Inhibition of HIV type 1 replication by simultaneous infection of peripheral blood lymphocytes with human immunodeficiency virus types 1 and 2.
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.
Deutsches Krebsforschungszentrum Heidelberg, Heidelberg 69120, Germany.
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Rübsamen-Waigmann
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Unger
D004279:DNA, Viral / Q000032:analysis; D016655:HIV Core Protein p24 / Q000378:metabolism*; D015699:HIV Envelope Protein gp120 / Q000378:metabolism; D015658:HIV Infections / Q000150:complications / Q000821:virology*; D015497:HIV-1 / Q000472:pathogenicity* / Q000502:physiology; D015498:HIV-2 / Q000472:pathogenicity* / Q000502:physiology; D006801:Humans; D008213:Lymphocyte Activation; D008214:Lymphocytes / Q000821:virology*; D010835:Phytohemagglutinins / Q000494:pharmacology; D014779:Virus Replication / Q000502:physiology*
D004279:DNA, Viral; D016655:HIV Core Protein p24; D015699:HIV Envelope Protein gp120; D010835:Phytohemagglutinins