Relation between HIV-2 proviral load and CD4(+) lymphocyte count differs in monotypic and dual HIV infections

Citation
Ad. Sarr et al., Relation between HIV-2 proviral load and CD4(+) lymphocyte count differs in monotypic and dual HIV infections, J HUMAN VIR, 2(1), 1999, pp. 45-51
Citations number
34
Categorie Soggetti
Microbiology
Journal title
JOURNAL OF HUMAN VIROLOGY
ISSN journal
10909508 → ACNP
Volume
2
Issue
1
Year of publication
1999
Pages
45 - 51
Database
ISI
SICI code
1090-9508(199901/02)2:1<45:RBHPLA>2.0.ZU;2-Z
Abstract
Objective: To explore and compare the relations between proviral DNA load a nd CD4(+) lymphocyte counts in both HIV-2 monotypic and HN dual infection. Study Design/Methods: In Dakar, Senegal, where the HN-I and HIV-2 epidemics overlap, serum and peripheral blood mononuclear cell (PBMC) DNA samples we re collected from registered female sex workers and hospitalized patients. Sera were evaluated for reactivity to antigens of HIV-1 and HIV-2 by immuno blot; dual reactivity was confirmed with recombinant envelope peptides for HIV-I and HIV-2. These samples were then subjected to HN-1 and HIV-2 provir al DNA polymerase chain reaction (PCR). To evaluate the HIV-2 cellular prov iral DNA loads, a quantitative competitive PCR (QC-PCR) was developed using nested primers to amplify the gag region of HIV-2. This assay used an inte rnal competitor generated by inserting 25 bp in the first-round PCR target sequence. T-lymphocyte subset counts were estimated by flow cytometry for b oth HIV-2 monotypic and dually infected persons. Results: 35 HIV-2-infected and 33 dually seroreactive samples were evaluate d in this study. The CD4(+) lymphocyte counts were similar ill both groups, with mean values of 449 +/- 390 cells/mm(3) for the HIV-2 monotypic infect ed persons and 476 +/- 308 cells/mm3 among the dually infected persons. How ever, the median proviral loads differed significantly, with those in the H IV-2 group ranging from 63.2 to 669.8 copies/10(5) CD4(+) cells and demonst rating an inverse correlation with CD4(+) lymphocyte count. The HIV dually infected persons showed less variation in viral load, ranging from 9.9 to 4 3.3 copies/10(5) CD4(+) cells. Among the HN dually infected persons, low HI V-2 proviral load was correlated with low CD4(+) lymphocyte counts. Conclusions: The HIV-2 proviral loads in HIV dually infected persons were s ignificantly lower than those in HIV-2 mono-typically infected individuals (P <.0001), despite comparable CD4(+) lymphocyte counts. These results sugg est that different HIV-2 proviral dynamics prevail in HIV dual infection.