Rab11-FIP1C Is Dispensable for HIV-1 Replication in Primary CD4+T Cells, but Its Role Is Cell Type Dependent in Immortalized Human T-Cell Lines

Author:

Fernandez-de Céspedes Melissa V.1ORCID,Hoffman Huxley K.2ORCID,Carter Hannah1ORCID,Simons Lacy M.3ORCID,Naing Lwar1ORCID,Ablan Sherimay D.1ORCID,Scheiblin David A.4ORCID,Hultquist Judd F.3ORCID,van Engelenburg Schuyler B.2ORCID,Freed Eric O.1ORCID

Affiliation:

1. HIV Dynamics and Replication Program, Center for Cancer Research, National Cancer Institute, Frederick, Maryland, USA

2. Biological Sciences, University of Denver, Denver, Colorado, USA

3. Division of Infectious Diseases, Center for Pathogen Genomics and Microbial Evolution, Havey Institute for Global Health, Northwestern University Feinberg School of Medicine, Chicago, Illinois, USA

4. Optical Microscopy and Analysis Laboratory, Cancer Research Technology Program, Frederick National Laboratory for Cancer Research, Frederick, Maryland, USA

Abstract

The incorporation of the HIV-1 envelope (Env) glycoproteins, gp120 and gp41, into virus particles is critical for virus infectivity. gp41 contains a long cytoplasmic tail that has been proposed to interact with host cell factors, including the trafficking factor Rab11a family interacting protein 1C (FIP1C). To investigate the role of FIP1C in relevant cell types—human T-cell lines and primary CD4+T cells—we used CRISPR-Cas9 to knock out FIP1C expression and examined the effect on HIV-1 Env incorporation and virus replication.

Funder

HHS | National Institutes of Health

Publisher

American Society for Microbiology

Subject

Virology,Insect Science,Immunology,Microbiology

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