"No. As the person you're responding to pointed out: "The viruses that cause colds, many of which are also coronaviruses, are pretty adept at hitting people throughout their life.""
Yes. I'm talking about the question of immunity, not whether or not it's possible to get re-infected by new strains of the same virus, or whether or not immunity fades over time. It would be unlikely that this virus didn't confer at least short-term immunity to the host.
The viruses that cause colds primarily re-infect because they mutate at a very high rate. We aren't seeing that with this particular virus.
One of the currently popular mutants of the virus has a mutation in the proof-reading exonuclease that causes the virus to mutate much more often than the original strain.
"that causes the virus to mutate much more often than the original strain."
This is not claimed anywhere in the paper you linked to. They show a non-synonymous mutation in RNA-dependent RNA polymerase, and hypothesized that it could impact drug resistance.
My bad, I was misremembering the paper, which mentions the exonuclease's role in fidelity. I meant RdRps. The conclusion was the same. Figure 4 shows quite clearly that the RdRp mutation is associated with further mutations.
> We found that viral strains with RdRp mutation have a median of 3 point mutations [range: 2–5], whereas viral strains with no RdRp mutation have a median of 1 mutation [range: 0–3] (p value < 0.001, Mann–Whitney test). The different distribution between the two groups relative to the number of mutations is statistically significant (Fig. 4).
Yes. I'm talking about the question of immunity, not whether or not it's possible to get re-infected by new strains of the same virus, or whether or not immunity fades over time. It would be unlikely that this virus didn't confer at least short-term immunity to the host.
The viruses that cause colds primarily re-infect because they mutate at a very high rate. We aren't seeing that with this particular virus.