The paper I’m discussing today came out last May in Science but, as you probably noticed, I’ve been busy posting about other things and neglected the science aspect of the CHIMERAS blog. Apologies to my science readers.
Viruses are pesky little things that have the innate ability of inserting genetic material into our cells. As such, they are capable of permanently changing our immune system: for one thing, our immune system learns to recognize the pathogen and that “memory” will be used to prevent future infections. Viruses can also alter the expression of certain genes within the infected cells, shutting off the production of proteins that would otherwise prevent the virus from replicating.
Viruses that infect preferentially cells from the immune system are particularly nasty. HIV, for example, gradually depletes the host’s reservoir of T-cells (the “sentinels” of the immune system) until patients die of a common infection simply because their body can no longer fight pathogens.
HIV is not the only virus that attacks the immune system. Measles is another one. The virus enters cells through a receptor that’s expressed on the surface of many immune cells such as dendritic cells, macrophages, and lymphocytes. All of these cells have a very important function: they retain “immune memory.” What does it mean? Every time the immune system encounters a new pathogen (a virus, a bacterium, etc.), bits of proteins from the pathogens are presented to the immune cells. The immune cells create an “impression” of these proteins so that they can bind to them and destroy them. using a metaphor, they create a “mold”, a special receptor that binds to the pathogen. Lots of cells with the special “mold” are created, so they can bind to the pathogen, capture it, and destroy it. A whole army of cells needs to be created in order to get rid of the million viral particles in the body, but once the infection is over and the full army is no longer needed, only a few of these cells with the special “mold” are saved. These few are the ones that preserve the memory of the specific pathogen, so that next time it enters the body it is recognized immediately and destroyed before it can start the infection.
Back to the measles virus. This nasty pathogen has a special receptor that allows it to enter the cell membrane of “mature” immune cells , i.e. cells that carry that special “mold” for a particular pathogen. By infecting and killing those cells, the measles virus effectively erases immune memory, making the host prone to be reinfected by pathogens it has already encountered. So, on the one hand, the virus stimulates immune responses that will protect from future measles infections. On the other hand, however, it erases some of the existing defenses against other pathogens. It’s called the “measles paradox.” Immune memory of previous pathogens is eared and replaced by measles-specific immune responses. 
A study published in Science last May  corroborated this finding by looking at child mortality data from England, Wales, the United States, and Denmark during the decades immediately preceding and following the introduction of the measles vaccine. The researchers showed that immune memory loss caused by measles infection lasted from 6 months to several years, and that vaccination against measles significantly reduced child mortality caused by non measles infections.
To further corroborate their analysis, the researchers applied the same techniques to pertussis, which is also known to cause immunosuppression. This time they found no correlation with the incidence of pertussis and non-pertussis infectious disease mortality, corroborating the hypothesis that it was the measles vaccine to cause the drop in mortality.
“MV infection and vaccination produce strong and durable herd immunity against subsequent epidemics. Our results thus suggest an extra dynamical twist: MV infections could also reduce population immunity against other infections in which MV immunomodulation could be envisioned as a measles-induced immune amnesia; hence, measles vaccination might also be preserving herd protection against nonmeasles infections .”
 Tahara, M., Takeda, M., Shirogane, Y., Hashiguchi, T., Ohno, S., & Yanagi, Y. (2008). Measles Virus Infects both Polarized Epithelial and Immune Cells by Using Distinctive Receptor-Binding Sites on Its Hemagglutinin Journal of Virology, 82 (9), 4630-4637 DOI: 10.1128/JVI.02691-07
 de Vries, R., & de Swart, R. (2014). Measles Immune Suppression: Functional Impairment or Numbers Game? PLoS Pathogens, 10 (12) DOI: 10.1371/journal.ppat.1004482
 Mina MJ, Metcalf CJ, de Swart RL, Osterhaus AD, & Grenfell BT (2015). Long-term measles-induced immunomodulation increases overall childhood infectious disease mortality. Science (New York, N.Y.), 348 (6235), 694-9 PMID: 25954009
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