Simian Immunodeficiency Virus Infection of Rhesus Macaques Results in Delayed Zika Virus Clearance

Author:

Vinton Carol L.1,Magaziner Samuel J.2,Dowd Kimberly A.3,Robertson Shelly J.4,Amaro-Carambot Emerito3,Karmele Erik P.5,Ortiz Alexandra M.1,Starke Carly E.1,Mudd Joseph C.1,Whitehead Stephen S.3,Best Sonja M.4,Pierson Theodore C.3,Hickman Heather D.2,Brenchley Jason M.1

Affiliation:

1. Barrier Immunity Section, Laboratory of Viral Diseases, NIAID/NIH, Bethesda, Maryland, USA

2. Viral Immunity and Pathogenesis Unit, Laboratory of Clinical Immunology & Microbiology, NIAID/NIH, Bethesda, Maryland, USA

3. Viral Pathogenesis Section, Laboratory of Viral Diseases, NIAID/NIH, Bethesda, Maryland, USA

4. Innate Immunity & Pathogenesis Section, Laboratory of Virology, NIAID/NIH, Hamilton, Montana, USA

5. Mucosal Immunobiology Section, Laboratory of Molecular Immunology, NIAID/NIH, Bethesda, Maryland, USA

Abstract

Immunocompromised individuals often become symptomatic with infections which are normally fairly asymptomatic in healthy individuals. The particular mechanisms that underlie susceptibility to coinfections in human immunodeficiency virus (HIV)-infected individuals are multifaceted. ZIKV and other flaviviruses are sensitive to neutralizing antibodies, whose production can be limited in HIV-infected individuals but are also sensitive to type I interferons, which are expressed at high levels in HIV-infected individuals. Data in this study highlight how individual components of the innate and adaptive immune responses which become perturbed in HIV-infected individuals influence ZIKV infection.

Funder

HHS | NIH | National Institute of Allergy and Infectious Diseases

Publisher

American Society for Microbiology

Subject

Virology,Microbiology

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