Adipocyte Plasma Membrane Protein (APMAP) promotes JC Virus (JCPyV) infection in human glial cells.

Autor: Haley SA; Department of Molecular Biology, Cell Biology and Biochemistry, Brown University, Providence, RI, USA. Electronic address: sheila_haley@brown.edu., O'Hara BA; Department of Molecular Biology, Cell Biology and Biochemistry, Brown University, Providence, RI, USA., Atwood WJ; Department of Molecular Biology, Cell Biology and Biochemistry, Brown University, Providence, RI, USA. Electronic address: walter_atwood@brown.edu.
Jazyk: angličtina
Zdroj: Virology [Virology] 2020 Sep; Vol. 548, pp. 17-24. Date of Electronic Publication: 2020 Jun 07.
DOI: 10.1016/j.virol.2020.06.002
Abstrakt: The demyelinating disease progressive multifocal leukoencephalopathy (PML) is caused by the human polyomavirus, JCPyV, under conditions of prolonged immunosuppression. Initial infection is asymptomatic, and the virus establishes lifelong persistence in the host. Following the loss of immune surveillance, the virus can traffic to the central nervous system and infect oligodendrocytes to cause demyelination and PML. The mechanisms involved in glial cell infection are not completely understood. In a screen for N-glycosylated proteins that influence JCPyV pathology, we identified Adipocyte Plasma Membrane Associated Protein (APMAP) as a host cell modulator of JCPyV infection. The removal of APMAP by small interfering siRNA as well as by CRISPR-Cas9 gene editing resulted in a significant decrease in JCPyV infection. Exogenous expression of APMAP in APMAP knockout cell lines rescued susceptibility to infection. These data suggest that virus infection of glial cells is dependent on APMAP.
(Copyright © 2020 Elsevier Inc. All rights reserved.)
Databáze: MEDLINE
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