Contrary to early theories, high rates of microcephaly and other neurological deficits recorded during a 2015 Zika outbreak in Brazil were not the result of modern mutations of the virus, scientists from the Columbia University Medical Center concluded in a report released this week.
Zika virus was first documented in 1947, but cases of human infections have been historically rare or mild. That changed in 2015 when a link emerged between pregnant mothers infected with Zika giving birth to babies with microcephaly in Brazil.
A team of Columbia University Medical Center researchers acquired various strains of the virus and developed a method to test its infectivity while growing it in cultured cells. Researchers discovered that every strain of the virus seemed capable of replicating in animal brain tissue — dispelling an earlier theory that a benign strain of the virus had gained the ability to cause neurological disease.
“The idea that the virus had evolved into this neurotropic pathogen was very aggressively put forward, everybody picked up on it,” Amy Rosenfeld, an associate research scientist in microbiology and immunology at the Columbia University Medical Center, said. “However, this new study found that the 1947 isolate of the virus infects brain slices just as strains from Brazil’s 2015 outbreak and those isolated elsewhere can; Zika virus has been able to infect brain tissue all along.”
Researchers found that the virus was not simply killing brain cells in slices of actual animal brains, but was causing “widespread chaos.” The virus derailed neuronal migration and disrupted scaffolds composed of vimentin protein that guides neuronal cells into final position, the study found.
There are a number of theories to explain why Zika virus was not linked to microcephaly prior to the 2015 outbreak in Brazil. A possible explanation includes genetic differences among those affected, concurrent or previous infections, and environmental factors.