TY - JOUR
T1 - Aspirin-like molecules that inhibit human immunodeficiency virus 1 replication
AU - Pereira, Cândida F.
AU - Paridaen, Judith T. M. L.
AU - Rutten, Karla
AU - Huigen, Marleen C. D. G.
AU - van de Bovenkamp, Marja
AU - Middel, Jeena
AU - Beerens, Nancy
AU - Berkhout, Ben
AU - Schuurman, Rob
AU - Marnett, Lawrence J.
AU - Verhoef, Jan
AU - Nottet, Hans S. L. M.
PY - 2003
Y1 - 2003
N2 - Some anti-inflammatory molecules are also known to possess anti-human immunodeficiency virus (HIV) activity. We found that o-(acetoxyphenyl)hept-2-ynyl sulfide (APHS), a recently synthesized non-steroidal anti-inflammatory molecule can inhibit HIV-1 replication. The aim of this study was to clarify the mechanism of action of APHS. When administered during the first steps of the infection, APHS was capable of inhibiting the replication of several HIV-1 strains (macrophage-tropic and/or lymphocytotropic) in a dose-dependent manner in both peripheral blood mononuclear cells (PBMC), monocyte-derived macrophages and peripheral blood lymphocytes with 50% inhibitory concentration values of approximately 10 muM. The 50% toxic concentration of APHS varied between 100 and 200 muM in the different primary cells tested. APHS did not affect HIV-1 replication once the provirus was already inserted into the cellular genome. APHS also did not inhibit HIV-1 entry into the host cells as determined by quantification of gag RNA inside PBMC 2 h after infection. However, APHS did inhibit gag DNA synthesis during reverse transcription in primary cells, which indicates that APHS may target the reverse transcription process. (C) 2003 Elsevier Science B.V. All rights reserved
AB - Some anti-inflammatory molecules are also known to possess anti-human immunodeficiency virus (HIV) activity. We found that o-(acetoxyphenyl)hept-2-ynyl sulfide (APHS), a recently synthesized non-steroidal anti-inflammatory molecule can inhibit HIV-1 replication. The aim of this study was to clarify the mechanism of action of APHS. When administered during the first steps of the infection, APHS was capable of inhibiting the replication of several HIV-1 strains (macrophage-tropic and/or lymphocytotropic) in a dose-dependent manner in both peripheral blood mononuclear cells (PBMC), monocyte-derived macrophages and peripheral blood lymphocytes with 50% inhibitory concentration values of approximately 10 muM. The 50% toxic concentration of APHS varied between 100 and 200 muM in the different primary cells tested. APHS did not affect HIV-1 replication once the provirus was already inserted into the cellular genome. APHS also did not inhibit HIV-1 entry into the host cells as determined by quantification of gag RNA inside PBMC 2 h after infection. However, APHS did inhibit gag DNA synthesis during reverse transcription in primary cells, which indicates that APHS may target the reverse transcription process. (C) 2003 Elsevier Science B.V. All rights reserved
U2 - https://doi.org/10.1016/S0166-3542(03)00006-8
DO - https://doi.org/10.1016/S0166-3542(03)00006-8
M3 - Article
C2 - 12767473
SN - 0166-3542
VL - 58
SP - 253
EP - 263
JO - Antiviral Research
JF - Antiviral Research
IS - 3
ER -