| Autor: |
Mu¨nch, Jan, Janardhan, Ajit, Stolte, Nicole, Stahl-Hennig, Christiane, ten Haaft, Peter, Heeney, Jonathan L., Swigut, Tomek, Kirchhoff, Frank, Skowronski, Jacek |
| Zdroj: |
The Journal of Virology; December 2002, Vol. 76 Issue: 23 p12360-12364, 5p |
| Abstrakt: |
ABSTRACTWe investigated the function of severely truncated simian immunodeficiency virus (SIV) Nef proteins (tNef) in vitro and in vivo. These variants emerged in rhesus monkeys infected with SIVmac239 containing a 152-bp deletion in the nef-unique region and have been suggested to enhance SIV virulence (E. T. Sawai, M. S. Hamza, M. Ye, K. E. Shaw, and P. A. Luciw, J. Virol. 74:2038-2045, 2000). We found that the tNef proteins were unable to down-regulate the cell surface expression of major histocompatibility complex class I proteins, CD4, and CD28 and neither stimulated SIV replication nor enhanced virion infectivity. The tNef proteins did efficiently down-regulate T-cell receptor (TCR):CD3 cell surface expression. Nevertheless, the SIVmac239 tnefvariants were strongly attenuated in six infected juvenile rhesus macaques. Thus, while the ability of SIV Nef to down-modulate TCR:CD3 cell surface expression apparently confers a selective advantage in vivo, it is insufficient for efficient viral replication in infected macaques. Additional mutations elsewhere in SIVmac239 tnefgenomes are required for a virulent phenotype. |
| Databáze: |
Supplemental Index |
| Externí odkaz: |
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