First, an update: There are few surprises in the progression of the outbreak. The more we test the more we find. Speaking of testing, some states are absolutely smashing it right now. 20-30k tests per day. Basically, once the restrictions were removed, the ingenuity of scientists and engineers let them retool their labs to work on this problem.
There is, however, huge discrepancies in testing at the state level. Not surprisingly, those with low test rates have low SARSCoV2 prevalence. In general, New England is testing well but still has a long way to go to get ahead of the epidemic curve. But, I believe that capacity is coming.
Bottom line, buckle up. There is an epidemic curve in every state (exponential growth), numbers of infected people in the USA are going to get really big. There is little doubt that we will be in the unenviable position of #1 infections in the world by the end of the week. The USA is the epicenter of this outbreak now.
Iceland: Iceland has one of the most progressive healthcare systems in the world. Their approach to this outbreak. Test everyone! They only have 364,000 citizens, but their plan is to test everyone on their island. This is a monumental science experiment that will benefit the rest of the world. We will get robust numbers on the numbers of people who are asymptomatic carriers in the population. They only started on Friday, but initial results show that half of those who tested positive are currently non-symptomatic. This reinforces the stay-at-home directives we all are currently experiencing: you could currently feel fine, but you are carrying and shedding the virus.
Viral Mutations: There was a wonderful piece written by Dr Trevor Bedford today that I will summarize here. I have seen a lot of people discuss new strains of SAVSCoV2 emerging and how this may lead to the vaccine not working. If we get a vaccine to work, viral mutations will not be a problem for some time.
SARSCoV2 is a RNA virus. Influenza is also an RNA virus. The molecular machinery RNA viruses use to replicate in the body is highly error prone. This results in rapid mutations.
If we look at influenza, and follow a transmission chain in which one person with the flu infects another person, and they infect another person and so on, you will find that the influenza virus mutates somewhere in its genome about once in every 10 days. Almost all of these mutations will have little to no effect on virus function. Evolution weeds out the mutations that "break" the virus. Mutations that make the virus replicate better are extremely rare. the majority of mutations have little to no functional benefit to the virus.
For influenza, the major driver of evolution is immunity. Mutations will occasionally appear in the genes that give rise to the virus's surface proteins (the H and N you see in flu designations). These mutations in the surface proteins cause people's existing immunity to no longer protect as efficiently against a newly emerged mutant virus. This is why the strain(s) used in the flu vaccine needs to be updated by WHO every year. Shown below, you can see the evolution of influenza H3N2 over the past 12 years, and the amount of "antigenic drift', ie evolution relevant to vaccines and immunity.
You can see with this tree, the original strain is at the bottom left (2008 - blue). The little branches that are all blue show new mutants, but few of them survive in the human population beyond that year. A new tree (green) starts above, and accumulates new mutations making multiple green branches. Some of these survive for a few years, before new branches (light green, yellow and orange) start breaking out. Basically, our immunity drives certain strains out of existence and only escape mutants, those which avoid our adaptive immunity, persist in the population. But they are eventually driven out of existence, and another new escape mutant emerges,
Importantly, this evolution takes years to occur. When pandemic swine flu emerged in 2009, it took the virus 3 years before we saw any evidence at all of antigenic drift.
Dr Bedford, estimates that SARSCoV2 will behave similarly to existing seasonal coronaviruses in its ability to mutate and avoid immunity. The primary protein targeted by immunity in CoV is the spike protein, and we see that in the human CoV OC43, that mutations in the spike protein do occur. But these mutations accumulate in the spike protein because of existing community immunity.
Again, the primary driver of accumulation of mutations is existing immunity in the population, of which (we) currently have none for the SARSCoV2. Therefore, the prediction is, mutations in the spike protein of SARSCoV2 will occur, but these mutations will require many years before they are relevant to escaping immunity from prior infection or immunity created from a vaccine in development.
This will allow vaccines under development to be tested and demonstrate their efficacy (and safety) and if they work, and the virus does mutate in the future, it will be easy to adjust the current vaccine to target the new mutant more efficiently.
So when you see someone talking about viral mutations and we are all doomed.... correct them. The science does not back up their beliefs.