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Viral and cellular gene expression in CD4+ human lymphoid cell lines infected by the simian immunodeficiency virus,
Insights
Simian immunodeficiency virus (SIV/Mne) does not inhibit host cell synthesis like HIV-1. SIV/Mne replication is restricted in certain CD4+ cells, suggesting a need for viral cofactors or specific cell surface molecules.
Area of Science:
- Virology
- Molecular Biology
- Immunology
Background:
- Human immunodeficiency virus type 1 (HIV-1) selectively inhibits host macromolecular synthesis.
- HIV-1 readily infects various CD4+ human lymphoid cell lines.
- Simian immunodeficiency virus (SIV/Mne) is being investigated for its infection mechanisms.
Purpose of the Study:
- To compare the effects of SIV/Mne infection on host macromolecular synthesis with HIV-1.
- To investigate the mechanisms restricting SIV/Mne infection in CD4+ cells susceptible to HIV-1.
Main Methods:
- Analysis of cellular and viral gene expression in CD4+ human lymphoid cell lines.
- Comparison of host macromolecular synthesis in HIV-1 and SIV/Mne infected cells.
- Polymerase Chain Reaction (PCR) analysis to detect viral DNA.
- Flow Cytometry analysis (FACS) for cell surface marker expression.
Main Results:
- SIV/Mne does not induce selective inhibition of cellular protein synthesis or mRNA degradation, unlike HIV-1.
- SIV/Mne efficiently infected only specific CD4+ cell lines (MT-4, C8166, 174 x CEM), with restricted replication in others (CEM, Jurkat, HUT 78).
- Susceptible SIV/Mne infected cells were virally transformed and expressed B cell markers (B7/BB1, CD40).
Conclusions:
- SIV/Mne replication is restricted at an early step in non-susceptible CD4+ cell lines.
- Efficient SIV/Mne replication may depend on viral transformation-induced cofactors or specific cell surface molecules.
- Significant differences exist between HIV-1 and SIV/Mne infection pathways and cellular requirements.
Abstract:
Our laboratory has undertaken an analysis of cellular and viral gene expression in CD4+ human lymphoid cell lines infected by the human and simian immunodeficiency viruses, HIV-1 and SIV/Mne, respectively. The purpose of the current study was to: (i) examine the effects of SIV/Mne infection on host macromolecular synthesis and compare the results to those in the HIV-1 system; and (ii) investigate the mechanisms responsible for the restriction of SIV/Mne infection in CD4 positive lymphoid cells which are readily infected by HIV-1. First we determined that SIV does not impose selective blocks on host macromolecular synthesis, unlike HIV-1, which induces both the selective inhibition of cellular protein synthesis and the degradation of cellular mRNAs (Agy, M., Wambach, M., Foy, K., and Katze, M. G., 1990, Virology 177, 251-258). No such selective reduction in cellular mRNA stability or protein synthesis was observed in cells infected by SIV/Mne. Additional differences between SIV and HIV-1 were observed using a panel of CD4+ human cell lines. While HIV-1-infected all cell lines. SIV/Mne efficiently infected only the MT-4, C8166, and 174 x CEM cell lines. Repeated efforts to infect CEM or Jurkat cells were unsuccessful as determined by PCR analysis of viral DNA. HUT 78 cells supported a limited infection detectable only by PCR analysis. These data suggest the block in viral replication in the nonsusceptible cell lines is at an early step. Interestingly, all the SIV susceptible cells were virally transformed, C8166 and MT-4 by HTLV-1, and 174 x CEM by Epstein-Barr virus. Furthermore FACS analysis revealed that all susceptible cells expressed two B cell associated markers, B7/BB1 and CD40. These observations taken together highlight differences between the HIV and SIV viruses, and suggest that for efficient replication, SIV/Mne may require an additional cell surface molecule, cofactors provided by transforming viruses, or a complex interplay between the two.
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