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J Gen Virol 71 (1990), 97-103; DOI 10.1099/0022-1317-71-1-97
© 1990 Society for General Microbiology

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Reciprocal Enhancement of Gene Expression and Viral Replication Between Human Cytomegalovirus and Human immunodeficiency Virus Type 1

Wen-Zhe Ho1, Janet M. Harouse2, Robert F. Rando3, Eva Gönczöl1, Alagarsamy Srinivasan1 and Stanley A. Plotkin1

The1 Wistar Institute of Anatomy and Biology, 36th Street at Spruce, Philadelphia, Pennsylvania 19104
2 Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania 19104
and3 Pennsylvania Hospital, Philadelphia, Pennsylvania 19107, U.S.A.

Biological interactions between human cytomegalovirus (HCMV) and the human immunodeficiency virus type 1 (HIV-1) were analysed in transfection and infection experiments, carried out in a human osteogenic sarcoma cell line (HOS) and in the same cell line chronically infected with HCMV (E155). When HOS and E155 cells were transfected with recombinant plasmids containing the HIV long terminal repeat (LTR) linked to the bacterial chloramphenicol acetyl-transferase (CAT) gene, LTR-directed CAT expression was 20 times higher in E155 cells than in HOS cells. HOS cells co-infected with HCMV and HIV-1 showed enhanced production of the HIV-1 p24 antigen. In reciprocal experiments, an increase in HCMV immediate early gene expression was observed when HCMV-infected HOS cells and E155 cells were either transfected with a recombinant plasmid containing the HIV transactivator gene (pTAT), or when infected with HIV-1. DNA hybridization analysis of E155 and HCMV-infected HOS cells revealed higher levels of HCMV DNA in cells transfected with pTAT than in cells transfected with other non-specific recombinant plasmids. E155 cells transfected with pTAT also produced higher titres of infectious HCMV than control cultures of E155 cells transfected with other recombinant plasmids, including pMTAT carrying a mutant tat gene. The functional reciprocity in vitro between HCMV and HIV is discussed with respect to its possible implications for the clinical development of AIDS.

Received 24 April 1989; accepted 12 September 1989.


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