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• W2292932153 abstract "ABSTRACT Endogenous retroviruses (ERVs), the majority of which exist as degraded remnants of ancient viruses, comprise approximately 8% of the human genome. The youngest human ERVs (HERVs) belong to the HERV-K(HML-2) subgroup and were endogenized within the past 1 million years. The viral envelope protein (ENV) facilitates the earliest events of endogenization (cellular attachment and entry), and here, we characterize the requirements for HERV-K ENV to mediate infectious cell entry. Cell-cell fusion assays indicate that a minimum of two events are required for fusion, proteolytic processing by furin-like proteases and exposure to acidic pH. We generated an infectious autonomously replicating recombinant vesicular stomatitis virus (VSV) in which the glycoprotein was replaced by HERV-K ENV. HERV-K ENV imparts an endocytic entry pathway that requires dynamin-mediated membrane scission and endosomal acidification but is distinct from clathrin-dependent or macropinocytic uptake pathways. The lack of impediments to the replication of the VSV core in eukaryotic cells allowed us to broadly survey the HERV-K ENV-dictated tropism. Unlike extant betaretroviral envelopes, which impart a narrow species tropism, we found that HERV-K ENV mediates broad tropism encompassing cells from multiple mammalian and nonmammalian species. We conclude that HERV-K ENV dictates an evolutionarily conserved entry pathway and that the restriction of HERV-K to primate genomes reflects downstream stages of the viral replication cycle. IMPORTANCE Approximately 8% of the human genome is of retroviral origin. While many of those viral genomes have become inactivated, some copies of the most recently endogenized human retrovirus, HERV-K, can encode individual functional proteins. Here, we characterize the envelope protein (ENV) of the virus to define how it mediates infection of cells. We demonstrate that HERV-K ENV undergoes a proteolytic processing step and triggers membrane fusion in response to acidic pH—a strategy common to many viral fusogens. Our data suggest that the infectious entry pathway mediated by this ENV requires endosomal acidification and the GTPase dynamin but does not require clathrin-dependent uptake. In marked contrast to other betaretroviruses, HERV-K ENV imparts broad species tropism in cultured cells. This work provides new insights into the entry pathway of an extinct human virus and provides a powerful tool to further probe the endocytic route by which HERV-K infects cells." @default.
• W2292932153 created "2016-06-24" @default.
• W2292932153 creator A5003654135 @default.
• W2292932153 creator A5077992307 @default.
• W2292932153 date "2016-04-01" @default.
• W2292932153 modified "2023-10-16" @default.
• W2292932153 title "Infectious Entry Pathway Mediated by the Human Endogenous Retrovirus K Envelope Protein" @default.
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• W2292932153 doi "https://doi.org/10.1128/jvi.03136-15" @default.
• W2292932153 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4794671" @default.
• W2292932153 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/26792739" @default.
• W2292932153 hasPublicationYear "2016" @default.
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