Why We Can't Just Get Rid of the Genes That Let Us Get Infected

By Veronique Greenwood
Feb 13, 2012 11:35 PMNov 19, 2019 8:55 PM


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Takin' one for the team.

What's the News: Clearly, as anyone suffering through a cold right now can tell you, our immune systems aren't all they could be when it comes to keeping us disease-free. And what's worse, the same viruses that have some people hawking up phlegm for weeks can give their roommates or spouses no more than a brief sniffle, hammering home the fact that the immune system wealth isn't distributed evenly. Why hasn't evolution dealt with this problem already and given us all impenetrable defenses? As it turns out, it's not just that evolution takes its own sweet time. It's also that a species benefits from having individuals be immune to some things and vulnerable to others, a new study shows

. What's the Context:

  • The study focused on proteins in a class known as the "major histocompatibility complex," or MHC. These proteins are, as their name suggests, major players in immunity. They sit on your cells' membranes and watch for specific signs that a cell is infected, such as molecules manufactured by a virus or bacterium. Once they pick up on those signs, they start to broadcast an alert that says: "We're under attack. And here's what we're up against." Each one is an SOS beacon that is able to recognize a certain set of signs of infection, so it pays to have a lot of different kinds of them to pick up different pathogens.

  • Vertebrates, in fact, have hundreds of types, and it's been suggested that when we like the smell of someone else's sweat, we're responding to the fact they have an MHC make-up that is very different from ours, so our prospective offspring would have a wide variety of these immune proteins. (And if you haven't heard this before, you need to read about the weird-but-fascinating sweaty T-shirt experiment. Go on. We'll wait.)

How the Heck:

  • What this study found was that viruses tend to evolve so that they target mice with specific sets of MHC proteins. Once a virus had evolved to wreak havoc in mice with one set of MHC proteins---possibly by changing its own molecules just enough to avoid notice by those particular proteins, or some other work-around---it had a really hard time infecting mice with a different set of proteins, which, of course, could still sniff it out just fine.

  • A population of mice with lots of different MHC proteins effectively has walls that keep a virus from spreading too quickly throughout the population, because if the virus evolves to work really well in one host, it sacrifices its chances of infecting a host with a different immune makeup.

Food for Thought:

  • When you whittle down the number of MHC proteins in a population, as has happened in dairy cows bred to produce lots of milk, you wind up with a situation where viruses and bacteria can spread like wildfire---perhaps one of the reasons why antibiotics use is so rampant in the livestock industry (h/t to Josh Fischman at the Percolator blog for pointing this out). It's basically analogous to the problem of agricultural monoculture: if you grow only one crop over a vast swath of land, it's easy for a fungus or beetle or disease to come in and destroy the lot in no time. Planting a variety of crops, or breeding cow populations with lots of different MHC genes, is probably a more resilient option.

  • When we extend this idea to humans, each one of us is, in a sense, an evolutionary red herring for viruses. If a virus evolves so it can really wreak havoc on one particular person, it's effectively closing the door on ravaging someone else with a different set of MHC genes. I guess those roommates and spouses should be really grateful that we're taking the fall for them...this time. Next time, they're up.

Reference: Kubinak JL, et al. Experimental viral evolution to specific host MHC genotypes reveals fitness and virulence trade-offs in alternative MHC types.

Proc Natl Acad Sci USA.

2012 Feb 7. Image courtesy of tanjila / flickr

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