Abstract:
:Besides its role in viral assembly, the vesicular stomatitis virus (VSV) matrix (M) protein causes cytopathic effects such as cell rounding (D. Blondel, G. G. Harmison, and M. Schubert, J. Virol. 64:1716-1725, 1990). DNA cotransfection assays demonstrated that VSV M protein was able to inhibit the transcription of a reporter gene (B. L. Black and D. S. Lyles, J. Virol. 66:4058-4064, 1992). We have confirmed these observations by using cotransfections with an infectious clone of human immunodeficiency virus type 1 (HIV-1) and found that the amino-terminal 32 amino acids of M protein which are essential for viral assembly were not required for this inhibition. For the study of the potential role of M protein in the shutoff of transcription from chromosomal DNA, we have isolated stable HeLa T4 cell lines which encode either a wild-type or a temperature-sensitive (ts) VSV M gene under control of the HIV-1 long terminal repeat promoter. Transcription of the M mRNA was transactivated after HIV-1 infections. A cell line which encodes the wild-type M protein was nonpermissive for either HIV-1 or HIV-2. A cell line that encodes the ts M gene was transfected with the infectious HIV-1 DNA or was infected with HIV-1 or HIV-2. In all cases, at 32 degrees C, the permissive temperature for M protein, the cells were nonpermissive for HIV replication. At 40 degrees C, the ts M protein was nonfunctional and both HIV-1 and HIV-2 were able to replicate at high levels. A comparison of the amounts of proviral HIV-1 DNAs and HIV-1 mRNAs at 10 and 36 h after HIV-1 infection demonstrated that proviral insertion had not been prevented by M protein and that the block in HIV-1 replication was at the level of proviral expression. The severe reduction of HIV-1 proviral transcripts demonstrates that the VSV M protein alone can inhibit expression from chromosomal DNA. These results strongly support the hypothesis that the VSV M protein is involved in the shutoff of host cell transcription. M protein was able to attenuate HIV-1 infections and protect the cell population from HIV-1 pathogenesis. The temperature-dependent switch from a persistent to a lytic HIV-1 infection in the presence of ts M protein could be useful for studies of HIV-1 replication and pathogenesis.
journal_name
J Viroljournal_title
Journal of virologyauthors
Paik SY,Banerjea AC,Harmison GG,Chen CJ,Schubert Mdoi
10.1128/JVI.69.6.3529-3537.1995subject
Has Abstractpub_date
1995-06-01 00:00:00pages
3529-37issue
6eissn
0022-538Xissn
1098-5514journal_volume
69pub_type
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pub_type: 杂志文章
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pub_type: 杂志文章
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pub_type: 杂志文章
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pub_type: 杂志文章
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pub_type: 杂志文章
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pub_type: 杂志文章
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pub_type: 杂志文章
doi:10.1128/JVI.61.7.2198-2207.1987
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pub_type: 杂志文章
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pub_type: 杂志文章
doi:10.1128/JVI.79.10.6260-6271.2005
更新日期:2005-05-01 00:00:00
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journal_title:Journal of virology
pub_type: 杂志文章
doi:10.1128/JVI.68.9.5882-5889.1994
更新日期:1994-09-01 00:00:00
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pub_type: 杂志文章
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pub_type: 杂志文章
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更新日期:1988-11-01 00:00:00
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pub_type: 杂志文章
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pub_type: 杂志文章
doi:10.1128/JVI.68.2.1103-1114.1994
更新日期:1994-02-01 00:00:00
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pub_type: 杂志文章
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pub_type: 杂志文章
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更新日期:2008-07-01 00:00:00
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更新日期:2014-05-01 00:00:00
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journal_title:Journal of virology
pub_type: 杂志文章
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更新日期:1986-12-01 00:00:00
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pub_type: 杂志文章
doi:10.1128/jvi.74.20.9412-9420.2000
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