Here’s a puzzle from Varki et al (2008). All simians and primates *except* humans are infected with a retrovirus called simian foamy virus (SFV). SFV is normally harmless, and reproduces by infecting cells, inserting itself into the host genome, and then at some point expressing the genes necessary to make new virus. The virus is ubiquitous, and newborns apparently catch it from their kin. The same is probably true for another group of lineage-specific viruses called simian infectious retroviruses (SIVs).
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Humans do not have these viruses, but we can catch them from chimps. So how did we lose these viruses if we are descended from primate ancestors who had them?
From the paper:
Indeed, given the remarkable corroboration between the phylogenetic trees of primates and their lineage-specific simian foamy viruses (SFVs), our common ancestors with other hominids almost certainly had SFVs. The same is probably true of the lineage-specific simian infectious retroviruses (SIVs) found in most non-human primates (NHPs). Assuming that the common ancestors of hominids carried multiple endemic infectious retroviruses, how did the human lineage eliminate them? Given that humans remain susceptible to re-infection with both SFVs and SIVs from other hominids, this seems unlikely to be explained solely on the basis of more efficient host restriction systems. Rather, there seems to have been an episode in which the ancestral human lineage was somehow ‘purged’ of these endemic viruses.
Now wait, before you get all excited, there is more to the story. Varki et al. suggest that humans lost the viruses because we lost the enzyme for making a particular glycoprotein that SIVs and SFVs use to make their envelope (outer coating of the infectious particle). These viruses are harmless, though, so there would be no selective benefit to eliminating that glycoprotein just to eliminate the viruses.
Rather, there might be a significant cost to inactivating the enzyme, since the glycoprotein we lost was important for cell recognition and immune responses ( based on its distribution in other mammals). Its loss would have to be compensated for by any lectins (proteins that bind to glycoproteins) that interacted with it, requiring multiple downstream changes, and likely affecting multiple biological processes.
Varki proposes that some other unknown lethal virus used the same glycoprotein to infect cells, so eliminating the glycoprotein to defend against infection was advantageous enough to overcome any other costs. (Alternatively, the loss could have been a random mutation that became fixed in the population due to a sudden population bottleneck.) The glycoprotein that we lost would then have to be replaced by another, similar glycoprotein that had some affinity for the same lectins. But that compensation would take time, whereas the loss of the glycoprotein would have an immediate effect on many cellular processes.
According to published work, 10 out of 60 genes involved in recognizing the replacement glycoprotein show evidence of rapid evolution (multiple mutations), dating back to around 1 to 1.2 million years ago. Even more interesting, the expression pattern of the replacement glycoprotein has changed—now it is expressed in the brain as well as other places. Furthermore, the inactivation of the enzyme to make the original glycoprotein apparently happened after our lineage split from chimps, and before the most rapid enlargement of our brains. Is there a causal relationship? Who knows?
Unfortunately, the loss of the enzyme and subsequent change to our glycoprotein repertoire may have left us with some immune-related vulnerabilities.
We have a complex story here, one that is mostly speculation with some indirect data. Would the loss of the enzyme, and thus the glycoprotein it made, have been enough to eliminate the endemic SIVs and SFVs? Was the loss of the glycoprotein due to drift, or some selective advantage against an unknown virus? Does the changed expression pattern of the substitute glycoprotein have anything to do with our larger brains and increased connectivity compared to chimps? Is the proposed scenario even feasible?
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To survive such a sudden change is unlikely, but not impossible. It would depend on what systems were affected by the loss of the glycoprotein. These probably included fertility, the immune system, and as evidence suggests, the nervous system. It may have also affected protein trafficking through the Golgi apparatus. The compensatory adaptive mutations to the interacting lectins would have to have occurred rapidly, but given our population size and mutation rate this is unlikely, unless the process was guided somehow.
It should be possible to examine the feasibility of some of these transitions. By doing so, we may arrive at a better understanding of what such a series of adaptations would really require. And whether we were wiped clean of SFVs and SIVs by design.