TY - JOUR
T1 - Inhibition of HIV type 1 replication by simultaneous infection of peripheral blood lymphocytes with human immunodeficiency virus types 1 and 2
AU - Dern, K.
AU - Rübsamen-Waigmann, H.
AU - Unger, R. E.
PY - 2001/3/1
Y1 - 2001/3/1
N2 - 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 SIVmac 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.
AB - 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 SIVmac 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.
UR - http://www.scopus.com/inward/record.url?scp=0035283057&partnerID=8YFLogxK
U2 - 10.1089/08892220150503672
DO - 10.1089/08892220150503672
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C2 - 11242517
AN - SCOPUS:0035283057
SN - 0889-2229
VL - 17
SP - 295
EP - 309
JO - AIDS Research and Human Retroviruses
JF - AIDS Research and Human Retroviruses
IS - 4
ER -