Photo of a needle going into a vaccine container.

Graphic by Luiscar74, Shutterstock.

Stanford Medicine Scope - June 27th, 2017 - by Bruce Goldman

A vaccine is, in essence, a “virtual-reality mug shot” that spurs the immune system to (among other things) generate antibodies that gum up whatever pathogen the vaccine is targeting. But viruses and bacteria have ways of defying vaccination.

For citizens of modern industrialized countries, maybe the most familiar example of viral wiliness is seasonal influenza. Every year, new strains of the virus emerge, forcing vaccinologists to make educated guesses about which of those strains are most likely to sweep across the globe in the coming months. The accuracy of these experts’ guesses determines, to a great extent, how effective any given year’s flu vaccine will be. It’s a game you never win for more than a year at a time.

Other viral menaces — HIV and hepatitis C come to mind — pose similar problems. This can be because they’re prone to frequent mutation and, therefore, rapid evolution into strains that defy a vaccine designed for a particular set of previously existing strains. Or it can come about just because so many strains already abound that no workable vaccine can be designed to take them all on at one shot.

A very commonly encountered but not so well-known pest (because it virtually never kills anyone in modern industrialized countries) is rotavirus. The leading cause of severe diarrhea in young children worldwide, rotavirus causes the deaths of something like 200,000 babies every year, according to Stanford virologist and vaccine pioneer Harry Greenberg, MD. He should know: It was Greenberg whose research was instrumental in producing the first-ever rotavirus vaccine, licensed in 1998.

A second-generation vaccine introduced since then has improved efficacy. Still, the existence of diverse viral strains mean that some of them get past the defense boosted by current rotavirus vaccines.

That could be about to change, though.

In a new study published in Science Translational Medicine, a team of researchers led by Greenberg and using state-of-the-art lab methods zeroed in on a few structural components of rotavirus that appear to be similar enough from one strain to the next that a single vaccine that could generate antibodies to these particular structural components might, in principle, be effective against all strains.

In this case, the virus’s Achilles heel turned out to be a portion of its stalk. Antibodies that target that portion proved effective against numerous viral strains tested in the study. This suggests the possibility of, someday, developing vaccines capable raising broad immunity to all or most rotavirus strains.

And that’s the good news. The bad news is that every viral type marches to its own evolutionary drum, and the weak points for HIV, hepatitis C virus, and all the rest all have to be found separately. But still. Progress in developing a vaccine that could save 200,000 infants lives per year is nothing to sneeze at.

Speaking of which, it would be nice, wouldn’t it, to find something along those lines for the thousand strains of rhinovirus responsible for the common cold.

Originally published at Stanford Medicine Scope Blog