I’ll comment here but first thanks to both Marielle and CellBioGuy.
Just as informational input I am curious if we have good understanding (meaning once we see a virus we can predict) of why some viruses would more easily make the jump repeatedly while others are perhaps highly unlikely mutations?
Also, more at CellBioGuy, have you seen any of the stories suggesting the outbreak in the Wuhan market was actually human-to-human and not wild-to-human? If it were the case that the COVID-19 outbreak really was not a jump from an infected animal to a human would that change anything to speak of?
Is that last statement just about the three coronaviruses or more generally about viral infection? And does that generalize to the more likely one is to die from some infection the less likely it is that you will actually become infected?
For things you’d want to look at to predict animal-to-human jump, I’d say probably look at...
viral-entry-method
the anchoring and docking protein, and its specificity, similarity between the animal and human (or even the absence/presence of the membrane protein it docks to in humans)
Similarity of immune system
Pigs and ferrets generally seem very human-close
the virus mutation rate
Actually quite different across viruses! Small RNA viruses are generally flirting with error catastrophe, while large DNA viruses are incentivized (and able) to be more careful. You can see something like 100x differences in mutation rates across radically different viruses.
Within-species diversity and population-density for the endemic host (tends to yield generally more powerful, adaptable, immune-evasive viruses)
Rats, mice, and bats (large populations, high genetic diversity; a lot of zoonotics seem to originate in these guys)
R0 is the more proximal metric that infections are sorta evolving to optimize. It is sometimes, but not always, harmed by excessively severe symptoms or high death-rates. I would say that “viruses are discouraged from having excessively high death rates” works okayish as a generalization, but not as a hard rule.
You can vaguely think of viruses as optimizing...
Infectivity * Duration
...and there are plenty of death-cases that don’t matter that much to this equation.
If a higher rate-of-death is linked to a proportional increase in infectivity (creating more virions faster, or something), a virus is not going to evolve to stop that. If the death-rate is mostly late, after the virus has done most of its transmission and replication, the virus does not care. If (as in this case) some transmission happens before people are symptomatic, there is much less pressure on the virus to decrease severity during the symptomatic infection. If you are a host on the side for a zoonotic that is actually endemic to bats, the virus will optimize severity for bats and not you and you will probably have a bad time if you catch it.
I’ll comment here but first thanks to both Marielle and CellBioGuy.
Just as informational input I am curious if we have good understanding (meaning once we see a virus we can predict) of why some viruses would more easily make the jump repeatedly while others are perhaps highly unlikely mutations?
Also, more at CellBioGuy, have you seen any of the stories suggesting the outbreak in the Wuhan market was actually human-to-human and not wild-to-human? If it were the case that the COVID-19 outbreak really was not a jump from an infected animal to a human would that change anything to speak of?
Is that last statement just about the three coronaviruses or more generally about viral infection? And does that generalize to the more likely one is to die from some infection the less likely it is that you will actually become infected?
For things you’d want to look at to predict animal-to-human jump, I’d say probably look at...
viral-entry-method
the anchoring and docking protein, and its specificity, similarity between the animal and human (or even the absence/presence of the membrane protein it docks to in humans)
Similarity of immune system
Pigs and ferrets generally seem very human-close
the virus mutation rate
Actually quite different across viruses! Small RNA viruses are generally flirting with error catastrophe, while large DNA viruses are incentivized (and able) to be more careful. You can see something like 100x differences in mutation rates across radically different viruses.
Within-species diversity and population-density for the endemic host (tends to yield generally more powerful, adaptable, immune-evasive viruses)
Rats, mice, and bats (large populations, high genetic diversity; a lot of zoonotics seem to originate in these guys)
R0 is the more proximal metric that infections are sorta evolving to optimize. It is sometimes, but not always, harmed by excessively severe symptoms or high death-rates. I would say that “viruses are discouraged from having excessively high death rates” works okayish as a generalization, but not as a hard rule.
You can vaguely think of viruses as optimizing...
Infectivity * Duration
...and there are plenty of death-cases that don’t matter that much to this equation.
If a higher rate-of-death is linked to a proportional increase in infectivity (creating more virions faster, or something), a virus is not going to evolve to stop that. If the death-rate is mostly late, after the virus has done most of its transmission and replication, the virus does not care. If (as in this case) some transmission happens before people are symptomatic, there is much less pressure on the virus to decrease severity during the symptomatic infection. If you are a host on the side for a zoonotic that is actually endemic to bats, the virus will optimize severity for bats and not you and you will probably have a bad time if you catch it.