[논문]Inhibition of HIV Type 1 Replication by Simultaneous Infection of Peripheral Blood Lymphocytes with Human Immunodeficiency Virus Types 1 and 2

Dern, Kirsten; Rü; bsamen-Waigmann, Helga; Unger, Ronald E.

doi:10.1089/08892220150503672

[해외논문] Inhibition of HIV Type 1 Replication by Simultaneous Infection of Peripheral Blood Lymphocytes with Human Immunodeficiency Virus Types 1 and 2

AIDS research and human retroviruses, v.17 no.4, 2001년, pp.295 - 309

Dern, Kirsten (Deutsches Krebsforschungszentrum Heidelberg, Heidelberg 69120, Germany.) , Rübsamen-Waigmann, Helga (Institute of Virology, Bayer AG, Wuppertal 42096, Germany.) , Unger, Ronald E. (Institute for Pathology, Johannes Gutenberg University, Mainz 55131, Germany.)

Abstract ▼ AI-Helper

A productive infection of peripheral blood lymphocytes by HIV-1 was severely inhibited by the simultaneous infection of these cells with HIV-2. A similar reciprocal effect on HIV-2 infection was not observed. The extent of virus replication was determined by virus-specific antigen capture assays of the supernatants of the infections. The inhibitory effect was observed with T cell-tropic, dual-tropic, as well as with primary HIV-1 isolates from different subtypes (A, B, C, E, F, and O). Infection of PBLs with different subtypes of HIV-2 (A and B) as well as with SIV(mac) resulted in the inhibition of HIV-1. However, the inhibitory effect was limited to PBLs; similar results were not observed in a T cell line. The inhibition of HIV-1 replication was independent of HIV-2 concentration; however, the infection by HIV-2 had to take place within 24 hr after PBLs were infected by HIV-1 for inhibition of HIV-1 replication to occur. The inhibition could be reversed by the addition of PHA. Analysis of HIV-1 RNA and DNA demonstrated that the inhibition was not at uptake or reverse transcription and that equal amounts of PBLs were infected by HIV-1 in single infections and coinfections. Immunocytochemical analysis of HIV-1 proteins demonstrated that equal numbers of cells were infected and that equal amounts of intracellular HIV-1 Env and Gag proteins were produced throughout the culture period. Therefore we conclude that HIV-2 can potently inhibit the productive infection of PBLs by HIV-1 and that the mechanism of this inhibition appears to prevent HIV-1 assembly or release from PBLs.

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