Have you ever heard of rotavirus? It’s a nasty bug that causes stomach and intestinal inflammation, leading to severe dehydration from relentless diarrhea. But fear not, for science has brought us two vaccines — Rotarix (RV1) and RotaTeq (RV5) — that have significantly slashed cases of debilitating illness caused by this troublesome virus.

However, as with all things in life, these vaccines are not foolproof shields against rotavirus. Some vaccinated children still find themselves battling the virus. Why is that? Well, enter Jiye Kwon, a dedicated PhD student from Yale School of Public Health who embarked on a mission to answer this puzzling question.

Kwon and his team delved into the intricate world of rotavirus genetics. While previous studies had mainly focused on two proteins on the virus’ surface, Kwon decided to take a different route. He wanted to explore whether the remaining nine genetic segments within the virus — what he calls the

“viral backbone”

— could hold the key to understanding why vaccine effectiveness varies among different rotavirus strains.

Their journey led them through 254 cases of rotavirus-related sickness spanning across seven medical sites in the US between 2012 and 2016. What they discovered was groundbreaking: vaccine effectiveness seemed to waver as the genetic gap widened between circulating strains and vaccine strains.

In Kwon’s own words,

“Previous research has focused on just the outer proteins of the virus, but rotavirus has a total of 11 genetic segments.”

This shift towards examining the full genome rather than just surface proteins opened up new avenues for understanding how these vaccines work their magic against rotavirus.

Through their meticulous analysis using cutting-edge techniques like sieve analysis, they found that individuals vaccinated with Rotarix were more susceptible to strains significantly different from those covered by the vaccine – more than 9.6% dissimilar in their genetic makeup.

This revelation was further illuminated when observing how vaccination patterns influenced which strains dominated in various locations. Places favoring Rotarix or RotaTeq saw genetically distant strains become prevalent over time due to natural viral evolution adapting in response to vaccine-induced immunity.

As co-senior author Virginia Pitzer puts it eloquently,

“Our study shows that looking at the entire genetic structure of rotavirus gives a much clearer picture of how well vaccines work compared to just looking at the two surface proteins.”

These findings shed light on an essential aspect of vaccination strategies; considering not only specific proteins but also comprehensively studying viral genomes can be crucial in designing effective vaccines against rapidly evolving viruses like rotavirus.