Title
Clinical and Virologie Efficacy of Herpes Simplex Virus Type 2 Suppression by Acyclovir in a Multicontinent Clinical Trial
Date Issued
15 April 2010
Access level
open access
Resource Type
journal article
Author(s)
Fuchs J.
Celum C.
Wang J.
Hughes J.
Sanchez J.
Cowan F.
Reid S.
Delany-Moretlwe S.
Corey L.
Wald A.
Abstract
Acyclovir suppressive therapy (400 mg twice daily) reduces herpes simplex virus (HSV) type 2-associated genital ulcer disease and lesionai HSV shedding. In an international trial of acyclovir for suppression of HSV type 2 to prevent human immunodeficiency virus (HIV) acquisition (HIV Prevention Trials Network 039), acyclovir had a smaller effect on the frequency of genital ulcer disease as well as a smaller effect on the frequency and quantity of lesional HSV DNA in Af-rican women and Peruvian men, compared with its effects in men in the United States. The observed regional varia-tion in the clinical and virologic efficacy of acyclovir for HSV suppression warrants further evaluation of determinants of responses to acyclovir. (ClinicalTrials.gov identifier: NCT00076232.) © 2010 by the Infectious Diseases Society of America, All rights reserved.
Start page
1164
End page
1168
Volume
201
Issue
8
Language
English
OCDE Knowledge area
Dermatología, Enfermedades venéreas
Virología
Enfermedades infecciosas
Farmacología, Farmacia
DOI
Scopus EID
2-s2.0-77950292824
PubMed ID
Source
Journal of Infectious Diseases
ISSN of the container
00221899
Sponsor(s)
Funding text 1
Financial support: National Institute of Allergy and Infectious Diseases, National Institutes of Health (grants U01 AI052054 and AI30731; grant K24 AI07113 to A.W.); HIV Prevention Trials Network (Cooperative Agreement U01 AI46749); National Institute of Child Health and Human Development; National Institute on Drug Abuse; National Institute of Mental Health; Office of AIDS Research; GlaxoSmithKline (grant for purchasing study drug).
Funding text 2
Potential conflicts of interest: C.C. has received research grant support from GlaxoSmithKline and has served on an advisory board to GlaxoSmithKline. J.S. has received grant support from GlaxoSmithKline. F.C. has received research grant support from GlaxoSmithKline. The University of Washington Virology Division has received grant funding from GlaxoSmithKline and Novartis to undertake herpes simplex virus serological assays and polymerase chain reaction assays for studies funded by these companies. L.C. directs these laboratories; he receives no salary support from these grants. A.W. has received grant support from GlaxoSmithKline, Antigenics, and Astellas. All other authors declare no conflict of interest.
Sources of information:
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