SARS-CoV2 is the same as HIV in this sense; it's descended from an animal virus but its (essentially only) tropism*** is human cells.
Which comes back to the original point; if we can control it well enough in humans, it will go away.
AFZ
***Tropism is the technical term. In this context it means the specific cells a virus can infect. No virus can infect all species or even all cell types within a species (AFAIK). For example, HIV's main tropism is CD4+ T-lymphocytes. These cells are critical to control and coordination of the immune system thus explaining why HIV causes such a massive failure of the immune system (AIDS). This paper (https://www.thelancet.com/journals/lanres/article/PIIS2213-2600(20)30193-4/fulltext) is an example of the work being done to understand the tropism of SARS-Cov2. The key here is that it essentially only infects human respiratory epithelium. The exceptions are well documented but there are few absolutes in biology, most things are a spectrum. The propensity of SARS-Cov2 to infect non-human mammals is very low. Low enough to ignore from a public health perspective. (On current evidence).
I’m surprised to hear that you’re so confident of this, particularly since the paper you link to doesn’t appear to discuss non-human infection, and the first paragraph contains the sentence “The transmissibility and pathogenesis of SARS-CoV-2 remain poorly understood.” It appears that some have reported infection of and efficient transmission between ferrets, and there seem to be numerous studies which use them as a model for studying SARS-CoV-2 infection and transmission.
SARS-CoV2 is the same as HIV in this sense; it's descended from an animal virus but its (essentially only) tropism*** is human cells.
Which comes back to the original point; if we can control it well enough in humans, it will go away.
AFZ
***Tropism is the technical term. In this context it means the specific cells a virus can infect. No virus can infect all species or even all cell types within a species (AFAIK). For example, HIV's main tropism is CD4+ T-lymphocytes. These cells are critical to control and coordination of the immune system thus explaining why HIV causes such a massive failure of the immune system (AIDS). This paper (https://www.thelancet.com/journals/lanres/article/PIIS2213-2600(20)30193-4/fulltext) is an example of the work being done to understand the tropism of SARS-Cov2. The key here is that it essentially only infects human respiratory epithelium. The exceptions are well documented but there are few absolutes in biology, most things are a spectrum. The propensity of SARS-Cov2 to infect non-human mammals is very low. Low enough to ignore from a public health perspective. (On current evidence).
I’m surprised to hear that you’re so confident of this, particularly since the paper you link to doesn’t appear to discuss non-human infection, and the first paragraph contains the sentence “The transmissibility and pathogenesis of SARS-CoV-2 remain poorly understood.” It appears that some have reported infection of and efficient transmission between ferrets, and there seem to be numerous studies which use them as a model for studying SARS-CoV-2 infection and transmission.
Sorry, I only linked to that paper to illustrate the concept of tropism for different cell types.
My confidence about the lack of animal reservoir for SARS-Cov2 comes from an epidemiological perspective mostly. This virus has swept the human world. Humanity lives side-by-side with multiple species in all cultures; be that pest animals or livestock or pets. I think if there was significant animal to human transmission we would have evidence of it. The absence of such is indeed reassuring in this case.
FWIW (not much) my best guess is that's not likely to be an issue. The way coronaviruses enter cells tends to make them quite restrictive on which cells they can enter. Hence apart from when species jumps occur (which is actually a rare phenomenon*) each of the known coronaviruses tend to infect only species predominantly (as far as I can remember). The handful of cases of human to animal transmissions do not a concern make especially as this appears to be a dead-end for the virus.**
Having said that, there is some evidence (according to the CDC) from Denmark that a variant of SARS-Cov2 might be able to spread from humans to mink and subsequently from mink to humans. That, if confirmed would raise my level of concern. However, I don't think that an insurmountable problem. Influenza-A is endemic in poultry and many strains can transmit from poultry to humans, so we're never (with current science and technology) going to get rid of it. Conversely culling a small number of mink is feasible.
I could be wrong about all this***, or simply out-of-date. The evidence is ever changing but as with the fact that the virus can survive on surfaces for upto 72 hours and can then infect another person, has shown to be of minimal importance in terms of the pandemic spread, it seems very likely than zoonotic spread if indeed it is occurring is of negligible significance. It is certainly not the case that we have an animal reservoir like Ebola.
AFZ
*This is intuitively true: there are literally millions of cases of human-to-human transmission of SARS-Cov2 and probably only one case of bat to human.
**As I said above, human-to-animal transmission alone is not concerning; it's animal to human that would ring alarm bells. Good examples of viral dead ends:
1) Polio
2) HIV in northern Africa due to circumcision.
I put these two examples here because they interest me and they illustrate the point:
Polio, oddly, is actually a gut infection. In fact, about 99% of people who have the virus, never know it. It is passed by the classic faecal-oral route; that is, the viral particles are shed in faeces and then either via the water supply or human hands or whatever enter the mouth of someone else. (Many, many pathogens do this). This is the normal life-cycle of the virus. For some odd, reason, in around 1 in 100 cases, the virus gets into the nervous system. This triggers inflammation which causes nerve damage which is the disease we know as polio. This is, however, a dead-end for the virus. It is not able to replicate in the human nervous system and then be transmitted to another person.
The HIV one is interesting as well and is held to be the reason why HIV is rampant in sub-Saharan Africa and rare in Northern Africa. HIV is not actually very easily transmitted but it is definitely more easily transmitted from males to females during intercourse. There is some direct evidence that for female-to-male transmission to occur the virus needs to bind to receptors found in the inner foreskin. Thus, it is very unlikely (in the absence of other lesions) for an infected woman to pass HIV to her male partner if he is circumcised. A key epidemiological point here is that in Africa the major means of transmission of HIV is heterosexual sexual contact. Hence in Northern Africa where the majority of the male population is circumcised, there is very little female-to-male transmission. Hence if a man gives HIV to his female partner, it is likely to be a dead-end for the virus.
The point of all this is, if the risk of animal to human transmission is very low (which it seems to be) then even though we have some well-documented cases of human-to-animal transmission it is a dead-end for the virus spread.
Once again, I want to point out that biology is rarely binary. Whilst some zoonotic transmission may be possible, it is definitely not (at this point in time) of a high enough level to make controlling the virus difficult if we can control its human-to-human spread. This is the key point, I'm making.
***ALWAYS a possibility, and I am happy to change my mind when the evidence leads that way. I have already of multiple aspects of Covid-19.
Every morning, my wife and I check the paper to see what the reported cases are for our county--it varies from the Coronavirus.us report some. Today we opened the paper to find our county had 12 new cases, but the neighboring county in Idaho had 24, and, population-wise, it is half the size of our county. The biggest difference is the governor of Idaho has refused to mandate a mask ordinance; whereas, Washington State does require masks in public. That, and, there is a congregation in that county that has refused to mask up. We suspect many of the people in that county are members of that congregation.
AFZ - I appreciate your point, but I wonder if we really are in a position to be confident we have a good estimate of the rate of animal-to-human transmission - a smaller but still significant amount might easily be masked by the huge amount of human-to-human transmission.
China might provide reassurance, though - since they’ve almost completely suppressed it in the human population, animal sources of infection would presumably be easier to spot. Still, I wouldn’t snuggle up with any ferrets or minks, whether zombie or not.
I would hope not. Nasty little beasts; they stink and they bite.
Barnabas62Purgatory Host, 8th Day Host, Epiphanies Host
edited January 10
Latest weekly update.
Week ending 9 January
Global:
Total cases: 90,059,506 (prev. 84,970,208)
New cases during the week: 5,089,298 (prev. 4,258,751)
Daily Average: 727,043 (prev. 608,393)
Total deaths: 1,933,708 (prev. 1,843,106)
New deaths during the week: 90,602 (prev. 78,682)
Daily Average: 12,943 (prev, 11,240)
Europe:
Total cases: 25,748,078 (prev, 24,037,052)
New cases during the week: 1,710,996
(prev. 1,475,693)
Daily Average: 244,428 (prev. 210,813)
Total deaths: 586,261 (prev. 550,454)
New deaths during the week: 35,807 (prev. 31,719)
Daily average: 5,115 (prev. 4,531)
USA:
Total cases: 22,699,938 (prev. 20,904,853)
New cases during the week: 1,795,085 (prev. 1,471,006
Daily Average: 256,441 (prev. 193,691)
Total deaths: 381,480 (prev, 358,685)
New deaths during the week: 22,795 (prev. 18,764)
Daily Average: 3,256 (prev. 2,681)
Europe, with about a tenth of the global population, accounted for 34% of the global new cases and 40% of the global deaths during the week.
The USA, with less than 5% of the global population, accounted for 35% of the global new cases and 25% of the global deaths during the week.
All weekly figures are up sharply. Within Europe, the sharp increase in UK figures is a significant factor.
In the rest of the world I noted that after a lull the Brazil figures are trending up sharply. And as MaryLouise has noted, figures are trending up sharply in South Africa.
Overall, a very grim picture just got even grimmer. The race to vaccinate looks even more important.
@Barnabas our Covid-19 stats are soaring faster than anyone predicted: a total of 1 214 176 cases have been reported with 21 606 new cases in the past 24 hours. So far there are 32 824 reported deaths, 399 in the past day.
Zimbabwe's Covid-19 infections are also reported to be out of control. We have a humanitarian crisis at South Africa's border (Beit Bridge over the Limpopo River) with Zimbabwe, where hundreds of migrant workers and refugees have been turned back following a national lockdown by the Zimbabwean government. Many of those wanting to cross over into South Africa for medical treatment have tested positive for Covid.
@Barnabas our Covid-19 stats are soaring faster than anyone predicted: a total of 1 214 176 cases have been reported with 21 606 new cases in the past 24 hours. So far there are 32 824 reported deaths, 399 in the past day.
Zimbabwe's Covid-19 infections are also reported to be out of control. We have a humanitarian crisis at South Africa's border (Beit Bridge over the Limpopo River) with Zimbabwe, where hundreds of migrant workers and refugees have been turned back following a national lockdown by the Zimbabwean government. Many of those wanting to cross over into South Africa for medical treatment have tested positive for Covid.
I feel bad changing the subject, MaryLouise, especially as my news is not good. Here is a link to a Guardian article on modelled rates of infection versus confirmed cases. If the models are close - and two separate models seem to support each other, though of course they can be wrong in the same way - then rates of past infection of 40-50% seem insufficient in a population to slow the current spread. We have further to go.
Here is a link to a Guardian article on modelled rates of infection versus confirmed cases. If the models are close - and two separate models seem to support each other, though of course they can be wrong in the same way - then rates of past infection of 40-50% seem insufficient in a population to slow the current spread. We have further to go.
I would view that as good news. Why?
It means the disease is less deadly than we thought (given that there are unlikely to be a whole bunch of corpses somewhere that haven’t been counted yet).
It also means the disease is far more likely to be asymptomatic (and therefore harmless) than we thought. From an individual point of view this provides reassurance that if any one of us catches it we’re far more likely to be completely unharmed than was previously thought.
It means more people have already had it, and so can’t catch it again. We’re considerably closer to herd immunity than we thought.
Remember, the total number of cases there have been or will be is not in and of itself a metric for how bad this pandemic is (for the same reason very few people care in the least how many cases of the common cold there are in a given year). What’s important is how many of the cases require hospitalisation and how many of them result in death or other serious long-term health issues. If what you report is correct, both percentages are considerably lower than has thus far been thought.
Assymptomatic is not harmless. Someone who is assymptomatic can still transmit the virus, and cause fatal or life changing illness in someone they love.
Also there is evidence that catching Covid19 once does not guarantee either that you will not catch it again or that you will not have worse symptoms the second time around. Plus the way we are helping the virus mutate means that becomes even more likely that people can catch another variant, and because people are infectious in the early asymptomatic stages, or asymptomatic, there is no driver for the virus to become less severe in its effects.
Repeated infections with variations of coronaviruses (and adenoviruses) are the cause of the common cold, which has never been cured or vaccinated against. The coronavirus link is why there were initial doubts that a vaccine would work to prevent Covid19.
There are still doubts as to how long immunity lasts with the current vaccines. This may require an annual vaccination.
There are still doubts as to how long immunity lasts with the current vaccines. This may require an annual vaccination.
It doesn’t have to last forever, just for long enough that the virus dies out for lack of new hosts to infect. A few months (plus additional measures such as a NZ-style strict quarantine for anyone new coming into the country) would be enough.
Here is a link to a Guardian article on modelled rates of infection versus confirmed cases. If the models are close - and two separate models seem to support each other, though of course they can be wrong in the same way - then rates of past infection of 40-50% seem insufficient in a population to slow the current spread. We have further to go.
I would view that as good news. Why?
It means the disease is less deadly than we thought (given that there are unlikely to be a whole bunch of corpses somewhere that haven’t been counted yet). .
The model estimates the number of cases in an areas by comparing its number of deaths against an estimated infection fatality rate.
They're taking the IFR as known and using that and the number of deaths to estimate the number of infections. You can't get a new value from the IFR from these results.
We have now seen three US representatives test positive for Covid-19 after having been forced to shelter from the rampaging mob in the Capitol for several hours in a confined space in the company of a number of maskless morons.
It has not been proven that one of these maskless Republicans was the source of the infection. Masks are not a panacea, and it is possible that the source of the infection was a person who was wearing their mask correctly, or attempting to do so.
If it could be proven that one of the maskless members was the source, then would they, by knowingly and recklessly refusing to wear a mask, have committed a criminal offense?
The model estimates the number of cases in an areas by comparing its number of deaths against an estimated infection fatality rate.
They're taking the IFR as known and using that and the number of deaths to estimate the number of infections. You can't get a new value from the IFR from these results.
I assume the number of COVID deaths is pretty much what it has always been reported as. Somebody would surely have noticed if the real number of deaths caused by the disease was significantly higher. That being the case, any additional case numbers (which must logically have been non-fatal) that get added retrospectively must by definition reduce the fatality rate.
Either they’re assuming all deaths in the period were due to COVID or they’re assuming an IFR that isn’t based on the reported numbers. Neither is a particularly compelling argument unless there’s additional supporting evidence that they didn’t share.
The model estimates the number of cases in an areas by comparing its number of deaths against an estimated infection fatality rate.
They're taking the IFR as known and using that and the number of deaths to estimate the number of infections. You can't get a new value from the IFR from these results.
I assume the number of COVID deaths is pretty much what it has always been reported as. Somebody would surely have noticed if the real number of deaths caused by the disease was significantly higher. That being the case, any additional case numbers (which must logically have been non-fatal) that get added retrospectively must by definition reduce the fatality rate.
Either they’re assuming all deaths in the period were due to COVID or they’re assuming an IFR that isn’t based on the reported numbers. Neither is a particularly compelling argument unless there’s additional supporting evidence that they didn’t share.
Presumably the IFR can be determined to a certain degree of accuracy from ONS survey testing, and the figure so derived used to project back from the number of known deaths to an estimate of the number of infections.
Testing says we’ve had x cases, and we know we’ve had y deaths. The IFR is therefore y/x.
So how can you then divide y by the IFR and get anything other than x?
Does the ONS track specific individuals that have tested positive and see how many of them die or something? That’s the only way I can think of that might get a lower IFR than the above method, but it’s still not taking into account the fact that getting a test at all is reliant on being symptomatic - at best it can estimate an IFR for symptomatic cases, but that still says nothing about the IFR for all cases because we simply don’t know how many asymptomatic cases there have been. For all we know 50% or more of the population could have had it asymptomatically by now.
Either way, what this research is saying is that covid is nowhere near as deadly as we thought.
If we assume that the threshold for admission to hospital is constant (it's not but probably close enough) then the data on mortality of those admitted to hospital with Covid-19 is easily calculated and meaningful.
But of course, those admitted are only a subset of those with symptomatic Covid-19. In turn, those are only a subset of all people infected with SARS-Cov2.
One of the most useful data sets is the ONS survey which they started in May. This samples the whole population regardless of symptoms. If this is a representative sample of the population then you don't need to follow up them at all to get an estimate of the mortality.
Using that number as the denominator for calculating a case-mortality rate makes a lot sense as one way of working out the actual mortality of this virus.
When you say that this virus is nowhere near as deadly as we thought, I'm not sure what you mean. Since very early on there have been estimates of mortality of less than 1%. I think that's about right. In certain transmission conditions and with certain underlying medical conditions, it is much more deadly. I don't think the evidence has changed much on this point.
But let's take that 1% figure and assume that at some point all of the population will be exposed then that's ~65,000 deaths in the UK. Again it gets more complex, because if healthcare systems are overloaded then Covid-19 deaths go up and all-cause mortality goes up. Moreover, the risk of infecting healthcare staff goes up when the hospitals are busier. As does the risk of healthcare staff dying. This is because there's good evidence that a larger infective dose of SARS-Cov2 makes for higher mortality. In an overstretched healthcare setting, staff are much more likely to struggle to use PPE correctly and that's if enough is available!
My point here is that the 'deadliness' is not a fixed number.
The ONS survey has been testing more regularly recently as a way of monitoring the spread of the disease. I know a family who are taking part and they started having weekly tests recently, compared with monthly in the summer.
Testing says we’ve had x cases, and we know we’ve had y deaths. The IFR is therefore y/x.
So how can you then divide y by the IFR and get anything other than x?
Does the ONS track specific individuals that have tested positive and see how many of them die or something? That’s the only way I can think of that might get a lower IFR than the above method, but it’s still not taking into account the fact that getting a test at all is reliant on being symptomatic - at best it can estimate an IFR for symptomatic cases, but that still says nothing about the IFR for all cases because we simply don’t know how many asymptomatic cases there have been. For all we know 50% or more of the population could have had it asymptomatically by now.
Either way, what this research is saying is that covid is nowhere near as deadly as we thought.
This report adds absolutely nothing to estimates of how deadly Covid-19 is - it isn't any kind of re-calculation of IFR.
They're taking the weekly reported deaths in each local area and dividing by an estimate of the local IFR (age-weighted to account for the age distribution of the local population) to estimate the weekly new cases. The spreadsheet column heading is literally this:
"Estimated weekly new cases - (Weekly deaths divided by regional IFR)"
For example - on March 20, 7 people died of Covid-19 in Barking and Dagenham; given an IFR of 0.004381, they estimate 1597.703 cases. So they're assuming an IFR of 0.4381%, not calculating it (and that's the number used for B&D up to mid-June, after which they assume it's 0.3402%.)
The age-specific IFR estimates themselves come from work done by the Cambridge University MRC Biostatistics Unit - you can see them on this page (the IFR tab under "Epidemic Summary"). MRC gives high, low, and median estimates for different age groups, with higher numbers for the early part of the pandemic and lower numbers for the later part. (The median estimate for the overall IFR was 1.3%; it's now 0.94% for the later part.)
If we assume that the threshold for admission to hospital is constant (it's not but probably close enough) then the data on mortality of those admitted to hospital with Covid-19 is easily calculated and meaningful.
But of course, those admitted are only a subset of those with symptomatic Covid-19. In turn, those are only a subset of all people infected with SARS-Cov2.
One of the most useful data sets is the ONS survey which they started in May. This samples the whole population regardless of symptoms. If this is a representative sample of the population then you don't need to follow up them at all to get an estimate of the mortality.
Using that number as the denominator for calculating a case-mortality rate makes a lot sense as one way of working out the actual mortality of this virus.
When you say that this virus is nowhere near as deadly as we thought, I'm not sure what you mean. Since very early on there have been estimates of mortality of less than 1%. I think that's about right. In certain transmission conditions and with certain underlying medical conditions, it is much more deadly. I don't think the evidence has changed much on this point.
But let's take that 1% figure and assume that at some point all of the population will be exposed then that's ~65,000 deaths in the UK. Again it gets more complex, because if healthcare systems are overloaded then Covid-19 deaths go up and all-cause mortality goes up. Moreover, the risk of infecting healthcare staff goes up when the hospitals are busier. As does the risk of healthcare staff dying. This is because there's good evidence that a larger infective dose of SARS-Cov2 makes for higher mortality. In an overstretched healthcare setting, staff are much more likely to struggle to use PPE correctly and that's if enough is available!
My point here is that the 'deadliness' is not a fixed number.
AFZ
M'lud - point of order; 1% of 65,000,000 is 650,000, not 65,000.
Suppose you have a population with no immunity. If each infected person transmits the virus to (say) two others, the number of new infections will grow exponentially (1,2,4,8,etc.) If, however, half the population is immune, then the same infected person will (on average) pass it on to only one other person (since half of the targets are now unavailable) - and if more than half the population is immune, then the number of new infections will eventually die out.
The key is the balance between how many new infections would be caused in a population with no immunity (the "Rt" number - in the example above, Rt=2) and what fraction of the population is effectively immune. Neglecting immunity from past infection, this last number is the product of the fraction of the population that has been vaccinated and the effectiveness of the vaccine. For the example above, if you can vaccinate 90% of the people and the vaccine is 70% effective, then the 63% of the population would be immune and the number of new infections would die out (because 63%>50%, the number required to stop a virus with Rt=2.)
But if you vaccinate 90% and the vaccine is only 50% effective, then only 45% of the population will be immune, and each new infection will still be transmitted to (on average) more than one person - the spread of the infection is slowed, but not stopped.
In general the rate of population immunity required to prevent exponential growth is given by 1-(1/Rt). If SARS-CoV-2 has an Rt of 3 (typical early estimate for the developed world with people taking no special precautions) this number is 67%; if the vaccine is 60% effective (about the effectiveness of the standard regimen of the Oxford/Astrazenica vaccine), even a 100% vaccination rate wouldn't be enough to reach herd immunity. If the effectiveness is 95% (BioNTech/Pfizer, Moderna) then a vaccination rate of about 71% or more would do the trick (the higher the better, of course.)
If we assume that the threshold for admission to hospital is constant (it's not but probably close enough) then the data on mortality of those admitted to hospital with Covid-19 is easily calculated and meaningful.
But of course, those admitted are only a subset of those with symptomatic Covid-19. In turn, those are only a subset of all people infected with SARS-Cov2.
One of the most useful data sets is the ONS survey which they started in May. This samples the whole population regardless of symptoms. If this is a representative sample of the population then you don't need to follow up them at all to get an estimate of the mortality.
Using that number as the denominator for calculating a case-mortality rate makes a lot sense as one way of working out the actual mortality of this virus.
When you say that this virus is nowhere near as deadly as we thought, I'm not sure what you mean. Since very early on there have been estimates of mortality of less than 1%. I think that's about right. In certain transmission conditions and with certain underlying medical conditions, it is much more deadly. I don't think the evidence has changed much on this point.
But let's take that 1% figure and assume that at some point all of the population will be exposed then that's ~65,000 deaths in the UK. Again it gets more complex, because if healthcare systems are overloaded then Covid-19 deaths go up and all-cause mortality goes up. Moreover, the risk of infecting healthcare staff goes up when the hospitals are busier. As does the risk of healthcare staff dying. This is because there's good evidence that a larger infective dose of SARS-Cov2 makes for higher mortality. In an overstretched healthcare setting, staff are much more likely to struggle to use PPE correctly and that's if enough is available!
My point here is that the 'deadliness' is not a fixed number.
AFZ
M'lud - point of order; 1% of 65,000,000 is 650,000, not 65,000.
Thank you... in my defence, typing on my phone whilst holding a 13 month old... indeed I forgot the zero.
I think it noteworthy that this figure isn't far away from the famous "half a million deaths" that came out of some modelling that really scared the government into acting. I haven't looked at that data in detail but I suspect the reason it's 500,000 rather than 650,000 (thanks!) Is that when things get REALLY bad human behaviour changes and you see some mitigation.
Anyway, the point I was making is that even a low individual mortality with a disease that everyone gets is still a high number. For example, the disease my research is into, Has an overall mortality of 24% but there are only about 1000 to 1500 cases per year in the UK.
Added to which is that the effectiveness quoted for the vaccines relates to preventing development of covid19. The effectiveness at preventing infection may be lower, and it's not clear whether the vaccine reduces the chances of an infected person transmitting the virus. It's possible (though unlikely) that if you put a vaccinated and unvaccinated person in the same situation they'll both have the same chances of getting infected, both would then have the same chance of producing the same number of virus particles while asymptomatic and hence pass it on to the same number of people - the difference being that the unvaccinated person is much less likely to develop symptoms. I say it's unlikely, because it's almost certain that the vaccine will result in a more rapid immune response, supressing the number of cells that get infected and hence reducing the number of virus particles produced and the duration over which someone produces the virus - thus, reducing transmission. The vaccine may even reduce the chances of being infected in the first place. And, of course, we only know how people respond over a few months after the second dose, and the effectiveness may reduce over the longer term. But, all we know is effectiveness against developing covid19 (for a specific dosing regime - if you change that 21d interval between doses then there's no guarantee that the effectiveness will be the same).
If the vaccine only protects against covid19 but has little impact on transmission of SARS-CoV-2 virus then this will reduce the rate of hospitalisation, death and long-covid (as well as sick leave from work and similar economic effects) all other things being equal, but will leave the virus circulating freely in the population. If vaccination protects 50% of the population from covid but doesn't significantly impact transmission then it would only be possible to relax restrictions by a small amount before the covid19 rate reaches the same levels and the strain on the health of our nations isn't changed. As I said, that's an unlikely scenario, the vaccine should make a significant reduction in transmission once it gets distributed widely enough (in particular among the younger part of the population who are more likely to be out and about, and thus exposing and being exposed, taking kids to school or going into work).
If we assume that the threshold for admission to hospital is constant (it's not but probably close enough) then the data on mortality of those admitted to hospital with Covid-19 is easily calculated and meaningful.
But of course, those admitted are only a subset of those with symptomatic Covid-19. In turn, those are only a subset of all people infected with SARS-Cov2.
One of the most useful data sets is the ONS survey which they started in May. This samples the whole population regardless of symptoms. If this is a representative sample of the population then you don't need to follow up them at all to get an estimate of the mortality.
Using that number as the denominator for calculating a case-mortality rate makes a lot sense as one way of working out the actual mortality of this virus.
When you say that this virus is nowhere near as deadly as we thought, I'm not sure what you mean. Since very early on there have been estimates of mortality of less than 1%. I think that's about right. In certain transmission conditions and with certain underlying medical conditions, it is much more deadly. I don't think the evidence has changed much on this point.
But let's take that 1% figure and assume that at some point all of the population will be exposed then that's ~65,000 deaths in the UK. Again it gets more complex, because if healthcare systems are overloaded then Covid-19 deaths go up and all-cause mortality goes up. Moreover, the risk of infecting healthcare staff goes up when the hospitals are busier. As does the risk of healthcare staff dying. This is because there's good evidence that a larger infective dose of SARS-Cov2 makes for higher mortality. In an overstretched healthcare setting, staff are much more likely to struggle to use PPE correctly and that's if enough is available!
My point here is that the 'deadliness' is not a fixed number.
AFZ
M'lud - point of order; 1% of 65,000,000 is 650,000, not 65,000.
Thank you... in my defence, typing on my phone whilst holding a 13 month old... indeed I forgot the zero.
You could probably add another zero for people needing hospital treatment and/or suffering long term poor health, and not be far off the right number. Another zero for close friends and family of those who have experience these serious effects ... and, oh, that's basically everyone.
This report adds absolutely nothing to estimates of how deadly Covid-19 is - it isn't any kind of re-calculation of IFR.
For most people (myself included), the figures they see are total confirmed daily cases and total daily deaths. Which means they’ll perceive the IFR as being much higher than it really is, because total reported daily cases is far lower than total actual daily cases due to so many cases being asymptomatic.
So while this may not be a recalculation of the IFR that scientists and researchers have been using, for the common man or woman trying to keep up with the news this increase in the estimated total cases that have happened so far represents a lessening of covid’s perceived deadliness. It also means we’re further along the road to herd immunity than we thought, which is also a good thing isn’t it?
No, herd immunity without vaccination is not a good thing. If 50% of the population are immune because they've already been infected by the SARS-CoV-2 virus then that would mean there were 250,000+ dead people in the UK alone, 100s of thousand more who were suffering long term health impacts.
the vaccine should make a significant reduction in transmission once it gets distributed widely enough (in particular among the younger part of the population who are more likely to be out and about, and thus exposing and being exposed, taking kids to school or going into work).
I agree. Which makes it all the more annoying that those people are literally last in line to get the vaccine. It’s like the people making the decisions don’t want lockdown to end any sooner than it absolutely has to...
No, herd immunity without vaccination is not a good thing. If 50% of the population are immune because they've already been infected by the SARS-CoV-2 virus then that would mean there were 250,000+ dead people in the UK alone, 100s of thousand more who were suffering long term health impacts.
You miss my point. I'm talking about the situation if there have really been considerably more cases than we are aware of. Those extra cases having already happened won't do anything to the death figure, because they've already happened. People aren't going to retrospectively die because it turns out they actually had Covid four months ago without anyone knowing about it.
the vaccine should make a significant reduction in transmission once it gets distributed widely enough (in particular among the younger part of the population who are more likely to be out and about, and thus exposing and being exposed, taking kids to school or going into work).
I agree. Which makes it all the more annoying that those people are literally last in line to get the vaccine. It’s like the people making the decisions don’t want lockdown to end any sooner than it absolutely has to...
The sooner the people most likely to need hospital treatment or die from the disease are vaccinated, the sooner the pressure will be released on the NHS and the sooner we can go back to normal. Vaccinating younger people so that they can get out and about will result in them infecting the vulnerable people they will then come into contact with while they themselves are unaffected.
If we're going to play "it's like..." paranoia games, we could say that a call to vaccinate the younger part of the population first would look like the people making the decisions don't want vulnerable people to survive.
You miss my point. I'm talking about the situation if there have really been considerably more cases than we are aware of. Those extra cases having already happened won't do anything to the death figure, because they've already happened. People aren't going to retrospectively die because it turns out they actually had Covid four months ago without anyone knowing about it.
The new coronavirus, Sars-CoV-2, has not been around long enough to know how long immunity lasts, but there are six other human coronaviruses that can give a clue.
Four produce the symptoms of the common cold and immunity is short-lived. Studies showed some patients could be re-infected within a year.
Research at King's College London also suggested levels of antibodies that kill coronavirus waned over the three month study.
Not all reinfections seen so far are milder. “We see all different combinations,” Reusken says. The second time Luciana Ribeiro, a surgeon in Rio de Janeiro, got sick, it was much worse. She was first infected by a colleague in March, developed mild symptoms, and tested negative afterward. Three months later, Ribeiro had symptoms again—she could no longer smell her breakfast, she says—but she didn’t immediately get a test because she thought she was immune. When she grew more and more tired, she requested a computerized tomography scan. “It showed that half of my lungs were affected,” Ribeiro says. “‘This clearly is COVID,’ the radiologist told me. I didn’t believe it, but I tested positive.”
And younger people have a relatively high chance of getting long covid compared to the fatality rate.
You miss my point. I'm talking about the situation if there have really been considerably more cases than we are aware of. Those extra cases having already happened won't do anything to the death figure, because they've already happened. People aren't going to retrospectively die because it turns out they actually had Covid four months ago without anyone knowing about it.
The new coronavirus, Sars-CoV-2, has not been around long enough to know how long immunity lasts, but there are six other human coronaviruses that can give a clue.
Four produce the symptoms of the common cold and immunity is short-lived. Studies showed some patients could be re-infected within a year.
Research at King's College London also suggested levels of antibodies that kill coronavirus waned over the three month study.
Not all reinfections seen so far are milder. “We see all different combinations,” Reusken says. The second time Luciana Ribeiro, a surgeon in Rio de Janeiro, got sick, it was much worse. She was first infected by a colleague in March, developed mild symptoms, and tested negative afterward. Three months later, Ribeiro had symptoms again—she could no longer smell her breakfast, she says—but she didn’t immediately get a test because she thought she was immune. When she grew more and more tired, she requested a computerized tomography scan. “It showed that half of my lungs were affected,” Ribeiro says. “‘This clearly is COVID,’ the radiologist told me. I didn’t believe it, but I tested positive.”
And younger people have a relatively high chance of getting long covid compared to the fatality rate.
Well if all that's true then there's nothing whatsoever that we can do to be rid of Covid. The vaccines will also fail after three months, and there's no way we could give everybody four boosters per year - even if it were possible to produce that many doses it would be logistically impossible to distribute them in such a short timeframe.
So what do you suggest we do? Just stay locked down forever? Hope that it mutates into a less dangerous form at some point in the next decade or so, even though there's minimal evolutionary pressure for it to do so? Lift lockdown and accept that a lot of people are going to die?
The sooner the people most likely to need hospital treatment or die from the disease are vaccinated, the sooner the pressure will be released on the NHS and the sooner we can go back to normal. Vaccinating younger people so that they can get out and about will result in them infecting the vulnerable people they will then come into contact with while they themselves are unaffected.
Unless the vulnerable are properly isolated/quarantined prior to getting their vaccination, of course. Which is exactly the situation they're in right now, so it's not even like we'd be expecting them to take on any extra hardship.
If we're going to play "it's like..." paranoia games, we could say that a call to vaccinate the younger part of the population first would look like the people making the decisions don't want vulnerable people to survive.
There's a fairly simple piece of maths. The probability of being infected per unit time = number of people you meet x the probability of them being infected x the probability of passing the virus on
None of those can ever be zero. Lockdown reduces the number of people you meet. Precautions such as hand washing and wearing masks reduces the probability of the virus being passed on. Both of these probably have a minimum value that it's going to be increasingly hard to reach. There comes a point where the only way of reducing the the probability of being infected is to reduce the probability of people you meet being infected - that is, to get community transmission under control. Without control of the virus in the community sooner or later the virus will get through all of the barriers we put up to protect the vulnerable - as we've seen recently with fellow Shipmates living in Florida where there has been criminal-level disregard for any measure to control the virus.
To control the virus in the community by vaccination we'd need to vaccinate the vast majority of people - in the UK, 50m people or there abouts. That's going to take all year. To protect the most vulnerable, we need to vaccinate a far smaller group, 10-15m, and that should be possible (if the government doesn't contract the job out to incompetents) by the start of April, possibly a fair bit sooner.
Test positivity rate here is 15.8%, 3 times higher than WHO suggests, meaning not enough testing is going on. We're at 315 cases per 100,000 population. The highest in Canada.
The right-wing gov't feels it is doing well, so long as they blame the federal gov't for everything. This picture of the premier today went up. The news conference ended with him not putting on a mask and opening a door with the hand he coughed into.
This is the same man who ordered mandatory masks in communities only with more than 5,000 people to appeal to his spreadneck rural base when we were at <40 cases with modelling clearly showing where it was going. And lied that the federal gov't told him to hold back the 2nd dose: been caught with this. Conservatives everywhere seem to have failed grade 9 science. Also ethics.
The only saving grace for Saskatchewan is that our population density is very low and because it is cold in the winter, refrigerator trucks aren't needed for bodies.
This report adds absolutely nothing to estimates of how deadly Covid-19 is - it isn't any kind of re-calculation of IFR.
For most people (myself included), the figures they see are total confirmed daily cases and total daily deaths. Which means they’ll perceive the IFR as being much higher than it really is, because total reported daily cases is far lower than total actual daily cases due to so many cases being asymptomatic.
So while this may not be a recalculation of the IFR that scientists and researchers have been using, for the common man or woman trying to keep up with the news this increase in the estimated total cases that have happened so far represents a lessening of covid’s perceived deadliness. It also means we’re further along the road to herd immunity than we thought, which is also a good thing isn’t it?
I suppose if that anxious follower of the news has been assiduously dividing daily deaths by daily reported cases but has unaccountably missed all the many articles noting the likelihood of a undetermined but large number of unrecorded infections, they might interpret this as surprising good news.
It also might be interpreted as reassuring by those who desperately grasp at any scrap of information to support their prior bias against treating Covid-29 as a serious, deadly disease.
As for "further along the road to herd immunity" - well, I suppose. Just do this four more times and you're there.
I started this off right around here. 40-50% are likely to have had the virus, in populations which show no sign of slowing rates of infection due to herd immunity - indeed where infection rates have recently accelerated. I viewed this as less than good news, but perhaps as is often the case, that is just me.
Well if all that's true then there's nothing whatsoever that we can do to be rid of Covid. The vaccines will also fail after three months,
This does not appear to be true. The vaccine does not fail after 3 months. There's no reason to think that immunity-due-to-vaccine and immunity-due-to-infection last the same length of time, although it's easy to think that they should be the same. Bodies are more complicated than that, though. (Basically the big difference between the vaccine and the illness is that the vaccine doesn't actually make you sick, so there's a whole bunch of stuff that goes on when you have Covid that doesn't go on when you have the vaccine.)
Comments
Thank you.
I’m surprised to hear that you’re so confident of this, particularly since the paper you link to doesn’t appear to discuss non-human infection, and the first paragraph contains the sentence “The transmissibility and pathogenesis of SARS-CoV-2 remain poorly understood.” It appears that some have reported infection of and efficient transmission between ferrets, and there seem to be numerous studies which use them as a model for studying SARS-CoV-2 infection and transmission.
I agree with this @alienfromzog ; please keep posting as you do.
Sorry, I only linked to that paper to illustrate the concept of tropism for different cell types.
My confidence about the lack of animal reservoir for SARS-Cov2 comes from an epidemiological perspective mostly. This virus has swept the human world. Humanity lives side-by-side with multiple species in all cultures; be that pest animals or livestock or pets. I think if there was significant animal to human transmission we would have evidence of it. The absence of such is indeed reassuring in this case.
FWIW (not much) my best guess is that's not likely to be an issue. The way coronaviruses enter cells tends to make them quite restrictive on which cells they can enter. Hence apart from when species jumps occur (which is actually a rare phenomenon*) each of the known coronaviruses tend to infect only species predominantly (as far as I can remember). The handful of cases of human to animal transmissions do not a concern make especially as this appears to be a dead-end for the virus.**
Having said that, there is some evidence (according to the CDC) from Denmark that a variant of SARS-Cov2 might be able to spread from humans to mink and subsequently from mink to humans. That, if confirmed would raise my level of concern. However, I don't think that an insurmountable problem. Influenza-A is endemic in poultry and many strains can transmit from poultry to humans, so we're never (with current science and technology) going to get rid of it. Conversely culling a small number of mink is feasible.
I could be wrong about all this***, or simply out-of-date. The evidence is ever changing but as with the fact that the virus can survive on surfaces for upto 72 hours and can then infect another person, has shown to be of minimal importance in terms of the pandemic spread, it seems very likely than zoonotic spread if indeed it is occurring is of negligible significance. It is certainly not the case that we have an animal reservoir like Ebola.
AFZ
*This is intuitively true: there are literally millions of cases of human-to-human transmission of SARS-Cov2 and probably only one case of bat to human.
**As I said above, human-to-animal transmission alone is not concerning; it's animal to human that would ring alarm bells. Good examples of viral dead ends:
1) Polio
2) HIV in northern Africa due to circumcision.
I put these two examples here because they interest me and they illustrate the point:
Polio, oddly, is actually a gut infection. In fact, about 99% of people who have the virus, never know it. It is passed by the classic faecal-oral route; that is, the viral particles are shed in faeces and then either via the water supply or human hands or whatever enter the mouth of someone else. (Many, many pathogens do this). This is the normal life-cycle of the virus. For some odd, reason, in around 1 in 100 cases, the virus gets into the nervous system. This triggers inflammation which causes nerve damage which is the disease we know as polio. This is, however, a dead-end for the virus. It is not able to replicate in the human nervous system and then be transmitted to another person.
The HIV one is interesting as well and is held to be the reason why HIV is rampant in sub-Saharan Africa and rare in Northern Africa. HIV is not actually very easily transmitted but it is definitely more easily transmitted from males to females during intercourse. There is some direct evidence that for female-to-male transmission to occur the virus needs to bind to receptors found in the inner foreskin. Thus, it is very unlikely (in the absence of other lesions) for an infected woman to pass HIV to her male partner if he is circumcised. A key epidemiological point here is that in Africa the major means of transmission of HIV is heterosexual sexual contact. Hence in Northern Africa where the majority of the male population is circumcised, there is very little female-to-male transmission. Hence if a man gives HIV to his female partner, it is likely to be a dead-end for the virus.
The point of all this is, if the risk of animal to human transmission is very low (which it seems to be) then even though we have some well-documented cases of human-to-animal transmission it is a dead-end for the virus spread.
Once again, I want to point out that biology is rarely binary. Whilst some zoonotic transmission may be possible, it is definitely not (at this point in time) of a high enough level to make controlling the virus difficult if we can control its human-to-human spread. This is the key point, I'm making.
***ALWAYS a possibility, and I am happy to change my mind when the evidence leads that way. I have already of multiple aspects of Covid-19.
China might provide reassurance, though - since they’ve almost completely suppressed it in the human population, animal sources of infection would presumably be easier to spot. Still, I wouldn’t snuggle up with any ferrets or minks, whether zombie or not.
Week ending 9 January
Global:
Total cases: 90,059,506 (prev. 84,970,208)
New cases during the week: 5,089,298 (prev. 4,258,751)
Daily Average: 727,043 (prev. 608,393)
Total deaths: 1,933,708 (prev. 1,843,106)
New deaths during the week: 90,602 (prev. 78,682)
Daily Average: 12,943 (prev, 11,240)
Europe:
Total cases: 25,748,078 (prev, 24,037,052)
New cases during the week: 1,710,996
(prev. 1,475,693)
Daily Average: 244,428 (prev. 210,813)
Total deaths: 586,261 (prev. 550,454)
New deaths during the week: 35,807 (prev. 31,719)
Daily average: 5,115 (prev. 4,531)
USA:
Total cases: 22,699,938 (prev. 20,904,853)
New cases during the week: 1,795,085 (prev. 1,471,006
Daily Average: 256,441 (prev. 193,691)
Total deaths: 381,480 (prev, 358,685)
New deaths during the week: 22,795 (prev. 18,764)
Daily Average: 3,256 (prev. 2,681)
Europe, with about a tenth of the global population, accounted for 34% of the global new cases and 40% of the global deaths during the week.
The USA, with less than 5% of the global population, accounted for 35% of the global new cases and 25% of the global deaths during the week.
All weekly figures are up sharply. Within Europe, the sharp increase in UK figures is a significant factor.
In the rest of the world I noted that after a lull the Brazil figures are trending up sharply. And as MaryLouise has noted, figures are trending up sharply in South Africa.
Overall, a very grim picture just got even grimmer. The race to vaccinate looks even more important.
Zimbabwe's Covid-19 infections are also reported to be out of control. We have a humanitarian crisis at South Africa's border (Beit Bridge over the Limpopo River) with Zimbabwe, where hundreds of migrant workers and refugees have been turned back following a national lockdown by the Zimbabwean government. Many of those wanting to cross over into South Africa for medical treatment have tested positive for Covid.
Total crisis for you all 😥. Praying for you 🕯.
I would view that as good news. Why?
Remember, the total number of cases there have been or will be is not in and of itself a metric for how bad this pandemic is (for the same reason very few people care in the least how many cases of the common cold there are in a given year). What’s important is how many of the cases require hospitalisation and how many of them result in death or other serious long-term health issues. If what you report is correct, both percentages are considerably lower than has thus far been thought.
Repeated infections with variations of coronaviruses (and adenoviruses) are the cause of the common cold, which has never been cured or vaccinated against. The coronavirus link is why there were initial doubts that a vaccine would work to prevent Covid19.
There are still doubts as to how long immunity lasts with the current vaccines. This may require an annual vaccination.
It doesn’t have to last forever, just for long enough that the virus dies out for lack of new hosts to infect. A few months (plus additional measures such as a NZ-style strict quarantine for anyone new coming into the country) would be enough.
It has not been proven that one of these maskless Republicans was the source of the infection. Masks are not a panacea, and it is possible that the source of the infection was a person who was wearing their mask correctly, or attempting to do so.
If it could be proven that one of the maskless members was the source, then would they, by knowingly and recklessly refusing to wear a mask, have committed a criminal offense?
I assume the number of COVID deaths is pretty much what it has always been reported as. Somebody would surely have noticed if the real number of deaths caused by the disease was significantly higher. That being the case, any additional case numbers (which must logically have been non-fatal) that get added retrospectively must by definition reduce the fatality rate.
Either they’re assuming all deaths in the period were due to COVID or they’re assuming an IFR that isn’t based on the reported numbers. Neither is a particularly compelling argument unless there’s additional supporting evidence that they didn’t share.
Presumably the IFR can be determined to a certain degree of accuracy from ONS survey testing, and the figure so derived used to project back from the number of known deaths to an estimate of the number of infections.
Testing says we’ve had x cases, and we know we’ve had y deaths. The IFR is therefore y/x.
So how can you then divide y by the IFR and get anything other than x?
Does the ONS track specific individuals that have tested positive and see how many of them die or something? That’s the only way I can think of that might get a lower IFR than the above method, but it’s still not taking into account the fact that getting a test at all is reliant on being symptomatic - at best it can estimate an IFR for symptomatic cases, but that still says nothing about the IFR for all cases because we simply don’t know how many asymptomatic cases there have been. For all we know 50% or more of the population could have had it asymptomatically by now.
Either way, what this research is saying is that covid is nowhere near as deadly as we thought.
If we assume that the threshold for admission to hospital is constant (it's not but probably close enough) then the data on mortality of those admitted to hospital with Covid-19 is easily calculated and meaningful.
But of course, those admitted are only a subset of those with symptomatic Covid-19. In turn, those are only a subset of all people infected with SARS-Cov2.
One of the most useful data sets is the ONS survey which they started in May. This samples the whole population regardless of symptoms. If this is a representative sample of the population then you don't need to follow up them at all to get an estimate of the mortality.
Using that number as the denominator for calculating a case-mortality rate makes a lot sense as one way of working out the actual mortality of this virus.
When you say that this virus is nowhere near as deadly as we thought, I'm not sure what you mean. Since very early on there have been estimates of mortality of less than 1%. I think that's about right. In certain transmission conditions and with certain underlying medical conditions, it is much more deadly. I don't think the evidence has changed much on this point.
But let's take that 1% figure and assume that at some point all of the population will be exposed then that's ~65,000 deaths in the UK. Again it gets more complex, because if healthcare systems are overloaded then Covid-19 deaths go up and all-cause mortality goes up. Moreover, the risk of infecting healthcare staff goes up when the hospitals are busier. As does the risk of healthcare staff dying. This is because there's good evidence that a larger infective dose of SARS-Cov2 makes for higher mortality. In an overstretched healthcare setting, staff are much more likely to struggle to use PPE correctly and that's if enough is available!
My point here is that the 'deadliness' is not a fixed number.
AFZ
They're taking the weekly reported deaths in each local area and dividing by an estimate of the local IFR (age-weighted to account for the age distribution of the local population) to estimate the weekly new cases. The spreadsheet column heading is literally this: For example - on March 20, 7 people died of Covid-19 in Barking and Dagenham; given an IFR of 0.004381, they estimate 1597.703 cases. So they're assuming an IFR of 0.4381%, not calculating it (and that's the number used for B&D up to mid-June, after which they assume it's 0.3402%.)
The age-specific IFR estimates themselves come from work done by the Cambridge University MRC Biostatistics Unit - you can see them on this page (the IFR tab under "Epidemic Summary"). MRC gives high, low, and median estimates for different age groups, with higher numbers for the early part of the pandemic and lower numbers for the later part. (The median estimate for the overall IFR was 1.3%; it's now 0.94% for the later part.)
M'lud - point of order; 1% of 65,000,000 is 650,000, not 65,000.
https://amp.9news.com.au/article/f0c9b151-e9cb-453e-8309-9fb6097c1f64
The key is the balance between how many new infections would be caused in a population with no immunity (the "Rt" number - in the example above, Rt=2) and what fraction of the population is effectively immune. Neglecting immunity from past infection, this last number is the product of the fraction of the population that has been vaccinated and the effectiveness of the vaccine. For the example above, if you can vaccinate 90% of the people and the vaccine is 70% effective, then the 63% of the population would be immune and the number of new infections would die out (because 63%>50%, the number required to stop a virus with Rt=2.)
But if you vaccinate 90% and the vaccine is only 50% effective, then only 45% of the population will be immune, and each new infection will still be transmitted to (on average) more than one person - the spread of the infection is slowed, but not stopped.
In general the rate of population immunity required to prevent exponential growth is given by 1-(1/Rt). If SARS-CoV-2 has an Rt of 3 (typical early estimate for the developed world with people taking no special precautions) this number is 67%; if the vaccine is 60% effective (about the effectiveness of the standard regimen of the Oxford/Astrazenica vaccine), even a 100% vaccination rate wouldn't be enough to reach herd immunity. If the effectiveness is 95% (BioNTech/Pfizer, Moderna) then a vaccination rate of about 71% or more would do the trick (the higher the better, of course.)
Thank you... in my defence, typing on my phone whilst holding a 13 month old... indeed I forgot the zero.
I think it noteworthy that this figure isn't far away from the famous "half a million deaths" that came out of some modelling that really scared the government into acting. I haven't looked at that data in detail but I suspect the reason it's 500,000 rather than 650,000 (thanks!) Is that when things get REALLY bad human behaviour changes and you see some mitigation.
Anyway, the point I was making is that even a low individual mortality with a disease that everyone gets is still a high number. For example, the disease my research is into, Has an overall mortality of 24% but there are only about 1000 to 1500 cases per year in the UK.
AFZ
If the vaccine only protects against covid19 but has little impact on transmission of SARS-CoV-2 virus then this will reduce the rate of hospitalisation, death and long-covid (as well as sick leave from work and similar economic effects) all other things being equal, but will leave the virus circulating freely in the population. If vaccination protects 50% of the population from covid but doesn't significantly impact transmission then it would only be possible to relax restrictions by a small amount before the covid19 rate reaches the same levels and the strain on the health of our nations isn't changed. As I said, that's an unlikely scenario, the vaccine should make a significant reduction in transmission once it gets distributed widely enough (in particular among the younger part of the population who are more likely to be out and about, and thus exposing and being exposed, taking kids to school or going into work).
For most people (myself included), the figures they see are total confirmed daily cases and total daily deaths. Which means they’ll perceive the IFR as being much higher than it really is, because total reported daily cases is far lower than total actual daily cases due to so many cases being asymptomatic.
So while this may not be a recalculation of the IFR that scientists and researchers have been using, for the common man or woman trying to keep up with the news this increase in the estimated total cases that have happened so far represents a lessening of covid’s perceived deadliness. It also means we’re further along the road to herd immunity than we thought, which is also a good thing isn’t it?
I agree. Which makes it all the more annoying that those people are literally last in line to get the vaccine. It’s like the people making the decisions don’t want lockdown to end any sooner than it absolutely has to...
You miss my point. I'm talking about the situation if there have really been considerably more cases than we are aware of. Those extra cases having already happened won't do anything to the death figure, because they've already happened. People aren't going to retrospectively die because it turns out they actually had Covid four months ago without anyone knowing about it.
The sooner the people most likely to need hospital treatment or die from the disease are vaccinated, the sooner the pressure will be released on the NHS and the sooner we can go back to normal. Vaccinating younger people so that they can get out and about will result in them infecting the vulnerable people they will then come into contact with while they themselves are unaffected.
If we're going to play "it's like..." paranoia games, we could say that a call to vaccinate the younger part of the population first would look like the people making the decisions don't want vulnerable people to survive.
Except, to reiterate, there is no guarantee that catching Covid19 gives immunity or for how long. From this BBC article from December 2020:
CDC advice recently says catching Covid19 doesn't even guarantee 3 months immunity.
Nor does catching it once ensure your second dose is milder - from Science Magazine from November 2020
And younger people have a relatively high chance of getting long covid compared to the fatality rate.
Well if all that's true then there's nothing whatsoever that we can do to be rid of Covid. The vaccines will also fail after three months, and there's no way we could give everybody four boosters per year - even if it were possible to produce that many doses it would be logistically impossible to distribute them in such a short timeframe.
So what do you suggest we do? Just stay locked down forever? Hope that it mutates into a less dangerous form at some point in the next decade or so, even though there's minimal evolutionary pressure for it to do so? Lift lockdown and accept that a lot of people are going to die?
Unless the vulnerable are properly isolated/quarantined prior to getting their vaccination, of course. Which is exactly the situation they're in right now, so it's not even like we'd be expecting them to take on any extra hardship.
True enough.
None of those can ever be zero. Lockdown reduces the number of people you meet. Precautions such as hand washing and wearing masks reduces the probability of the virus being passed on. Both of these probably have a minimum value that it's going to be increasingly hard to reach. There comes a point where the only way of reducing the the probability of being infected is to reduce the probability of people you meet being infected - that is, to get community transmission under control. Without control of the virus in the community sooner or later the virus will get through all of the barriers we put up to protect the vulnerable - as we've seen recently with fellow Shipmates living in Florida where there has been criminal-level disregard for any measure to control the virus.
To control the virus in the community by vaccination we'd need to vaccinate the vast majority of people - in the UK, 50m people or there abouts. That's going to take all year. To protect the most vulnerable, we need to vaccinate a far smaller group, 10-15m, and that should be possible (if the government doesn't contract the job out to incompetents) by the start of April, possibly a fair bit sooner.
The right-wing gov't feels it is doing well, so long as they blame the federal gov't for everything. This picture of the premier today went up. The news conference ended with him not putting on a mask and opening a door with the hand he coughed into.
This is the same man who ordered mandatory masks in communities only with more than 5,000 people to appeal to his spreadneck rural base when we were at <40 cases with modelling clearly showing where it was going. And lied that the federal gov't told him to hold back the 2nd dose: been caught with this. Conservatives everywhere seem to have failed grade 9 science. Also ethics.
The only saving grace for Saskatchewan is that our population density is very low and because it is cold in the winter, refrigerator trucks aren't needed for bodies.
It also might be interpreted as reassuring by those who desperately grasp at any scrap of information to support their prior bias against treating Covid-29 as a serious, deadly disease.
As for "further along the road to herd immunity" - well, I suppose. Just do this four more times and you're there.
This does not appear to be true. The vaccine does not fail after 3 months. There's no reason to think that immunity-due-to-vaccine and immunity-due-to-infection last the same length of time, although it's easy to think that they should be the same. Bodies are more complicated than that, though. (Basically the big difference between the vaccine and the illness is that the vaccine doesn't actually make you sick, so there's a whole bunch of stuff that goes on when you have Covid that doesn't go on when you have the vaccine.)