Does one acquire immunity after going through CoV infection? What about SARS/MERS?
If I understand correctly there are many strains of influenza and they mutate. That's why new vaccines are needed.
What about SARS/MERS? Did they mutate too?
If I understand correctly there are many strains of influenza and they mutate. That's why new vaccines are needed.
What about SARS/MERS? Did they mutate too?
From my understanding (I.e. someone who wasn't a doctor or biologist once told me), the flu virus is special in that it is very big for a virus and has something akin to primitive sexual reproduction: it is made of six(?) parts and if two strains of flu infect the same cell, the cell will give birth to viruses that have each part chosen at random from one of the two strains (e.g. aBCdEF or AbcdEf etc').
That's why there are so many strains of flu and the vaccine changes every year.
Apart from that, every virus mutates, and from what I've read there are already at least two known functionally different strains of nCov-2019 (one more aggressive than the other). However, I'd wager the same vaccines and medicines would work for both - to get resistance you need selection pressure or the amount of variance you get from sexual reproduction.
Edit: oh, and nCov-2019 attacks the immune system in a way that seems to lower or prevent acquiring immunity from reinfection.
The study that suggested ADE for this virus showed a very mild effect in vitro. However, antibodies still prevented infection. More crucially yet, a high number of viruses exhibit ADE in vitro, yet only two exhibit ADE in vivo. Moreover, even in vitro, infection of immune cells by the virus did not lead to viral replication. It's therefore unlikely that it shows ADE in humans, especially since its far less severe than viruses that do.
You might notice that for critical cases, lymphocytes counts are down. The issue is that lymphocyte counts are low, yet those patients show very high cytokine levels, and lymphocytes also exhibit exhaustion. Studies in a clinical setting have shown that indeed cytokine levels are a good predictor of lower lymphocyte counts. Thus this seems better explained by the cytokine storm.
Another thing that's good to know is that this coronavirus seems to have a very good exoribonuclease, which is an error checking enzyme. Mutation rates are also quite low, empirically. It is thus probable that this virus will not evolve too much.
Finally, the study that suggests that there are two lineages is deeply flawed. When you take into account the founder effect of international dissemination right before border controls are implemented, and the low mutation rate, you will find that the observation that led to the conclusions that there are two strains is not significantly more likely than the null hypothesis that this is simply a coincidence. Therefore it is not possible to make conclusions about the existence of strains, and certainly not possible to suggest they would behave differently in any way.
(One of which was that biologists have a more specific definition of "virus attacks X system" than computer security researchers, so my wording seems to have been off there. I was trying to say "seems to do something against its effectiveness, because we see cases of reinfection after a short time")
We should talk about the test error intervals.
With that small amount of secondary cases, maybe it was a false positive the first time. No procedure is 100% failsafe and this is a price that we pay for being in the real world. Maybe the test was not applied correctly, was not stored accurately or was triggered by some artifact.