With just 141 confirmed deaths so far, an interesting question is whether the 2009 H1N1 influenza virus could mutate into something more lethal (“How a Mild Virus Might Turn Vicious“). Of course it could – but is it beneficial for the virus?
A fundamental principle of viral evolution is that viruses must spread from host to host to maintain the viral population. A virus spreads only if an infected individual passes the virus on to more than one new host. Furthermore, infection can spread only if population density exceeds a minimal value.
Some scientists believe that increased viral virulence reduces transmissibility. When infected hosts die faster, exposure to uninfected hosts is reduced. According to Ian Lipkin:
“A really aggressive flu that quickly kills its host” – like SARS and H5N1 avian flu – “gives itself a problem”.
According to this hypothesis, virulence is selected against as the virus spreads in humans. This idea leads to statements like this one:
In the last year, dozens of H5N1 cases have been confirmed in toddlers, almost all of whom have survived – which led some experts to speculate that those are cases of a less lethal version of H5N1 that is better adapted to humans.
Why is reduced lethality equated with being better adapted to humans? And how could the virus become better adapted to humans when human to human transmission has been minimal?
There is insufficient evidence to conclude that increased viral virulence leads to reduced transmission. For example, the 1918 influenza virus strain was extremely virulent, yet spread very efficiently among humans. SARS and H5N1 influenza aren’t good examples – SARS transmission was probably stopped by containment efforts, and H5N1 influenza virus hasn’t transmitted well among humans, if at all.
In today’s highly crowded and mobile society, even a very lethal virus can be transmitted well. Acute viral infections are preceded by an incubation period, during which virus is shed but symptoms are not yet severe enough to lead to hospitalization. And even a highly pathogenic virus will cause mild or no disease in some individuals – further increasing the chances of spreading infection.
It seems more likely that increased viral virulence could lead to better transmission. For example, a more virulent influenza virus might cause more coughing and sneezing, which would be more effective in transmitting infection. Perhaps we should focus on transmissibility, not virulence, as the property that drives viral evolution. Viruses evolve so they can be efficiently transmitted to other hosts. According to this hypothesis, any other properties that accompany transmissibility, such as virulence, are secondary effects. If this idea were true, then all viruses would evolve to be maximally infectious and avirulent. But this is not the case. Perhaps, as Peter Palese said, viral virulence has unknown benefits:
Look, I believe in Darwin. Yes, the fittest virus survives. But it’s not clear what the ultimate selection parameter is. A mutation that confers lethality, he explained, may confer another advantage scientists have not pinned down.
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