Accéder au contenu
Merck

Determinants of Zika virus host tropism uncovered by deep mutational scanning.

Nature microbiology (2019-03-20)
Yin Xiang Setoh, Alberto A Amarilla, Nias Y G Peng, Rebecca E Griffiths, Julio Carrera, Morgan E Freney, Eri Nakayama, Shinya Ogawa, Daniel Watterson, Naphak Modhiran, Faith Elizabeth Nanyonga, Francisco J Torres, Andrii Slonchak, Parthiban Periasamy, Natalie A Prow, Bing Tang, Jessica Harrison, Jody Hobson-Peters, Thom Cuddihy, Justin Cooper-White, Roy A Hall, Paul R Young, Jason M Mackenzie, Ernst Wolvetang, Jesse D Bloom, Andreas Suhrbier, Alexander A Khromykh
RÉSUMÉ

Arboviruses cycle between, and replicate in, both invertebrate and vertebrate hosts, which for Zika virus (ZIKV) involves Aedes mosquitoes and primates1. The viral determinants required for replication in such obligate hosts are under strong purifying selection during natural virus evolution, making it challenging to resolve which determinants are optimal for viral fitness in each host. Herein we describe a deep mutational scanning (DMS) strategy2-5 whereby a viral cDNA library was constructed containing all codon substitutions in the C-terminal 204 amino acids of ZIKV envelope protein (E). The cDNA library was transfected into C6/36 (Aedes) and Vero (primate) cells, with subsequent deep sequencing and computational analyses of recovered viruses showing that substitutions K316Q and S461G, or Q350L and T397S, conferred substantial replicative advantages in mosquito and primate cells, respectively. A 316Q/461G virus was constructed and shown to be replication-defective in mammalian cells due to severely compromised virus particle formation and secretion. The 316Q/461G virus was also highly attenuated in human brain organoids, and illustrated utility as a vaccine in mice. This approach can thus imitate evolutionary selection in a matter of days and identify amino acids key to the regulation of virus replication in specific host environments.