I Wonder What Tara Would Make of This?

John J. Dennehy (Yale University), Nicholas A. Friedenberg (Dartmouth College), Robert D. Holt (University of Florida), and Paul E. Turner (Yale University), “Viral ecology and the maintenance of novel host use”


Infectious diseases often mysteriously appear and disappear in populations. On some occasions small outbreaks rapidly die out; on others, epidemics ensue. Dennehy et al. explore the dynamics of pathogen emergence using viruses and their host bacteria as a study system. A mathematical model was constructed from basic demographic data to predict transmission rates required for persistence of viruses on their native and novel hosts. The model was validated with serial passage experiments revealing a range of transmission rates where virus populations were sustained on the native host, but went extinct on the novel host. In this critical region, periodic exposure to native hosts allowed the viruses to survive on novel hosts, an unanticipated result. The mechanism behind this phenomenon may be a “host legacy” effect. Dennehy et al. observe that viruses previously reared on the native host showed greater productivity on the novel host than did viruses previously reared on the novel host. This experimental demonstration of a host legacy effect has important implications. The capacity of a virus to propagate upon a novel host apparently is conditional on the recent experience of preceding generations. This is intrinsically interesting, suggesting a kind of complexity in pathogen population dynamics that has not been widely regarded. Second, given this host legacy effect, the total viral population size experiencing the novel environment is greater than would otherwise be expected. Because the amount of genetic variation that can be exposed to selection via novel mutations should scale with population size, this provides a more fertile ground for adaptive evolution to the new host.
Just Curious…

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3 Responses

  1. Tara wishes she had more time to dig into the study! Sounds very cool, though–maybe I can take time to actually read the whole thing next week after grants are off. And how appropriate for profs from Yale and Dartmouth to be talking about a “legacy effect…”

  2. How intriguing. So basically, the virus can go back to it’s natural host for a bit of R’n’R before having another crack at the novel host?
    I think I can see how it would arise. When a virus first moves into the novel host, obviously there’ll be a large pressure to fix adaptations that favour transmission in the novel host. However, that could cause a selective sweep fixing a bunch of other slightly deleterious mutations.
    You can then shed these if you can repair it based on the ancestral genotype by moving back into the original host.
    Say you have a virus with segments A-H. It moves to a novel host, and a mutation A -> A’ allows better transmission and gets fixed. That may drag along with it a bunch of other deleterious mutations B -> B’, C-> C’, and so on.
    Going back into the original host and reassorting would allow them to dump their damaged B’-H’ segments but retain the A’ adaptation to the new host, if it’s selectively neutral in the native host.
    This suggests that the “legacy effect” will be more pronounced in viruses that have multiple independent nucleic acid strands (and thus can reassort with the ancestral strain).
    Doesn’t have to be reassortment, it could also be a back mutation, but that seems like it should be less probable. Could be way off on that though.

  3. Of course, it needn’t involve genetic change at all.
    Say an encapsulated virus normally picks up host proteins when budding, and these are useful to the virus in some way (maybe it tethers its coat proteins to them, or something). They aren’t virally encoded proteins, but they’re still necessary for full virulence.
    In the novel host, the virus won’t be fully adapted to use the homologous proteins.
    So your virus picks up some adaptive genetic mutations that favour transmission in the novel host – then returns to the native host to get a proper capsule.
    This mechanism looks like the legacy effect should only affect the first round of viral replication on each host switch, so it’s probably less likely.
    (Disclaimer: IANA virologist :-) )

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