SAN FRANCISCO — Disrupting the Zika enzyme NS3 could help stop the virus. NS3 causes problems when it gloms on to centrioles, structures inside cells needed to divvy up chromosomes when cells divide, Andrew Kodani, a cell biologist at Boston Children’s Hospital, reported December 6 at the American Society for Cell Biology’s annual meeting.
Zika, dengue and other related viruses, known as flaviviruses, all use a version of NS3 to chop joined proteins apart so they can do their jobs. (Before chopping, Zika’s 10 proteins are made as one long protein.) But once NS3 finishes slicing virus proteins, it moves to the centrioles and can interfere with their assembly, Kodani and colleagues found. Something similar happens in some genetic forms of microcephaly.
Kodani and colleagues found that small amounts of a chemical called anthracene can prevent NS3 from tinkering with the centrioles. So far the work has been done only in lab dishes.
A.T. Kodani et al. Zika infection disrupts centriole biogenesis. American Society for Cell Biology Annual Meeting, December 6, 2016.
M. Rosen. This week in Zika: Vaginal vulnerability, disease double trouble and more. Science News Online. November 17, 2016.