Genomic Epidemiology of 2015–2016 Zika Virus Outbreak in Cape Verde
Oumar Faye, Maria de Lourdes Monteiro, Bram Vrancken, Matthieu Prot, Sébastian Lequime, Maryam Diarra, Oumar Ndiaye, Tomás Valdez, Sandra Tavarez, Jéssica Fernandes Ramos, Silvânia da Veiga Leal, Cecílio Mendes Pires, António Moreira, Maria Filomena Tavares, Linete Fernandes, Jorge Barreto, Maria do Céu Esteves Amaral Teixeira, Maria da Luz Lima Mendonça, Carolina Cardoso da Silva Leite Gomes, Mariano Salazar Castellon, Laurence Ma, Frédéric Lemoine, Fabiana Gámbaro-Roglia, Déborah Delaune, Gamou Fall, Ibrahima Socé Fall, Mamadou Diop, Anavaj Sakuntabhai, Cheikh Loucoubar, Philippe Lemey, Edward C. Holmes, Ousmane Faye, Amadou Alpha Sall, Etienne Simon‐Lorière
Abstract
Z ika virus (ZIKV), first discovered in Uganda in 1947 and sporadically found in Africa and Asia, was long believed to only cause mild disease in humans (1). ZIKV isolates are classified into 1 of 2 lineages, representing the African and Asian genotypes. ZIKVs of the African lineage have been isolated from many regions of Africa (2), mostly through entomologic investigations, and serologic evidence suggests that ZIKV infections in humans are frequent (3). However, until the 2000s, the virus had seldom been detected in humans. The Asian lineage has spread throughout the Pacific, causing outbreaks in humans in Yap, Federated States of Micronesia, in 2007 and in French Polynesia during 2013-2014, where an association with neurologic afflictions was first detected (4). Zika cases were first reported in Brazil in May 2015, and from there, the virus quickly spread to most of the Americas (5). The high number of cases led to the discovery of an association between congenital ZIKV infection and neonatal neurologic complications, particularly microcephaly (6,7).