Not your grandfather’s Zika
How an unfamiliar virus led to a global epidemic
How does a formerly harmless and obscure virus like Zika transform itself into a feared pathogen inflicting a devastating impact on global health?
A new UCLA study suggests that the virus possesses the ability to mutate rapidly, increasing its power to invade the human body and allowing the current outbreak to spread swiftly around the world. Published April 15 by the journal Cell Host & Microbe, the findings sparked coverage by TIME, NBC News, The Scientist, Baltimore Sun, KCBS-Channel 2 and others.
“The Zika virus has undergone significant genetic changes in the past 70 years,” explained senior author Genhong Cheng, a professor of microbiology, immunology and molecular genetics at the David Geffen School of Medicine at UCLA. “By tracing its genetic mutations, we aimed to understand how the virus is transmitted from person to person and how it causes different types of disease.”
First isolated in 1947, the Zika virus only sporadically caused disease in Africa and Asia until 2007. Scientists previously believed that infection was spread solely by mosquitoes and caused only mild illnesses.
The latest epidemic has linked the virus to fetal brain-development disorders and Guillain-Barre syndrome. New modes of transmission, including infection through sexual contact and from mother to fetus, have also surfaced.
“We don’t know why Zika infection was not associated with serious human disease, especially in newborns, until recently,” said co-author Dr. Stephanie Valderramos, a fellow in obstetrics-gynecology at the Geffen School. “We hoped that taking a closer look at the virus’ genetic changes over time would reveal clues to this mystery.”
Cheng’s laboratory collaborated with researchers in China to compare genetic differences among 41 strains of Zika virus. Thirty strains originated from humans, 10 from mosquitoes and one from monkeys.
In sequencing the virus, the team identified substantial DNA changes between the strains, showing a major split between the Asian and African lineages, as well as the human and mosquito versions.
“We suspect these mutations could help the virus replicate more efficiently, evade the body’s immune response or invade new tissues that provide a safe harbor for it to spread,” said co-author Lulan Wang, a graduate student researcher in Cheng’s laboratory.
Cheng and his colleagues’ next step will be to analyze the viral strains causing the current epidemic and look for genetic targets for drug and vaccine development.