ncbi.nlm.nih.gov/32142651/ I'd read a bit about the drug, camostat, that has been suggested as being a possible option, which is partly what this paper from "Cell" discusses. A couple of things: 1) Camostat is already approved in Japan and Korea for pancreatitis. It does not follow that this drug would be able to target cells in the respiratory system at all or with the same efficacy as it targets pancreatic cells. That remains to be deduced. 2) The Danes are already trialling it (camostat) so there should be some data in the next few months. 3) The research was done in cell lines in-vitro, and with anything, again does not guarantee the same response in the whole organism (in-vivo). The Danes might be able to expand on that soon. 4) The cross efficacy of plasma from recovered SARS patients is interesting. We are trialling already the use of plasma from recovered Covid-19 patients, to see if that can reduce severity or to shorten the stays in critical care/ICU. Its worth noting that neither of the things above are cures and at best, would perhaps reduce severity, reduce duration of symptoms etc, if they work in the real life patient at all. To many unknowns again, unfortunately! " Thanks, appreciate your reply and original post. So you're saying it doesn't seem to be genetic differences or viral load. Weight makes a difference but isn't there something else? In harbin, super spreader flew in from miami. She infected 44 other people (known because of contact tracing) of which 19 were asymptomatic. 19/44 is huge. Surely there's a major factor at play in why so many people are asymptomatic? | |||
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" Thanks, appreciate your reply and original post. So you're saying it doesn't seem to be genetic differences or viral load. Weight makes a difference but isn't there something else? In harbin, super spreader flew in from miami. She infected 44 other people (known because of contact tracing) of which 19 were asymptomatic. 19/44 is huge. Surely there's a major factor at play in why so many people are asymptomatic? " Hey, it's fine, I'm on a busman's holiday here - I could chat shit about biology until someone tells me get stuffed! Asymptomatic is a big difference to the whole severity thing. Recent data discussed in the BMJ suggests that as many as 4/5 cases of Covid-19 are asymptomatic https://www.bmj.com/content/369/bmj.m1375 I don't think we fully understand the reason why, but it's probably related to how people's immune systems react to the infection. The asymptomatic people can still infect others - they are infected and shedding virus, but they aren't showing symptoms. Now, how the immune system responds to infection is, in part, genetic. What the research I shared earlier said is that it is unlikely to be genetic differences in the sequences of ACE2 that determine the severity. It doesn't mean there are no genetic factors at all. The fact that the vast majority of children and people under about 16-18 are either asymptomatic or have very short duration symptoms would suggest that genetic factors of the immune response aren't the only factors though. Not all children worldwide have the same immune system from a genetic perspective. It is likely that the very low likelihood of comorbidities in children, such as a low likelihood of cardiovascular disease relating to blood pressure/atherosclerosis; low/no smoking etc are having strong contributions too. Basically, until we get a lot more data on the rate of infection population wide, how many of those people had symptoms, how many were severely ill or died, what comorbidities they had or not etc etc, then a lot is simply hypothetical. | |||
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"I’m not a scientist either and I await the microbiologist reply. I believe that it’s to do with viral load. If you touched a surface that had a small amount of the virus and then that got into your system, if you are otherwise healthy, then your immune system should be able to fight it off. If you are in a hospital and the virus is everywhere and when you do get exposed to it there is a chance that someone is sneezing on you then when you get it your viral load is a lot higher. It is then harder for your immune system to cope and therefore you are more likely to get more seriously ill. " This is about right. They've tested this theory with other viruses on mice etc and found it to be the case. A virolologist on the radio last week was saying they thought this was the same for Covid although they haven't tested it yet. | |||
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"Question. How come some people can get covid 19 with little or no effects while others die? Especially healthy nurses and healthy bus drivers. I pondered this and came up with the following hypothesis. The common cold aka Rhino virus can be caught twice at the same time. Or " A cold on top of a cold." And inevitably your symptoms will be worse. This lends itself to the notion that covid can be the same. "Covid on top of covid." With the same result of worse symptoms. If this is correct. It would explain why there is such a dramatic variation of the severity of symptoms. Particularly to those who are likely to have repeated exposure to covid ie. Nurses and bus drivers. Is there anything in this or do I just have a great imagination? I'm not a scientist. But it seems logical. But like I said don't know shit because I'm not a scientist. Hence I'm asking the question?
As a scientist involved in infectious disease (bacterial not viral) there are a couple of assumptions you made which need correcting The number of viruses which cause the common cold are in the 100s, including 4 coronaviruses. So if you do have cold on top of a cold, it's because they're different viruses. This isn't possible with COVID-19 as it's one virus, like you can't get HIV on top of HIV (which would be fucking awful if it were the case!).
The main variation is due to underlying co-morbitities, esp in the older patients. But this is a virus to which we've not had exposure before, and currently we don't quite know why some do better and others (without a co-morbitity) do worse. The specialists at my company are discussing that the virus may not be causing what's called ARDS but something else, esp in direct damage to the lungs (vascular injury).
Also if you want another overview to help, check Dr Mike Hansen on YouTube as he has a vid on why it kills some but not others. "You can get multiple strains of HIV just to let you know. 2 main types of HIV and then there is sub strains so you can be infected with more than 1 strain at the same time. Which is a problem since most people think there's only 1 hiv so people who are hiv positive neglect to use protection when having sex then soon discover they have 2 strains of hiv which complicates matters. Not all the drugs for HIV work since they focus on the largest group infected with HIV 1 sub strain b. So yeah it's fucking awful just to catch one let alone two. People think there's a treatment for all HIV that isn't the case. | |||
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" Thanks, appreciate your reply and original post. So you're saying it doesn't seem to be genetic differences or viral load. Weight makes a difference but isn't there something else? In harbin, super spreader flew in from miami. She infected 44 other people (known because of contact tracing) of which 19 were asymptomatic. 19/44 is huge. Surely there's a major factor at play in why so many people are asymptomatic? Hey, it's fine, I'm on a busman's holiday here - I could chat shit about biology until someone tells me get stuffed! Asymptomatic is a big difference to the whole severity thing. Recent data discussed in the BMJ suggests that as many as 4/5 cases of Covid-19 are asymptomatic https://www.bmj.com/content/369/bmj.m1375 I don't think we fully understand the reason why, but it's probably related to how people's immune systems react to the infection. The asymptomatic people can still infect others - they are infected and shedding virus, but they aren't showing symptoms. Now, how the immune system responds to infection is, in part, genetic. What the research I shared earlier said is that it is unlikely to be genetic differences in the sequences of ACE2 that determine the severity. It doesn't mean there are no genetic factors at all. The fact that the vast majority of children and people under about 16-18 are either asymptomatic or have very short duration symptoms would suggest that genetic factors of the immune response aren't the only factors though. Not all children worldwide have the same immune system from a genetic perspective. It is likely that the very low likelihood of comorbidities in children, such as a low likelihood of cardiovascular disease relating to blood pressure/atherosclerosis; low/no smoking etc are having strong contributions too. Basically, until we get a lot more data on the rate of infection population wide, how many of those people had symptoms, how many were severely ill or died, what comorbidities they had or not etc etc, then a lot is simply hypothetical. " Not sure if you've seen the news but France have an aircraft carrier that got infected. It's got roughly 2,000 people onboard and 49% tested positive. Would you suppose that 51% didn't get exposed to the virus or that there's some mechanism by which they can't be infected? I'm a bit confused whether an immune person tests as nothing or asymptomatic. Aircraft carriers are the biggest ship the French have, but there are 3 instances of ships getting outbreaks and in all cases, less than half got infected. | |||
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"OK, here goes, and sorry if I miss any points raised by previous commentators: 1) Viral load theory (the theory that people are infected with more particles of SARS-Cov-2 are more likely to have more severe disease) - This works out for some diseases, but the evidence so far for SARS-CoV-2 is that this is not the case. Two studies (obviously not huge scale) have disproven this theory. One in Lombardy, the most affected part of Italy, and another in China, found no difference in viral load and severity of disease. What viral load will indicate is how infectious an individual might be, because viral load correlates to viral shedding. We don't yet know the infectious dose for SARS-CoV-2, but it is likely to be fairly low, given the ease at which is seems to pass from person to person. This New Scientist article deals with the viral load hypothesis in fairly easy to understand terms: https://www.newscientist.com/article/2238819-does-a-high-viral-load-or-infectious-dose-make-covid-19-worse/ 2) Why are apparently healthy medics, bus drivers etc succumbing to Covid-19? - A few things here. 1) Apparently healthy and actually healthy are two different things. People may walk around without any obvious signs/symptoms of an underlying medical condition for some considerable time, and it is often routine screening that uncovers issues before people show symptoms. An example would be that hypertension does not really cause any observable outward symptoms in the patient, but it easily identified with a blood pressure test and the patient is usually totally unaware they have it. For example, evidence from routine screening is that far more people have high blood pressure than realise it (e.g. when they do drop-in screening in shopping centres etc). Also, we don't know if any of the individuals smoked (smoking increases the risk of any respiratory disease being severe) or any other information about lifestyle, which might pre-dispose them to poorer outcomes. 2) Weight seems to be playing a huge factor in the severity of disease; quote: "Data from the first 2204 patients admitted to 286 NHS ICUs with COVID- 19 reveal that 72.7% of them were overweight or obese. We shouldn’t ignore the fact that 50-60% % of the 1.4 million NHS workforce are themselves overweight or obese too." Data for the ICU admissions here: https://www.icnarc.org/DataServices/Attachments/Download/c31dd38d-d77b-ea11-9124-00505601089b Evidence for the data on NHS workforce obesity/weight: https://bmjopen.bmj.com/content/7/12/e018498 It is also true that the chronic stress associated with working long shifts, including overnights and the general level of stress associated with healthcare roles causes chronic inflammation and this might also cause a more severe set of symptoms too. Bus/public transport drivers tend to work shifts too, especially in London, where it would seem a larger number of such workers have been affected. Up here in't North, for example, bus and train services have been severely curtailed since the lockdown began, with services starting later and ending earlier in the day than is usual. I believe TfL are still operating nightbuses etc; whereas we don't actually have nightbuses even on a "good" day here in Manchester anymore really. They were withdrawn a couple of years ago by TfGM. 3) ACE2 and its role in SARS-CoV-2 - OK, so this is where it might be harder to stay away from the complex science that I love so much
ACE stands for angiotensin-cleaving enzyme. Put simply, this is an enzyme found in the cell membranes of many human cells that is involved in the chopping (cleaving) of a hormone called angiotensin. Among many things, angiotensin is responsible for regulating blood pressure, through the constriction of the muscle within blood vessels. Higher active angiotensin = constriction of blood vessels; less active angiotensin = relaxation of blood vessels. ACE2 is the "opposite number" ACE. ACE2 causes the chopped angiotensin, that causes constriction of blood vessels, to be converted into a different form that is biologically inactive, therefore blood vessels dilate again. ACE2 was identified in the last SARS outbreak, in 2004, as the binding site for some coronaviruses, including SARS viruses and a couple of other coronaviruses. Viruses must enter into a host cell to reproduce themselves, as they do not contain the cellular machinery required to copy their own genetic information, so viruses effectively "trick" cells into allowing them to enter. This is a complex thing which I won't go into much, but suffice to say it is like a lock and key situation. The lock is the receptor (in this case, ACE2) and the key would usually be the biologically active form of angiotensin. All proteins have a specific 3D shape, but viral proteins on their surface mimic these "key" shapes, to facilitate entry to cells, a bit like a master key allowing access to any lock.
ACE and ACE2 are found in considerable levels in specific cells of the alveoli (the deepest parts of the lung, found at the end of the bronchioles); the small intestine and in smaller amounts in the kidney and other organs. This makes sense, because regulation of blood pressure is especially fundamental in organs that rely on specific pressures for normal function (OK, all organs rely on this, but the lungs require very specific blood pressures in order to efficiently exchange oxygen and carbon dioxide). The small intestine is exceptionally vascular, as this is the site of the absorption of the micronutrients from digestion, and absorption is directly into blood vessels. We require oxygen via the lungs, and glucose via the small intestine to perform aerobic respiration (the means by which we can convert the energy from nutrients into a form available for us to use for movement etc). The kidneys are the site of the majority of the fluid balancing via excretion of water and also considerably involve in regulation of ions, such as sodium and potassium. These ions are also involved in maintenance of normal blood pressure and so the presence of large concentrations of ACE and ACE2 make sense. I hope I did not digress too much.
We all have different genetic sequences (ish) that generate overall the same protein, so one (wo)man's ACE/ACE2 is not the same as another's. Plenty of research has gone into polymorphisms (the genetic variations found between people) and concluded that polymorphisms did not contribute to the difference in disease processes in the SARS outbreak in 2004. This SARS-CoV-2 is exceptionally similar to SARS, and so it is likely this is also the case this time: Info here, for example: https://academic.oup.com/clinchem/article/50/9/1683/5640134
- ACE2 is coded for on the human X-chromosome. As we probably know, human females have 2 X chromosomes, and human males have 1 X chromosome. There is a hypothesis that due to males only having the 1 copy of ACE2, that they might be more susceptible, but that would only hold water if having genetic variants of ACE2 was significant, which the research above from the SARS outbreak said was not. That doesn't mean 100% that it isn't and it's probably too early yet to have enough data from the SARS-CoV-2 outbreak to back that up. The increased severity/deaths in males might be related to males being more likely to have the co-morbidities that we know increase risk (heart conditions, diabetes, etc); because males are more likely to smoke and consume alcohol in excess; because males are less likely to seek medical advice early/visit doctors for routine health screening that might pick up underlying conditions. There are too many unknowns right now to fully explain that stat, but if you look at the ICU admission data above, the rate of admission of men vs women is pretty stark: 72.5% male for Covid-19 related admissions vs 54.3% males for non-Covid related pneumonias. However, note the data set of the non-Covid related pneumonias spans two calendar years (2017-19), so there will be varying pathogens circulating; both bacterial and viral, and the number of patients in the non-Covid data set is about double that of the Covid-19 dataset, so that allows smaller numbers to be seen more prominently in the overall percentages.
OK, that's enough science for now, and sorry for waffling on
N
BSc (Hons) Microbiology; lecturer of biology, physiology and medical health sciences in an institution somewhere in the vicinity of Manchester "So to sum up. I'm a man over 50, I'm over weight but quite muscular, I have type 2 diabetes, high cholesterol, severe asthma and high blood pressure. I'm fucked right? | |||
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"This is about right. They've tested this theory with other viruses on mice etc and found it to be the case. A virolologist on the radio last week was saying they thought this was the same for Covid although they haven't tested it yet." Viral load does not refer to the amount of exposure pre infection; it refers to the amount of viral particles that can be isolated from the patient after infection. The number of particles needed to causes infection (symptomatic or asymptomatic) is unknown at the moment, but is likely to be pretty small, considering how easy it is to acquire this infection. The number of initial particles a person is infected with doesn't necessarily correlate with viral load (amount that can be isolated from the patient post-infection) It is possible that a higher initial infectious dose (ie more viral particles at the start of the infection) might correlate with symptom severity, as it does in some other viral illness. Small scale data from the 2004 SARS outbreak, from Hong Kong, does not support this theory, but the data set is very small. We need far more data before we can conclude if higher infectious doses, which healthcare workers may be exposed to, are linked to poorer outcomes. | |||
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" So to sum up. I'm a man over 50, I'm over weight but quite muscular, I have type 2 diabetes, high cholesterol, severe asthma and high blood pressure. I'm fucked right?" Not fucked, just at increased risk of a more severe illness. Having comorbidities does not guarantee worse outcome, but it does make it more likely, unfortunately. | |||
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" So to sum up. I'm a man over 50, I'm over weight but quite muscular, I have type 2 diabetes, high cholesterol, severe asthma and high blood pressure. I'm fucked right? Not fucked, just at increased risk of a more severe illness. Having comorbidities does not guarantee worse outcome, but it does make it more likely, unfortunately. " No worries I know one of them is going to get me eventually. | |||
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" Not sure if you've seen the news but France have an aircraft carrier that got infected. It's got roughly 2,000 people onboard and 49% tested positive. Would you suppose that 51% didn't get exposed to the virus or that there's some mechanism by which they can't be infected? I'm a bit confused whether an immune person tests as nothing or asymptomatic. Aircraft carriers are the biggest ship the French have, but there are 3 instances of ships getting outbreaks and in all cases, less than half got infected. " I have indeed seen. Due to incubation period, it is possible more will test positive in the coming days/two weeks or so. They have quarantined those who tested negative I believe. So, just because they were negative upon docking does not mean that they will remain so. During the incubation period, there will be insufficient viral RNA to produce a positive result. Asymptomatic is not the same as negative. An asymptomatic person is infected with the virus and tests positive, but has no symptoms. This is pretty common in viral infections, either for the duration of the infection or for certain periods of the infection. Eg, someone with herpes simplex (cold sore virus) is asymptomatic for prolonged periods, sometimes many years, but is still infected with the virus for life after they acquire it. | |||
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" Not sure if you've seen the news but France have an aircraft carrier that got infected. It's got roughly 2,000 people onboard and 49% tested positive. Would you suppose that 51% didn't get exposed to the virus or that there's some mechanism by which they can't be infected? I'm a bit confused whether an immune person tests as nothing or asymptomatic. Aircraft carriers are the biggest ship the French have, but there are 3 instances of ships getting outbreaks and in all cases, less than half got infected. I have indeed seen. Due to incubation period, it is possible more will test positive in the coming days/two weeks or so. They have quarantined those who tested negative I believe. So, just because they were negative upon docking does not mean that they will remain so. During the incubation period, there will be insufficient viral RNA to produce a positive result. Asymptomatic is not the same as negative. An asymptomatic person is infected with the virus and tests positive, but has no symptoms. This is pretty common in viral infections, either for the duration of the infection or for certain periods of the infection. Eg, someone with herpes simplex (cold sore virus) is asymptomatic for prolonged periods, sometimes many years, but is still infected with the virus for life after they acquire it. " Thanks, really appreciate your time. I really want a test since I know I've been exposed, up close and personal with people who had it. So I really want to know if I test negative or asymptomatic. | |||
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" Not sure if you've seen the news but France have an aircraft carrier that got infected. It's got roughly 2,000 people onboard and 49% tested positive. Would you suppose that 51% didn't get exposed to the virus or that there's some mechanism by which they can't be infected? I'm a bit confused whether an immune person tests as nothing or asymptomatic. Aircraft carriers are the biggest ship the French have, but there are 3 instances of ships getting outbreaks and in all cases, less than half got infected. I have indeed seen. Due to incubation period, it is possible more will test positive in the coming days/two weeks or so. They have quarantined those who tested negative I believe. So, just because they were negative upon docking does not mean that they will remain so. During the incubation period, there will be insufficient viral RNA to produce a positive result. Asymptomatic is not the same as negative. An asymptomatic person is infected with the virus and tests positive, but has no symptoms. This is pretty common in viral infections, either for the duration of the infection or for certain periods of the infection. Eg, someone with herpes simplex (cold sore virus) is asymptomatic for prolonged periods, sometimes many years, but is still infected with the virus for life after they acquire it. " While making total sense (they tell you to wait 2 weeks after unprotected sex before you test for stds so you get an accurate result) ... it hadnt occurred to me before that people could have the virus, still be incubating and test negative ... the thought it terrifying for what that means in terms of testing being enough to get us all back out and about | |||
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" Not sure if you've seen the news but France have an aircraft carrier that got infected. It's got roughly 2,000 people onboard and 49% tested positive. Would you suppose that 51% didn't get exposed to the virus or that there's some mechanism by which they can't be infected? I'm a bit confused whether an immune person tests as nothing or asymptomatic. Aircraft carriers are the biggest ship the French have, but there are 3 instances of ships getting outbreaks and in all cases, less than half got infected. I have indeed seen. Due to incubation period, it is possible more will test positive in the coming days/two weeks or so. They have quarantined those who tested negative I believe. So, just because they were negative upon docking does not mean that they will remain so. During the incubation period, there will be insufficient viral RNA to produce a positive result. Asymptomatic is not the same as negative. An asymptomatic person is infected with the virus and tests positive, but has no symptoms. This is pretty common in viral infections, either for the duration of the infection or for certain periods of the infection. Eg, someone with herpes simplex (cold sore virus) is asymptomatic for prolonged periods, sometimes many years, but is still infected with the virus for life after they acquire it. While making total sense (they tell you to wait 2 weeks after unprotected sex before you test for stds so you get an accurate result) ... it hadnt occurred to me before that people could have the virus, still be incubating and test negative ... the thought it terrifying for what that means in terms of testing being enough to get us all back out and about " I wish to furnish this with a reply, but am switching off science mode for tonight and am instead going to take pictures of my arse
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" Not sure if you've seen the news but France have an aircraft carrier that got infected. It's got roughly 2,000 people onboard and 49% tested positive. Would you suppose that 51% didn't get exposed to the virus or that there's some mechanism by which they can't be infected? I'm a bit confused whether an immune person tests as nothing or asymptomatic. Aircraft carriers are the biggest ship the French have, but there are 3 instances of ships getting outbreaks and in all cases, less than half got infected. I have indeed seen. Due to incubation period, it is possible more will test positive in the coming days/two weeks or so. They have quarantined those who tested negative I believe. So, just because they were negative upon docking does not mean that they will remain so. During the incubation period, there will be insufficient viral RNA to produce a positive result. Asymptomatic is not the same as negative. An asymptomatic person is infected with the virus and tests positive, but has no symptoms. This is pretty common in viral infections, either for the duration of the infection or for certain periods of the infection. Eg, someone with herpes simplex (cold sore virus) is asymptomatic for prolonged periods, sometimes many years, but is still infected with the virus for life after they acquire it. Thanks, really appreciate your time. I really want a test since I know I've been exposed, up close and personal with people who had it. So I really want to know if I test negative or asymptomatic. "Some private clinics can test you (if you are willing to spend quite a lot) they have both PCR and antibody tests. But some antibody tests don't work very well so you might end up wasting money. (yes UK govern wasn't able to buy tests that work, but they do exist) Anyway this is the most interesting thread in this forum. Thanks to Kinky_couple2020 and to OP. | |||
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" Not sure if you've seen the news but France have an aircraft carrier that got infected. It's got roughly 2,000 people onboard and 49% tested positive. Would you suppose that 51% didn't get exposed to the virus or that there's some mechanism by which they can't be infected? I'm a bit confused whether an immune person tests as nothing or asymptomatic. Aircraft carriers are the biggest ship the French have, but there are 3 instances of ships getting outbreaks and in all cases, less than half got infected. I have indeed seen. Due to incubation period, it is possible more will test positive in the coming days/two weeks or so. They have quarantined those who tested negative I believe. So, just because they were negative upon docking does not mean that they will remain so. During the incubation period, there will be insufficient viral RNA to produce a positive result. Asymptomatic is not the same as negative. An asymptomatic person is infected with the virus and tests positive, but has no symptoms. This is pretty common in viral infections, either for the duration of the infection or for certain periods of the infection. Eg, someone with herpes simplex (cold sore virus) is asymptomatic for prolonged periods, sometimes many years, but is still infected with the virus for life after they acquire it. Thanks, really appreciate your time. I really want a test since I know I've been exposed, up close and personal with people who had it. So I really want to know if I test negative or asymptomatic.
Some private clinics can test you (if you are willing to spend quite a lot) they have both PCR and antibody tests. But some antibody tests don't work very well so you might end up wasting money. (yes UK govern wasn't able to buy tests that work, but they do exist)
Anyway this is the most interesting thread in this forum. Thanks to Kinky_couple2020 and to OP."I'm interested but I'm not £375 interested | |||
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"OK, here goes, and sorry if I miss any points raised by previous commentators: 1) Viral load theory (the theory that people are infected with more particles of SARS-Cov-2 are more likely to have more severe disease) - This works out for some diseases, but the evidence so far for SARS-CoV-2 is that this is not the case. Two studies (obviously not huge scale) have disproven this theory. One in Lombardy, the most affected part of Italy, and another in China, found no difference in viral load and severity of disease. What viral load will indicate is how infectious an individual might be, because viral load correlates to viral shedding. We don't yet know the infectious dose for SARS-CoV-2, but it is likely to be fairly low, given the ease at which is seems to pass from person to person. This New Scientist article deals with the viral load hypothesis in fairly easy to understand terms: https://www.newscientist.com/article/2238819-does-a-high-viral-load-or-infectious-dose-make-covid-19-worse/ 2) Why are apparently healthy medics, bus drivers etc succumbing to Covid-19? - A few things here. 1) Apparently healthy and actually healthy are two different things. People may walk around without any obvious signs/symptoms of an underlying medical condition for some considerable time, and it is often routine screening that uncovers issues before people show symptoms. An example would be that hypertension does not really cause any observable outward symptoms in the patient, but it easily identified with a blood pressure test and the patient is usually totally unaware they have it. For example, evidence from routine screening is that far more people have high blood pressure than realise it (e.g. when they do drop-in screening in shopping centres etc). Also, we don't know if any of the individuals smoked (smoking increases the risk of any respiratory disease being severe) or any other information about lifestyle, which might pre-dispose them to poorer outcomes. 2) Weight seems to be playing a huge factor in the severity of disease; quote: "Data from the first 2204 patients admitted to 286 NHS ICUs with COVID- 19 reveal that 72.7% of them were overweight or obese. We shouldn’t ignore the fact that 50-60% % of the 1.4 million NHS workforce are themselves overweight or obese too." Data for the ICU admissions here: https://www.icnarc.org/DataServices/Attachments/Download/c31dd38d-d77b-ea11-9124-00505601089b Evidence for the data on NHS workforce obesity/weight: https://bmjopen.bmj.com/content/7/12/e018498 It is also true that the chronic stress associated with working long shifts, including overnights and the general level of stress associated with healthcare roles causes chronic inflammation and this might also cause a more severe set of symptoms too. Bus/public transport drivers tend to work shifts too, especially in London, where it would seem a larger number of such workers have been affected. Up here in't North, for example, bus and train services have been severely curtailed since the lockdown began, with services starting later and ending earlier in the day than is usual. I believe TfL are still operating nightbuses etc; whereas we don't actually have nightbuses even on a "good" day here in Manchester anymore really. They were withdrawn a couple of years ago by TfGM. 3) ACE2 and its role in SARS-CoV-2 - OK, so this is where it might be harder to stay away from the complex science that I love so much
ACE stands for angiotensin-cleaving enzyme. Put simply, this is an enzyme found in the cell membranes of many human cells that is involved in the chopping (cleaving) of a hormone called angiotensin. Among many things, angiotensin is responsible for regulating blood pressure, through the constriction of the muscle within blood vessels. Higher active angiotensin = constriction of blood vessels; less active angiotensin = relaxation of blood vessels. ACE2 is the "opposite number" ACE. ACE2 causes the chopped angiotensin, that causes constriction of blood vessels, to be converted into a different form that is biologically inactive, therefore blood vessels dilate again. ACE2 was identified in the last SARS outbreak, in 2004, as the binding site for some coronaviruses, including SARS viruses and a couple of other coronaviruses. Viruses must enter into a host cell to reproduce themselves, as they do not contain the cellular machinery required to copy their own genetic information, so viruses effectively "trick" cells into allowing them to enter. This is a complex thing which I won't go into much, but suffice to say it is like a lock and key situation. The lock is the receptor (in this case, ACE2) and the key would usually be the biologically active form of angiotensin. All proteins have a specific 3D shape, but viral proteins on their surface mimic these "key" shapes, to facilitate entry to cells, a bit like a master key allowing access to any lock.
ACE and ACE2 are found in considerable levels in specific cells of the alveoli (the deepest parts of the lung, found at the end of the bronchioles); the small intestine and in smaller amounts in the kidney and other organs. This makes sense, because regulation of blood pressure is especially fundamental in organs that rely on specific pressures for normal function (OK, all organs rely on this, but the lungs require very specific blood pressures in order to efficiently exchange oxygen and carbon dioxide). The small intestine is exceptionally vascular, as this is the site of the absorption of the micronutrients from digestion, and absorption is directly into blood vessels. We require oxygen via the lungs, and glucose via the small intestine to perform aerobic respiration (the means by which we can convert the energy from nutrients into a form available for us to use for movement etc). The kidneys are the site of the majority of the fluid balancing via excretion of water and also considerably involve in regulation of ions, such as sodium and potassium. These ions are also involved in maintenance of normal blood pressure and so the presence of large concentrations of ACE and ACE2 make sense. I hope I did not digress too much.
We all have different genetic sequences (ish) that generate overall the same protein, so one (wo)man's ACE/ACE2 is not the same as another's. Plenty of research has gone into polymorphisms (the genetic variations found between people) and concluded that polymorphisms did not contribute to the difference in disease processes in the SARS outbreak in 2004. This SARS-CoV-2 is exceptionally similar to SARS, and so it is likely this is also the case this time: Info here, for example: https://academic.oup.com/clinchem/article/50/9/1683/5640134
- ACE2 is coded for on the human X-chromosome. As we probably know, human females have 2 X chromosomes, and human males have 1 X chromosome. There is a hypothesis that due to males only having the 1 copy of ACE2, that they might be more susceptible, but that would only hold water if having genetic variants of ACE2 was significant, which the research above from the SARS outbreak said was not. That doesn't mean 100% that it isn't and it's probably too early yet to have enough data from the SARS-CoV-2 outbreak to back that up. The increased severity/deaths in males might be related to males being more likely to have the co-morbidities that we know increase risk (heart conditions, diabetes, etc); because males are more likely to smoke and consume alcohol in excess; because males are less likely to seek medical advice early/visit doctors for routine health screening that might pick up underlying conditions. There are too many unknowns right now to fully explain that stat, but if you look at the ICU admission data above, the rate of admission of men vs women is pretty stark: 72.5% male for Covid-19 related admissions vs 54.3% males for non-Covid related pneumonias. However, note the data set of the non-Covid related pneumonias spans two calendar years (2017-19), so there will be varying pathogens circulating; both bacterial and viral, and the number of patients in the non-Covid data set is about double that of the Covid-19 dataset, so that allows smaller numbers to be seen more prominently in the overall percentages.
OK, that's enough science for now, and sorry for waffling on
N
BSc (Hons) Microbiology; lecturer of biology, physiology and medical health sciences in an institution somewhere in the vicinity of Manchester
So to sum up.
I'm a man over 50, I'm over weight but quite muscular, I have type 2 diabetes, high cholesterol, severe asthma and high blood pressure.
I'm fucked right?" | |||
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"OK, here goes, and sorry if I miss any points raised by previous commentators: 1) Viral load theory (the theory that people are infected with more particles of SARS-Cov-2 are more likely to have more severe disease) - This works out for some diseases, but the evidence so far for SARS-CoV-2 is that this is not the case. Two studies (obviously not huge scale) have disproven this theory. One in Lombardy, the most affected part of Italy, and another in China, found no difference in viral load and severity of disease. What viral load will indicate is how infectious an individual might be, because viral load correlates to viral shedding. We don't yet know the infectious dose for SARS-CoV-2, but it is likely to be fairly low, given the ease at which is seems to pass from person to person. This New Scientist article deals with the viral load hypothesis in fairly easy to understand terms: https://www.newscientist.com/article/2238819-does-a-high-viral-load-or-infectious-dose-make-covid-19-worse/ 2) Why are apparently healthy medics, bus drivers etc succumbing to Covid-19? - A few things here. 1) Apparently healthy and actually healthy are two different things. People may walk around without any obvious signs/symptoms of an underlying medical condition for some considerable time, and it is often routine screening that uncovers issues before people show symptoms. An example would be that hypertension does not really cause any observable outward symptoms in the patient, but it easily identified with a blood pressure test and the patient is usually totally unaware they have it. For example, evidence from routine screening is that far more people have high blood pressure than realise it (e.g. when they do drop-in screening in shopping centres etc). Also, we don't know if any of the individuals smoked (smoking increases the risk of any respiratory disease being severe) or any other information about lifestyle, which might pre-dispose them to poorer outcomes. 2) Weight seems to be playing a huge factor in the severity of disease; quote: "Data from the first 2204 patients admitted to 286 NHS ICUs with COVID- 19 reveal that 72.7% of them were overweight or obese. We shouldn’t ignore the fact that 50-60% % of the 1.4 million NHS workforce are themselves overweight or obese too." Data for the ICU admissions here: https://www.icnarc.org/DataServices/Attachments/Download/c31dd38d-d77b-ea11-9124-00505601089b Evidence for the data on NHS workforce obesity/weight: https://bmjopen.bmj.com/content/7/12/e018498 It is also true that the chronic stress associated with working long shifts, including overnights and the general level of stress associated with healthcare roles causes chronic inflammation and this might also cause a more severe set of symptoms too. Bus/public transport drivers tend to work shifts too, especially in London, where it would seem a larger number of such workers have been affected. Up here in't North, for example, bus and train services have been severely curtailed since the lockdown began, with services starting later and ending earlier in the day than is usual. I believe TfL are still operating nightbuses etc; whereas we don't actually have nightbuses even on a "good" day here in Manchester anymore really. They were withdrawn a couple of years ago by TfGM. 3) ACE2 and its role in SARS-CoV-2 - OK, so this is where it might be harder to stay away from the complex science that I love so much
ACE stands for angiotensin-cleaving enzyme. Put simply, this is an enzyme found in the cell membranes of many human cells that is involved in the chopping (cleaving) of a hormone called angiotensin. Among many things, angiotensin is responsible for regulating blood pressure, through the constriction of the muscle within blood vessels. Higher active angiotensin = constriction of blood vessels; less active angiotensin = relaxation of blood vessels. ACE2 is the "opposite number" ACE. ACE2 causes the chopped angiotensin, that causes constriction of blood vessels, to be converted into a different form that is biologically inactive, therefore blood vessels dilate again. ACE2 was identified in the last SARS outbreak, in 2004, as the binding site for some coronaviruses, including SARS viruses and a couple of other coronaviruses. Viruses must enter into a host cell to reproduce themselves, as they do not contain the cellular machinery required to copy their own genetic information, so viruses effectively "trick" cells into allowing them to enter. This is a complex thing which I won't go into much, but suffice to say it is like a lock and key situation. The lock is the receptor (in this case, ACE2) and the key would usually be the biologically active form of angiotensin. All proteins have a specific 3D shape, but viral proteins on their surface mimic these "key" shapes, to facilitate entry to cells, a bit like a master key allowing access to any lock.
ACE and ACE2 are found in considerable levels in specific cells of the alveoli (the deepest parts of the lung, found at the end of the bronchioles); the small intestine and in smaller amounts in the kidney and other organs. This makes sense, because regulation of blood pressure is especially fundamental in organs that rely on specific pressures for normal function (OK, all organs rely on this, but the lungs require very specific blood pressures in order to efficiently exchange oxygen and carbon dioxide). The small intestine is exceptionally vascular, as this is the site of the absorption of the micronutrients from digestion, and absorption is directly into blood vessels. We require oxygen via the lungs, and glucose via the small intestine to perform aerobic respiration (the means by which we can convert the energy from nutrients into a form available for us to use for movement etc). The kidneys are the site of the majority of the fluid balancing via excretion of water and also considerably involve in regulation of ions, such as sodium and potassium. These ions are also involved in maintenance of normal blood pressure and so the presence of large concentrations of ACE and ACE2 make sense. I hope I did not digress too much.
We all have different genetic sequences (ish) that generate overall the same protein, so one (wo)man's ACE/ACE2 is not the same as another's. Plenty of research has gone into polymorphisms (the genetic variations found between people) and concluded that polymorphisms did not contribute to the difference in disease processes in the SARS outbreak in 2004. This SARS-CoV-2 is exceptionally similar to SARS, and so it is likely this is also the case this time: Info here, for example: https://academic.oup.com/clinchem/article/50/9/1683/5640134
- ACE2 is coded for on the human X-chromosome. As we probably know, human females have 2 X chromosomes, and human males have 1 X chromosome. There is a hypothesis that due to males only having the 1 copy of ACE2, that they might be more susceptible, but that would only hold water if having genetic variants of ACE2 was significant, which the research above from the SARS outbreak said was not. That doesn't mean 100% that it isn't and it's probably too early yet to have enough data from the SARS-CoV-2 outbreak to back that up. The increased severity/deaths in males might be related to males being more likely to have the co-morbidities that we know increase risk (heart conditions, diabetes, etc); because males are more likely to smoke and consume alcohol in excess; because males are less likely to seek medical advice early/visit doctors for routine health screening that might pick up underlying conditions. There are too many unknowns right now to fully explain that stat, but if you look at the ICU admission data above, the rate of admission of men vs women is pretty stark: 72.5% male for Covid-19 related admissions vs 54.3% males for non-Covid related pneumonias. However, note the data set of the non-Covid related pneumonias spans two calendar years (2017-19), so there will be varying pathogens circulating; both bacterial and viral, and the number of patients in the non-Covid data set is about double that of the Covid-19 dataset, so that allows smaller numbers to be seen more prominently in the overall percentages.
OK, that's enough science for now, and sorry for waffling on
N
BSc (Hons) Microbiology; lecturer of biology, physiology and medical health sciences in an institution somewhere in the vicinity of Manchester
So to sum up.
I'm a man over 50, I'm over weight but quite muscular, I have type 2 diabetes, high cholesterol, severe asthma and high blood pressure.
I'm fucked right?"no. But I bet you'd like to be | |||
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"Just wanted to thank all those who took part. I don't have a conclusion to my question. However I have learnt so much and as they say Knowledge is power. Thank you all for taking part good luck, wash well, stay safe. "If you ask the unresolved question(s), again, we'll give it a bash to answer. | |||
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"There was a news story the other day stating that ace2 is more comman in men than woman with a higher concentration in your bollox which could explain the higher infection and mortality rate of men. I would take any report that talks like that with a pinch of salt (yes I know they wouldn't have said bollox). There are potential sex differences, but the easiest answer is women are more likely to raise concern and see a doctor than men and men's lifestyle habits. We don't know at this stage whether sex hormones or chromosomal differences play a part. Nor if there are racial differences but probably will once there is more data. More of concern is those with underlying issues and elderly, not whether you have a pair of balls "It is true that men have a greater expression of ACE2, because ACE2 is present in Sertoli cells (cells that assist in the maturation of sperm); spermatocytes (cells that go onto become sperm) and also in the testes elsewhere. There is data to suggest that Asian men express greater levels of ACE2 (https://www.thelancet.com/journals/lanres/article/PIIS2213-2600(20)30117-X/fulltext) and this might so someway to explain why men from this ethnic group seem to be more pre-disposed to severe illness. The testes theory is also being investigated as a reason why men are experiencing more severe disease. This is pre-peer review: https://www.medrxiv.org/content/10.1101/2020.04.16.20060566v1 | |||
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" I have indeed seen. Due to incubation period, it is possible more will test positive in the coming days/two weeks or so. They have quarantined those who tested negative I believe. So, just because they were negative upon docking does not mean that they will remain so. During the incubation period, there will be insufficient viral RNA to produce a positive result. Asymptomatic is not the same as negative. An asymptomatic person is infected with the virus and tests positive, but has no symptoms. This is pretty common in viral infections, either for the duration of the infection or for certain periods of the infection. Eg, someone with herpes simplex (cold sore virus) is asymptomatic for prolonged periods, sometimes many years, but is still infected with the virus for life after they acquire it. While making total sense (they tell you to wait 2 weeks after unprotected sex before you test for stds so you get an accurate result) ... it hadnt occurred to me before that people could have the virus, still be incubating and test negative ... the thought it terrifying for what that means in terms of testing being enough to get us all back out and about I wish to furnish this with a reply, but am switching off science mode for tonight and am instead going to take pictures of my arse
I'll come back to this tomorrow! "When you become infected with a virus, there is a lag period during which you are infected (and therefore might be infectious), but the viral particles that started the infection are too few to cause overt symptoms. Viral particles manage to "hide" within cells initially and therefore are hidden from the immune system. Once the virus has successfully replicated itself, in order to infect more cells, the viral particles must burst out of cells and it is at this point that the masquerade ends and the immune system becomes aware of the infection. By this time, infection is well established. The symptoms you get with a viral infection are principally due to the reaction of the immune system and the damage to the infected cells which burst and need to be "hoovered" up by the immune system. | |||
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" I have indeed seen. Due to incubation period, it is possible more will test positive in the coming days/two weeks or so. They have quarantined those who tested negative I believe. So, just because they were negative upon docking does not mean that they will remain so. During the incubation period, there will be insufficient viral RNA to produce a positive result. Asymptomatic is not the same as negative. An asymptomatic person is infected with the virus and tests positive, but has no symptoms. This is pretty common in viral infections, either for the duration of the infection or for certain periods of the infection. Eg, someone with herpes simplex (cold sore virus) is asymptomatic for prolonged periods, sometimes many years, but is still infected with the virus for life after they acquire it. While making total sense (they tell you to wait 2 weeks after unprotected sex before you test for stds so you get an accurate result) ... it hadnt occurred to me before that people could have the virus, still be incubating and test negative ... the thought it terrifying for what that means in terms of testing being enough to get us all back out and about I wish to furnish this with a reply, but am switching off science mode for tonight and am instead going to take pictures of my arse
I'll come back to this tomorrow!
When you become infected with a virus, there is a lag period during which you are infected (and therefore might be infectious), but the viral particles that started the infection are too few to cause overt symptoms. Viral particles manage to "hide" within cells initially and therefore are hidden from the immune system. Once the virus has successfully replicated itself, in order to infect more cells, the viral particles must burst out of cells and it is at this point that the masquerade ends and the immune system becomes aware of the infection. By this time, infection is well established. The symptoms you get with a viral infection are principally due to the reaction of the immune system and the damage to the infected cells which burst and need to be "hoovered" up by the immune system."This is all really interesting ... thanks for your reply | |||
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"Yes We Did - no worries. S and I both think we had it, we'd love to know for sure too, and seeing as he has the cough still a full 3 weeks after initially starting, we'd be interested to know if he's still infectious. We're assuming he is and he's staying at home all the time. He feels otherwise well, by the way. Data from China says the longest measured infectious period was something like 37 days, so it's perfectly possible. We'd love to have the tech at home to experiment on ourselves, saddos, eh "Is there any way you're aware that children could be carriers but not spread the virus? It sounds pretty strange. We know they get it, thousands did in China, but some people are claiming they don't spread it. I could understand them not spreading it as much, but is there aren't biological mechanism that could mean they can't spread at all? | |||
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) back in 2007.
Mr Bicpl | |||
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"Yes We Did - no worries. S and I both think we had it, we'd love to know for sure too, and seeing as he has the cough still a full 3 weeks after initially starting, we'd be interested to know if he's still infectious. We're assuming he is and he's staying at home all the time. He feels otherwise well, by the way. Data from China says the longest measured infectious period was something like 37 days, so it's perfectly possible. We'd love to have the tech at home to experiment on ourselves, saddos, eh
Is there any way you're aware that children could be carriers but not spread the virus? It sounds pretty strange. We know they get it, thousands did in China, but some people are claiming they don't spread it. I could understand them not spreading it as much, but is there aren't biological mechanism that could mean they can't spread at all? "Thanks to work getting in the way, only just getting round to answering these, sorry. In short, there is no mechanism I can think of whereby a child might be an asymptomatic "carrier" or reservoir of the virus, without also being infectious. There is, of course, limited data, but the best two pieces I can find shows some very intriguing things like: Children who have radiological signs of pneumonia (aka X-rays show they have pneumonia) BUT they remain asymptomatic. https://www.nejm.org/doi/full/10.1056/NEJMc2005073 This article also discusses asymptomatic infection in children, but also suggests children are potential vectors, whilst asymptomatic: https://www.thelancet.com/journals/laninf/article/PIIS1473-3099(20)30236-X/fulltext | |||
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"Thanks to Kinky_Couple, with whom have corresponded before (I'm a vaccine scientist), it's good to have a proper explanation rather than all the non-science (are you listening, Daily Mail) that is terrifying people. Question for Kinky, however: do you think that that SARS-COV-2 is able to be a more efficient replicant than, say another RNA virus, like 'flu, because of the positive-sense ssRNA? I haven't seen comment on this anywhere, apart from a paper in Clinical Microbiology Reviews (which I know you read at night ) back in 2007.
Mr Bicpl"Thanks, Mr BiCpl
I don't know of any specific data/papers which might state this for certain, but it makes sense that the positive-sense ssRNA viruses might replicate more quickly/effiently than the negative-sense ssRNA viruses. An example of +ve sense ssRNA viruses we know are efficient replicators/infectors are rhinoviruses (majority of common colds). Influenza viruses (orthomyxoviridae) are -ve sense ssRNA and we know the infectious dose needed to develop symptoms of 'flu (anything from 10^3 - 10^7 viral particles) are higher than the dose of rhinovirus needed to develop a cold (anything from 10^-1 to 10^5 viral particles). However, I don't have anything more empirical and it's impossible to compare the infectious doses of all the various +ve/-ve sense viruses.
It makes sense in theory that avoiding the need to transcribe the viral RNA would mean +ve sense ssRNA viruses would replicate more efficiently, yes, but that's only a theoretical suggestion. What do you think, Mr BiCpl? | |||
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"Thanks to Kinky_Couple, with whom have corresponded before (I'm a vaccine scientist), it's good to have a proper explanation rather than all the non-science (are you listening, Daily Mail) that is terrifying people. Question for Kinky, however: do you think that that SARS-COV-2 is able to be a more efficient replicant than, say another RNA virus, like 'flu, because of the positive-sense ssRNA? I haven't seen comment on this anywhere, apart from a paper in Clinical Microbiology Reviews (which I know you read at night ) back in 2007.
Mr Bicpl
Thanks, Mr BiCpl
I don't know of any specific data/papers which might state this for certain, but it makes sense that the positive-sense ssRNA viruses might replicate more quickly/effiently than the negative-sense ssRNA viruses. An example of +ve sense ssRNA viruses we know are efficient replicators/infectors are rhinoviruses (majority of common colds). Influenza viruses (orthomyxoviridae) are -ve sense ssRNA and we know the infectious dose needed to develop symptoms of 'flu (anything from 10^3 - 10^7 viral particles) are higher than the dose of rhinovirus needed to develop a cold (anything from 10^-1 to 10^5 viral particles). However, I don't have anything more empirical and it's impossible to compare the infectious doses of all the various +ve/-ve sense viruses.
It makes sense in theory that avoiding the need to transcribe the viral RNA would mean +ve sense ssRNA viruses would replicate more efficiently, yes, but that's only a theoretical suggestion. What do you think, Mr BiCpl?"Well, Kinky, that's what I assume - I'll try to find a virologist (if any will engage with me right now!) and see if there is an established view. Cheers, Mr BiCpl | |||
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