Reference

Differential diffusions of indinavir and lopinavir in genital secretions of human immunodeficiency virus-infected women

Differential diffusions of indinavir and lopinavir in genital secretions of human immunodeficiency virus-infected women. Launay, Odile; Tod, Michel; Louchahi, Kamel; Belarbi, Linda; Bouchaud, Olivier; Memain, Nathalie; Petitjean, Olivier; Robineau, Michel; Guillevin, Loic; Lortholary, Olivier (Federation de Medecine Interne, Maladies Infectieuses et Tropicales and UPRES EA 3409, Hopital Avicenne, AP-HP, Universite Paris-Nord, Bobigny, Fr.). Antimicrobial Agents and Chemotherapy, 48(2), 632-634 (English) 2004 American Society for Microbiology. CODEN: AMACCQ. ISSN: 0066-4804. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacology) Plasma and cervicovaginal secretion (CVS) samples were collected from 19 human immunodeficiency virus type 1-infected women on lopinavir- or indinavir-contg. regimens. 155213-67-5 and 150378-17-9 are also in the experiment. Lopinavir and indinavir were detectable in 29 and 93% of CVS samples, resp., a finding that may be ascribed to these drugs' differences in protein binding and pKa. The relationship between lopinavir and indinavir pharmacodynamics and viral evolution in the female genital tract should be assessed over time. .

Productive infection maintains a dynamic steady state of residual viremia in human immunodeficiency virus type 1-infected persons treated with suppressive antiretroviral therapy for five years

Productive infection maintains a dynamic steady state of residual viremia in human immunodeficiency virus type 1-infected persons treated with suppressive antiretroviral therapy for five years. Havlir, Diane V.; Strain, Matthew C.; Clerici, Mario; Ignacio, Caroline; Trabattoni, Daria; Ferrante, Pasquale; Wong, Joseph K. (Department of Medicine, San Francisco General Hospital, University of California, San Francisco, CA 94110, USA).Chemicals with cas numbers 150378-17-9 and 136470-78-5 also play role. Journal of Virology, 77(20), 11212-11219 (English) 2003 American Society for Microbiology. CODEN: JOVIAM. ISSN: 0022-538X. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacology) Section cross-reference(s): 14 To provide insight into the dynamics and source of residual viremia in human immunodeficiency virus (HIV) patients successfully treated with antiretroviral therapy, 14 intensely monitored patients treated with indinavir and efavirenz sustaining HIV RNA at <50 copies/mL for >5 yr were studied. Abacavir was added to the regimen of eight patients at year 5. After the first 9 mo of therapy, HIV RNA levels had reached a plateau ("residual viremia") that persisted for over 5 yr. Levels of residual viremia differed among patients and ranged from 3.2 to 23 HIV RNA copies/mL. Baseline HIV DNA was the only significant pretreatment predictor of residual viremia in regression models including baseline HIV RNA, CD4 count, and patient age. In the four of five patients with detectable viremia who added abacavir to their regimen after 5 yr, HIV RNA levels declined rapidly. The estd. half-life of infected cells was 6.7 days. Decrease in activated memory cells and a redn. in gamma interferon prodn. to HIV Gag and p24 antigen in ELISpot assays were obsd., consistent with a decrease in HIV replication. Thus, in patients treated with efavirenz plus indinavir, levels of residual viremia were established by 9 mo, were predicted by baseline proviral DNA, and remained const. for 5 yr. Even after years of highly suppressive therapy, HIV RNA levels declined rapidly after the addn. of abacavir, suggesting that productive infection contributes to residual ongoing viremia and can be inhibited with therapy intensification. .