Objective: The aims of this study were to compare the intensity of human immunodeficiency virus (HIV)-RNA genital shedding among postmenopausal (PM) and fertile-aged (F) women and to investigate the association between viral shedding and gynecological features, HIV plasma viral loads, and other markers of HIV disease progression.
Methods: We interviewed 146 HIV-infected women (73 PM/73 F) in search of gynecological complaints and signs and symptoms of HIV disease and obtained additional information concerning HIV infection by medical chart review. Cervicovaginal lavages (CVLs) were collected for assessment of HIV shedding. Laboratory analyses included CD4+ cell counts, HIV-RNA quantitation in plasma and CVL, and screening for concurrent genital infections.
Results: HIV-RNA genital shedding was detected in 16.4% of PM and 21.9% of F women (P = 0.400), and the intensity of HIV shedding did not differ between both groups (means—PM: 1.4log/mL; F: 1.4log/mL; P = 0.587). Three women (2 PM/1 F) exhibited viral shedding in the absence of detectable viremia. HIV plasma viral loads correlated with HIV shedding in both groups. In multivariable analysis, HIV plasma viral loads were independently associated with HIV shedding in both groups. Moreover, the intensity of shedding was independently associated with vaginal pH, tumor necrosis factor α concentrations in CVL, and HIV plasma viral loads.
Conclusions: Despite significant changes that occur in the vaginal mucosa of PM women, HIV cervicovaginal shedding was not significantly influenced by this state in our cohort. In contrast, increased vaginal pH and genital inflammation, evidenced by increased tumor necrosis factor α concentrations in CVL and HIV plasma viral loads, were independently associated with the intensity of HIV shedding in PM and F women.
This article describes an original investigation of human immunodeficiency virus cervicovaginal shedding among postmenopausal women from S&#x00E3;o Paulo, Brazil, and compares the intensity of viral shedding in this age group with that in their fertile-aged counterparts.
From the 1Virology Laboratory (LIM-52), Department of Infectious Diseases, School of Medicine, University of São Paulo; and 2Department of Physiology, Santa Casa Medical School, São Paulo, Brazil.
Received March 11, 2011; revised and accepted June 7, 2011.
Funding/support: This study was funded by Fundação de Amparo à Pesquisa do Estrado de São Paulo (Research Grant No. 2005/50182-1) and Conselho de Desenvolvimento Cientifico e Tecnológico (PhD grant given to K.C.M.).
Financial disclosure/conflicts of interest: The authors declare no conflict of interest.
Address correspondence to: Aluisio Cotrim Segurado, MD, PhD, Av. Dr. Eneas de Carvalho Aguiar 470, 05403-000 São Paulo, SP, Brazil. E-mail: email@example.com