Coronavirus ability to mutate vastly underestimated, some strains more deadly
 

The most aggressive strains of Sars-CoV-2 could generate 270 times as much viral load as the least potent type

New York may have a deadlier strain imported from Europe, compared to less deadly viruses elsewhere in the United States.

Coronavirus’s ability to mutate has been vastly underestimated, and mutations affect deadliness of strains, Chinese study finds | South China Morning Post

Full paper here:

Patient-derived mutations impact pathogenicity of SARS-CoV-2 | medRxiv

If they are right this will complicate vaccine development, drug therapies, results from clinical trials etc. Also might be why we are starting to see studies showing large numbers with antibodies but never had symptoms, they were exposed to a weaker strain.

It at least offers an explanation why some have little or no symptoms and others get gravely ill. It explains why mortality can be in the low single digits and yet 4 individuals from the same family have a fatal result. The next question is do antibodies from the weaker strain provide immunity from the stronger strain.

At this point we don't know if antibodies from any strain make you immune or for how long.

Severe vs mild mutations of the Covid-19 virus
 

In order to replicate and survive the virus needs host cells. The so called weak mutation of the virus which causes only mild symptoms will soon drive out the severe form of the virus because it ( the weak form) can infect many more victims while the the severe form kills off its host too fast and thus will produce fewer numbers of severe viruses as compared to large numbers of weak viruses.

The science of this pandemic is above my pay grade. I’m just praying that we have an affective vaccine by fall of this year. ������

Pray harder

I read, but didn't really understand, the whole paper. They did genetic sequencing on the viral samples from 11 patients all hospitalized in a single hospital. All but one were directly connected to early cases from Wuhan but in a city several hundred miles away.

None of the 11 had identical genomes. Every single strain differed if I'm reading the paper correctly. They did not comment on whether variations that had produced higher viral replication in their cell tissue model were from those who were clinically sicker.

None of these strains were subclinical in these patients, all were hospitalized. This is going to be very complex. In producing a vaccine it will have to target a stable protein on the virus, or have components targeting several variations of those proteins, as is done with influenza. This is potentially bad news in the hope for an early vaccine.