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Rhesus monkey TRIM5α has distinct HIV-1 restriction activity among different mammalian cell lines
Jian Gong1, Xi-Hui Shen, Hui Qiu
1The State Key Laboratory of Virology, Wuhan Institute of Virology, Chinese Academy of Sciences, Xiaohongshan 44, Wuhan 430071, China.
Abstract:
Rhesus monkey TRIM5α (TRIM5α(rh)), a member of the tripartite motif (TRIM) family, was identified as the main restriction factor responsible for resistance of old world monkey cells to HIV-1 infection. However, the precise mechanism of HIV-1 infection inhibition by TRIM5α remains elusive and appears to be related to some cellular cofactors. Here we reported that TRIM5α(rh) can significantly reduce the infection efficiency of VSV-G pseudotyped HIV-1/MA-YFP virus in human epithelial carcinoma (HeLa) cells, moderately reduce in porcine kidney (PK-15) cells and have no effect on the pseudotyped virus infection in Madin-Darby canine kidney (MDCK) cells. Furthermore, we found that the different HIV-1 restriction activities have no relation with the intracellular localization of TRIM5α(rh). These results indicate that the cellular environment is very important for the efficient anti-HIV-1 activity of TRIM5α(rh). We speculate that some unknown factors required for HIV-1 infection inhibition activity are adequately expressed in HeLa cells, inadequately expressed in PK-15 cells and absent in MDCK cells.
Insights
Rhesus TRIM5α protein restricts HIV-1 infection, but its effectiveness varies by cell type. Cellular cofactors, not protein location, likely determine this anti-HIV-1 activity.
Area of Science:
- Virology
- Immunology
- Cell Biology
Background:
- The tripartite motif (TRIM) family protein, Rhesus monkey TRIM5α (TRIM5α(rh)), is a key factor in restricting HIV-1 infection in Old World monkey cells.
- The exact mechanism by which TRIM5α inhibits HIV-1 remains unclear and may involve cellular cofactors.
Purpose of the Study:
- To investigate the anti-HIV-1 activity of TRIM5α(rh) in different cell types.
- To determine if intracellular localization of TRIM5α(rh) influences its HIV-1 restriction capabilities.
Main Methods:
- Infection of human epithelial carcinoma (HeLa), porcine kidney (PK-15), and Madin-Darby canine kidney (MDCK) cells with VSV-G pseudotyped HIV-1/MA-YFP virus.
- Analysis of TRIM5α(rh) intracellular localization.
Main Results:
- TRIM5α(rh) significantly reduced HIV-1 infection in HeLa cells, moderately in PK-15 cells, and had no effect in MDCK cells.
- The observed differences in HIV-1 restriction activity did not correlate with TRIM5α(rh) intracellular localization.
Conclusions:
- The cellular environment plays a crucial role in the anti-HIV-1 activity of TRIM5α(rh).
- Differential expression of unknown cellular cofactors in HeLa, PK-15, and MDCK cells likely accounts for the varying levels of HIV-1 restriction by TRIM5α(rh).
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