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Published December 1990 | public
Journal Article

A human cell factor is essential for HIV-1 Rev action

Abstract

To examine the restriction of HIV growth in murine cells, we infected NIH 3T3 cells with HIV pseudotyped by Moloney murine leukemia virus. The virus, which carried a dominant selectable marker under the control of the HIV LTR, gave large numbers of resistant clones, showing that murine cells are permissive for HIV uncoating, reverse transcription, nuclear transport and integration. However, we found that several murine cell lines, as well as CHO cells, could not support the function of rev, the viral regulatory gene which, in human cells, induces the cytoplasmic expression of the incompletely spliced class of HIV mRNAs that encode the viral structural proteins. Transfection of the HIV‐infected murine cells with a HTLV‐1 rex‐expressing vector failed to rescue the rev‐ phenotype, indicating that the block extended to rex function. Most importantly, we could complement the rev defect by fusing the infected murine with uninfected human cells. We conclude that HIV tropism is partly a consequence of a trans‐acting cellular factor critical for Rev function.

Additional Information

© 1990 Oxford University Press. Received on April 18, 1990; revised on August 20, 1990. We thank W. J. Nir for excellent technical assistance, M. Feinberg, M. Muesing and R. Pomerantz for helpful discussions, O. Danos and R.C. Mulligan for pCRIP-gag-2, W. Greene for pcRex, M. Feinberg and M. Muesing for pSV-Rev, pSVRev* and pSP73-HTLVl-CAT, J. Cunningham for EJ-Al, M. Sy for 5D5, and D.Patterson for the CHO cell derivative. This work was supported by a grant from NIH.

Additional details

Created:
August 19, 2023
Modified:
October 20, 2023