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Egress of HSV-1 capsid requires the interaction of VP26 and a cellular tetraspanin membrane protein.

ABSTRACT: HSV-1 viral capsid maturation and egress from the nucleus constitutes a self-controlled process of interactions between host cytoplasmic membrane proteins and viral capsid proteins. In this study, a member of the tetraspanin superfamily, CTMP-7, was shown to physically interact with HSV-1 protein VP26, and the VP26-CTMP-7 complex was detected both in vivo and in vitro. The interaction of VP26 with CTMP-7 plays an essential role in normal HSV-1 replication. Additionally, analysis of a recombinant virus HSV-1-UG showed that mutating VP26 resulted in a decreased viral replication rate and in aggregation of viral mutant capsids in the nucleus. Together, our data support the notion that biological events mediated by a VP26 - CTMP-7 interaction aid in viral capsid enveloping and egress from the cell during the HSV-1 infectious process.

SUBMITTER: Wang L

PROVIDER: S-EPMC2913958 | biostudies-other | 2010

REPOSITORIES: biostudies-other

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Egress of HSV-1 capsid requires the interaction of VP26 and a cellular tetraspanin membrane protein.

Wang Lei L Liu Longding L Che Yanchun Y Wang Lichun L Jiang Li L Dong Chenghong C Zhang Ying Y Li Qihan Q

Virology journal 20100714

HSV-1 viral capsid maturation and egress from the nucleus constitutes a self-controlled process of interactions between host cytoplasmic membrane proteins and viral capsid proteins. In this study, a member of the tetraspanin superfamily, CTMP-7, was shown to physically interact with HSV-1 protein VP26, and the VP26-CTMP-7 complex was detected both in vivo and in vitro. The interaction of VP26 with CTMP-7 plays an essential role in normal HSV-1 replication. Additionally, analysis of a recombinant ...[more]

PMID: 20630051

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