How Did Zika Virus Emerge in the Pacific Islands and Latin America?

Author:

Pettersson John H.-O.12,Eldholm Vegard1,Seligman Stephen J.34,Lundkvist Åke2,Falconar Andrew K.5,Gaunt Michael W.6,Musso Didier7,Nougairède Antoine89,Charrel Remi89,Gould Ernest A.8,de Lamballerie Xavier89

Affiliation:

1. Department of Infectious Disease Epidemiology and Modelling/Molecular Biology, Domain for Infection Control and Environmental Health, Norwegian Institute of Public Health, Oslo, Norway

2. Department of Medical Biochemistry and Microbiology (IMBIM), Zoonosis Science Center, Uppsala University, Uppsala, Sweden

3. St. Giles Laboratory of Human Genetics of Infectious Diseases, The Rockefeller University, New York, New York, USA

4. Department of Microbiology and Immunology, New York Medical College, Valhalla, New York, USA

5. Departmento de Medicina, Universidad del Norte, Barranquilla, Colombia

6. London School of Hygiene and Tropical Medicine, London, United Kingdom

7. Pôle de Recherche et de Veille sur les Maladies Infectieuses Émergentes, Institut Louis Malardé, Tahiti, French Polynesia

8. UMR Emergence des Pathologies Virales (EPV: Aix-Marseille Université-IRD 190-INSERM 1207-EHESP), Marseille, France

9. Institut Hospitalo-Universitaire Méditerranée Infection, APHM Public Hospitals of Marseille, Marseille, France

Abstract

ABSTRACT The unexpected emergence of Zika virus (ZIKV) in the Pacific Islands and Latin America and its association with congenital Zika virus syndrome (CZVS) (which includes microcephaly) and Guillain-Barré syndrome (GBS) have stimulated wide-ranging research. High densities of susceptible Aedes spp., immunologically naive human populations, global population growth with increased urbanization, and escalation of global transportation of humans and commercial goods carrying vectors and ZIKV undoubtedly enhanced the emergence of ZIKV. However, flavivirus mutations accumulate with time, increasing the likelihood that genetic viral differences are determinants of change in viral phenotype. Based on comparative ZIKV complete genome phylogenetic analyses and temporal estimates, we identify amino acid substitutions that may be associated with increased viral epidemicity, CZVS, and GBS. Reverse genetics, vector competence, and seroepidemiological studies will test our hypothesis that these amino acid substitutions are determinants of epidemic and neurotropic ZIKV emergence.

Publisher

American Society for Microbiology

Subject

Virology,Microbiology

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