Abstract
The interferon-induced host cell factor tetherin inhibits release of human immunodeficiency virus (HIV) from the plasma membrane of infected cells and is counteracted by the HIV-1 protein Vpu. Influenza A virus (FLUAV) also buds from the plasma membrane and is not inhibited by tetherin. Here, we investigated if FLUAV encodes a functional equivalent of Vpu for tetherin antagonism. We found that expression of the FLUAV protein NS1, which antagonizes the interferon (IFN) response, did not block the tetherin-mediated restriction of HIV release, which was rescued by Vpu. Similarly, tetherin-mediated inhibition of HIV release was not rescued by FLUAV infection. In contrast, FLUAV infection induced tetherin expression on target cells in an IFN-dependent manner. These results suggest that FLUAV escapes the antiviral effects of tetherin without encoding a tetherin antagonist with Vpu-like activity.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Antigens, CD / biosynthesis*
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Cell Line, Tumor
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Cell Membrane / virology
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Flow Cytometry / methods
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GPI-Linked Proteins / biosynthesis
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Gene Expression Regulation, Viral*
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HEK293 Cells
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HIV-1 / metabolism
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HeLa Cells
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Human Immunodeficiency Virus Proteins / metabolism*
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Humans
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Influenza A virus / metabolism*
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Interferons / metabolism*
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Plasmids / metabolism
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Viral Regulatory and Accessory Proteins / metabolism*
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Virion / metabolism
Substances
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Antigens, CD
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BST2 protein, human
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GPI-Linked Proteins
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Human Immunodeficiency Virus Proteins
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Viral Regulatory and Accessory Proteins
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vpu protein, Human immunodeficiency virus 1
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Interferons
Grants and funding
The study was supported by the Leibniz Association (MW SB IN ASM UG AK and SP), Sonderforschungsbereich 900 (CK SP), International Research Training Group 1273 (MK) and Center for Infection Biology of Hannover Medical School (KG). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.