Hacker News Reader

Comment by weaksauce | Hacker News Reader

different strains?

afaik there havent we havent observed major functional mutations in the virus

We haven't confirmed functional mutations. One of currently known mutations (D614G being a prime suspect) can be functional and we can't rule out the possibility.

The Strain that was seen in ny was more deadly than the strain seen on the west coast. And I’m not sure how many others are out there.

they have a different lineage, but as I stated previously, no major functional mutations were observed.

We don't yet know why (or even if) more people died in New York than on the west coast, per capita. We certainly cannot yet attribute it to a different strain.

You want to use the word isolate. The SARS2 virus is a strain of the original SARS virus I think

Viruses tend to become less lethal as time passes, not more.

I keep reading people asserting this, and I assume it's because we believe that a virus that becomes less lethal would have an evolutionary advantage.

But, wouldn't lengthening the incubation period also be a successful evolutionary strategy regardless of lethality?

It seems to me that there are many possible strategies that a mutating virus might gain an advantage and we shouldn't just assume that the only one that they would use would be to become more mild.

Luckily, sars-cov-2 seems relatively stable.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4873896/

> Trade-offs between different components of parasite fitness provide the dominant conceptual framework for understanding the adaptive evolution of virulence (Alizon et al. 2009).

...

> By far, the most widely studied trade-off involves transmission and virulence (Anderson and May, 1982; Frank, 1996; Alizon et al. 2009). Transmission and virulence are linked by within-host replication: increasing parasite abundance increases the likelihood of transmission, but also increases the likelihood of host death; mathematically, this assumption can be formalized by making transmission rate β an increasing function of parasite-induced mortality rate ν. Nearly all of the literature we summarize below assumes this trade-off. However, another potential trade-off suggested by an examination of R0 involves virulence and recovery rate (Anderson and May, 1982; Frank, 1996). This trade-off is also mediated by replication rate, with high abundance increasing the likelihood of host death, but also decreasing the likelihood of the host clearing the infection (Antia et al. 1994); mathematically, this assumption makes recovery rate γ a decreasing function of parasite-induced mortality rate ν.

'Tend to' doesn't mean some conscious, directed effort. On large enough scale, this is generally the more probable direction, and that's about it. Its truly random by nature.

It can very well go the other way as with 1918 'spanish' flu. Or it can change in ways that won't affect overall mortality much.

It's interesting you should mention the 1918 flu. That one had two waves, the first one less lethal... Evolution is random, add you say, but that's not quite what happened.

It was in the middle of world war 1. Soldiers were infected, and the ones that became the most ill were sent home to recuperate, or die. Either way they spread the virus better than the ones who weren't as ill, and who stayed in the field.

So the usual evolutionary pressure was upside down here.

> On large enough scale, this is generally the more probable direction, and that's about it. Its truly random by nature.

If it's truly random it wouldn't be directional, yeah?

The genetic mutations are random, the survival of a lineage based on pressures and fitness can be "directional" by the human definition.

You're neglecting the other side of things in that analysis. The more successful deadly viruses tend to eliminate their victims, so the surviving population has a higher concentration of people who are resistant or immune to it, including those who acquire immunity after being exposed to the virus.

Reply on news.ycombinator.com