It turns out that people aren’t the only ones who can be stodgy curmudgeons unwilling to get with the times. The viruses that infect us can be sticks in the mud too, according to a new study published in Cell Reports. It found that one of our long-time microbial foes, the measles virus (MeV), is unable to tolerate mutations in the two surface proteins crucial to bypassing our cellular defenses, especially when compared to presumingly hipper viruses like Influenza A and hepatitis C.  

Though not technically living, it would be a mistake to think of viruses as unchanging forces of nature. Like their single- and multi-celled counterparts, viruses evolve too, usually in response to pressures placed upon them by the lifeforms they hijack in order to produce more copies. This evolution is by no means perfect, happening via the random adoption, mutation, and discarding of genetic material, but it allows the virus to maintain an arms race against their living cousins. Some changes enable the virus to more easily bypass the host cells’ defenses, others affect its infectious or disease-causing potential, while many turn out to be nothing more than the viral equivalent of tattoos — possibly cool-looking, but either worthless or harmful to later reproduction.

But just like certain animals on the food chain that have remained relatively genetically similar over the eons — viruses can be somewhat unchanging too (the term 'living fossil' is a bit of a misnomer; while some animals like the goblin shark or coelacanth represent the last vestiges of evolutionary lines created hundreds of millions of years ago, they’re still genetically different than they were in the past. Everything evolves, but some species do it slower than others because there isn’t much pressure on them to change)

In the case of measles, a RNA virus that has infected humans with a blotchy rash and high fever for over a millennia, the researchers of this newest study found that it doesn’t take kindly to certain kinds of change. They induced mutations all along measles’ entire genetic structure and found that while most mutated versions of the virus could still infect human cells, it couldn’t when two of its glycoproteins, the hemagglutinin (H) and the fusion protein (F) underwent mutation. Most notably, these results explain both why the measles vaccine is very effective and confers lifelong immunity, and why the flu vaccine isn’t and requires annual booster shots. The measles vaccine (and infection) creates antibodies that specifically target the H and F protein, which, since these proteins hardly ever mutate, renders the germ permanently harmless. On the opposite end of the spectrum, other RNA viruses like influenza change their structure constantly, leaving scientists at their wits’ end trying to predict which strain of the virus will be most prevalent in the world in any one year.

"These data suggest that the MeV hemagglutinin and fusion proteins are very rigid when compared to the influenza A virus hemagglutinin under essentially the same experimental conditions," the authors wrote.

As to why measles evolved into a stickler and influenza became the microscopic version of a college student trying to really find themselves, the researchers don’t have a conclusive answer, but they speculate that it might have to do with how measles infects cells. Regardless, their results do shine a light on the diversity of strategies and tradeoffs viruses take on in order to infect our supple flesh.

"There are many potential explanations for why measles virus proteins can't tolerate insertional mutations, from changing protein stability to changing the structure or function of the proteins," senior study author Nicholas Heaton, a microbiologist at the Icahn School of Medicine at Mount Sinai, New York, said in a press release. "If we can better understand why flexibility or rigidity is imposed at a molecular level, we may be able to understand more about why we see different dynamics of viral evolution."  

Source: Fulton B, Sachs D, Beaty S, et al. Mutational Analysis of Measles Virus Suggests Constraints on Antigenic Variation of the Glycoproteins. Cell Reports. 2015.