On Monday, officials detected the first confirmed case of P.1 in the U.S., specifically in Minnesota. The state Department of Health picked up the case by randomly sequencing 50 nasal swabs from positive patients each week. The person infected with P.1. had previously traveled to Brazil.
“If you were to ask me right now, what’s most concerning of all the things that I’ve heard so far, it’s the fact that they are reporting a sudden increase in cases in Manaus, Brazil,” virus expert Jeremy Luban at the University of Massachusetts told NPR two weeks ago before the variant arrived in the United States. "Manaus already had 75% of people infected [in the spring of last year]."
While the variant from the U.K. took about three months to dominate the outbreak in England, P.1 took only about a month to dominate the outbreak in Manaus. In addition, Manaus had already been hit extremely hard by the virus in April. One study estimated that the population should have reached herd immunity and the virus shouldn’t be able to spread easily in the community. So why would the city see an even bigger surge 10 months later? Could P.1 be evading the antibodies made against the previous version of the virus, making reinfections easier? Could it just be significantly more contagious? Could both be true?
Looks probable that the mutations on the spike proteins are substantial enough to allow someone who had been infected with an existing strain to get sick from this new one.
I don’t think they know yet whether these new strains are more virulent or just more easily transmitted. Becoming more transmissible makes sense. The virus wants to spread so any variant that has spike protein mutations that make it easier for the virus to bind to human ACE2 receptors would have an advantage.
Selective pressures would probably favor the virus becoming less virulent over time, but you could certainly see more virulent strains emerge before they peter out.
That said, if P.1 is more virulent, it would be interesting to know if the worst cases are in people who already recovered from another strain. If they are, it would raise the possibility of anitbody-dependent enhancement, which is what happens to some people who get dengue for a second time.
Mutations can make a virus either more or less virulent. A common theory is that virulence will only change — either upwards or downwards — if it increases the transmission rate of the virus, which effectively means an increase in the number of virus ‘offspring’. However, high virulence may (although by no means always) reduce transmissibility if the host is too sick to expose others.
The lethality of the coronavirus is so comparatively small with most people surviving that this mechanism is unlikely to apply a lot. A lot of people will survive who can transmit the virus without immediately dying and thereby ending the transmission chain
That is the natural evolution of the virus. It is trying to remain alive so it is adapting to our immune bodies response. Dr’s are concerned about his rapid rollout of vaccines and how that might affect changes in the viruses behaviour. When movement restrictions were introduced the virus changed by living for longer periods on stagnant surfaces. When effective treatments, such as retrovirals and steroids, were introduced things seemed to stabilise for several months until the protein spike adapted. The changes to the protein spike made it much more difficult for our bodies immune response to identify and attack, essentially a kind of cell camouflage.
The new worry is that these recent strains, UK, B119, SA, and P1, are responses to the vaccine trials. Certainly the first 3 correlate with the stage 1, 2, and 3 trial periods. Who knows whether the P1 strain can be lumped in with that lot. There’s enough rich people in Brazil that might have queue jumped and paid for access to the trial vaccine (think Trump when he was infected in October) and then exposed that to low paid workers that then transmitted that through the favelas.
So essentially the virus is a basic form of life. It is trying to survive. It is adapting to our efforts to eradicate it. Therefore it is becoming more virulent. So far it has not become more deadly but that is mostly because of applicable treatment models (specifically the use of steroids). If the virus overcomes the steroid treatment then it will become much more deadly however that sort of defies the purpose. A dead host means a dead virus (sort of anyway even if it would take a few more weeks for the virus remnants on surfaces to die naturally).
The reason why the lethality dropped so quickly was because of the relatively quick identification of dexamethasone (steroids) as an early treatment option. This helped bring the average death rate from roughly 3% down to the current 0.3%. Dexamethasone is relatively cheap too. And there have been multiple trials across the world in the last year looking for contraindications between dexamethasone and other kinds of medications.
Pfizer Chief Executive Albert Bourla said there was “a high possibility” that emerging variants may eventually render the company’s vaccine ineffective.
“This is not the case yet … but I think it’s a very high likelihood that one day that will happen,” Bourla said at the World Economic Forum. The drugmaker is considering whether its vaccine needs to be altered to defend against the South African variant.