Roles of clinical and subclinical reactivated herpes simplex virus type 2 infection and human immunodeficiency virus type 1 (HIV-1)-induced immunosuppression on …
N Nagot, A Ouedraogo, I Konate… - The journal of …, 2008 - academic.oup.com
N Nagot, A Ouedraogo, I Konate, HA Weiss, V Foulongne, MC Defer, A Sanon, P Becquart…
The journal of infectious diseases, 2008•academic.oup.comBackground. Few longitudinal studies have described the interactions between reactivation
of herpes simplex virus type 2 (HSV-2) infection (hereafter,“HSV-2 reactivation”) and genital
and systemic replication of human immunodeficiency virus type 1 (HIV-1). Methods. Women
in Burkina Faso who were seropositive for both HIV-1 and HSV-2 were enrolled in a
randomized placebo-controlled trial of therapy to suppress reactivation of HSV-2 infection
(hereafter,“HSV suppressive therapy”). During the baseline phase, 6 enriched …
of herpes simplex virus type 2 (HSV-2) infection (hereafter,“HSV-2 reactivation”) and genital
and systemic replication of human immunodeficiency virus type 1 (HIV-1). Methods. Women
in Burkina Faso who were seropositive for both HIV-1 and HSV-2 were enrolled in a
randomized placebo-controlled trial of therapy to suppress reactivation of HSV-2 infection
(hereafter,“HSV suppressive therapy”). During the baseline phase, 6 enriched …
Abstract
Background. Few longitudinal studies have described the interactions between reactivation of herpes simplex virus type 2 (HSV-2) infection (hereafter, “HSV-2 reactivation”) and genital and systemic replication of human immunodeficiency virus type 1 (HIV-1).
Methods. Women in Burkina Faso who were seropositive for both HIV-1 and HSV-2 were enrolled in a randomized placebo-controlled trial of therapy to suppress reactivation of HSV-2 infection (hereafter, “HSV suppressive therapy”). During the baseline phase, 6 enriched cervicovaginal lavage specimens were obtained over 12 weeks to detect and quantify the HIV-1 RNA and HSV-2 DNA loads.
Results. Women with genital ulcer disease (GUD) detected at least once were more likely than women in whom GUD was not detected (risk ratio [RR], 1.23; 95% confidence interval [CI], 1.09–1.37) to have genital HIV-1 RNA detected during ⩾1 visit. Similarly, women with genital HSV-2 DNA detected during ⩾1 clinic visit were more likely than women in whom genital HSV-2 DNA was not detected (RR, 1.17; 95% CI, 1.01–1.34) to have genital HIV-1 RNA detected at least once. In addition, the mean genital HIV-1 RNA loads for women with GUD detected during ⩾1 visit and women with HSV-2 genital shedding detected during ⩾1 visit were greater than that for women in whom genital HSV-2 DNA or GUD was never detected. The plasma HIV-1 RNA load was increased among women for whom ⩾1 visit revealed GUD (+0.25 log10 copies/mL; 95% CI, −0.05–0.55) or genital HSV-2 DNA (+0.40 log10 copies/mL; 95% CI, 0.15–0.66), compared with women who did not experience GUD or HSV-2 genital shedding, respectively. The association of HSV-2 reactivations on HIV-1 replication tended to be stronger in patients with a higher CD4+ cell count (i.e., >500 cells/µL). The contribution of HSV-2 to HIV-1 replication among women with CD4+ cell count of ≤500 cells/µL was reduced because almost all experienced HIV-1 genital shedding.
Conclusions. Both clinical and subclinical HSV-2 reactivations play a role in increasing the rate of HIV-1 replication. HSV suppressive therapy is a promising tool for HIV control. Initiation of such therapy when the CD4+ cell count is >500 cells/µL deserves further investigation.
Clinical trials registration. The ANRS 1285 Study is registered with the National Institutes of Health (registration number NCT00158509).
Oxford University Press