The Impact of Active Herpes Simplex Virus Infection on Human Immunodeficiency Virus Load

• Published in: The Journal of infectious diseases Vol. 176; no. 3; pp. 766 - 770
• Main Authors: Mole, Larry, Ripich, Stefan, Margolis, Dan, Holodniy, Mark
• Format: Journal Article
• Language: English
• Published: Chicago, IL The University of Chicago Press 01.09.1997; University of Chicago Press; Oxford University Press
• Subjects: AIDS; AIDS-Related Opportunistic Infections - epidemiology; AIDS-Related Opportunistic Infections - virology; Antiretrovirals; Biological and medical sciences; Blood plasma; CD4 Lymphocyte Count; Concise Communications; Female; Gene Products, gag - blood; Gene Products, gag - genetics; Herpes Simplex - complications; HIV; HIV 1; HIV Core Protein p24 - blood; HIV-1 - genetics; HIV-1 - growth & development; Humans; Immunodeficiencies; Immunodeficiencies. Immunoglobulinopathies; Immunopathology; Infections; Male; Medical sciences; Messenger RNA; RNA; RNA, Viral - blood; Simplexvirus; Viral Load; Viruses; Human; Immunopathology; Mixed infection; Herpesviridae; Alphaherpesvirinae; Retroviridae; AIDS; Immune deficiency; Infection; Virus; Viral disease; Lentivirinae; Herpesvirus hominis; Human immunodeficiency virus
• ISSN: 0022-1899; 1537-6613
• DOI: 10.1086/517297

The effect of a concurrent herpes simplex virus (HSV) infection on human immunodeficiency virus type 1 (HIV-1) load was evaluated. Sixteen subjects were identified with an active HSV infection and had pre-outbreak, acute-phase, and post-outbreak plasma (n = 16) and peripheral blood mononuclear cell (PBMC) (n = 8) samples for evaluation. All subjects were treated for an acute HSV outbreak with acyclovir for 10 days, followed by chronic prophylaxis. HIV-1 plasma RNA levels were determined by branched DNA, and intracellular HIV gag mRNA copy numbers were determined by quantitative reverse transcriptase-polymerase chain reaction ELISA. Plasma virus load increased a median of 3.4-fold during the acute outbreak (range, 0- to 10-fold; P = .002), while post-outbreak levels (30–45 days after the appearance of lesions) remained above pre-outbreak, baseline levels in some subjects. Intracellular HIV gag mRNA increased during the outbreak as well. Thus, an acute HSV episode can result in increased HIV transcription and plasma virus load.