Looker KJ, Garnett GP, Schmid GPAn estimate of the global prevalence and incidence of herpes simplex virus type 2 infection. Bull World Health Organ 86:805-812

Department of Infectious Disease Epidemiology, Imperial College London, London, England.
Bulletin of the World Health Organisation (Impact Factor: 5.09). 11/2008; 86(10):805-12, A. DOI: 10.2471/BLT.07.046128
Source: PubMed


To estimate the global prevalence and incidence of herpes simplex virus type 2 (HSV-2) infection in 2003.
A systematic review was undertaken of published seroprevalence surveys describing the prevalence or incidence of HSV-2 by age and gender. For each of 12 regions, pooled prevalence values by age and gender were generated in a random-effect model. HSV-2 incidence was then estimated from these pooled values using a constant-incidence model. Values of the HSV-2 seroprevalence from the model fits were applied to the total population to estimate the numbers of people infected.
The total number of people aged 15-49 years who were living with HSV-2 infection worldwide in 2003 is estimated to be 536 million, while the total number of people who were newly infected with HSV-2 in 2003 is estimated to be 23.6 million. While the estimates are limited by poor availability of data, general trends are evident. For example, more women than men were infected, and the number infected increased with age. Although prevalence varied substantially by region, predicted prevalence was mostly higher in developing regions than developed regions.
The prevalence of HSV-2 is relatively easy to measure since infection is lifelong and has a specific serological test. The burden of disease is less easy to quantify. Despite the often sparse data on which these estimates are based, it is clear that HSV-2 infection is widespread. The dramatic differences in prevalence between regions are worthy of further exploration.

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    • "The World Health Organization estimated that over 500 million people are infected with HSV-2 worldwide with approximately 20 million new cases annually (Looker et al., 2008). The extremely high prevalence of HSV-2 in sub-Saharan Africa (∼70%) (Looker et al., 2008) may contribute more to the spread of HIV-1 than number of sex partners or other sexually transmitted infections (Freeman et al., 2006; Chen et al., 2007). Moreover, as HSV establishes latency in neurons with frequent subclinical or clinical reactivations, there is a lifelong impact of infection. "

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    • "The WHO estimates that 536 million people, aged 15 -49 are infected with HSV-2 type 2, the causative agent of genital herpes. Annually approximately 23.6 million people in this age group become newly infected with HSV-2 [11]. The epidemiology of each STI is different and is influenced by various factors, including sexual mixing patterns (moderated by protective behaviours), the transmissibility of each pathogen, and the duration of infectiousness (moderated by access to effective treatment), demographics, and social circumstances [12]. "

    Open Journal of Obstetrics and Gynecology 01/2015; 05(07):385-399. DOI:10.4236/ojog.2015.57056
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    • "This rate reaches more than 80% of subjects co-infected by both HIV and HSV-2 [Weiss, 2004; Looker et al., 2008]. Many epidemiologic studies have addressed the potential risk of acquisition of HIV-1 in case of genital herpes infection [Wald and Link, 2002; Freeman et al., 2006]. "
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    ABSTRACT: Herpes simplex virus type 2 (HSV-2) is the most common cause of genital ulcer disease worldwide. While the contribution of HSV-2 to acquisition and course of human immunodeficiency virus (HIV) infection has been well described, less attention has been paid to the impact of HIV infection on the variability and the pathophysiology of HSV-2 infection. The goal of the present study was to characterize genotypically and phenotypically HSV-2 strains isolated from 12 patients infected by HIV-1 and from 12 HIV-negative patients. Replication capacity analyses were carried out in Vero cells and full-length nucleotide sequences were determined for glycoproteins B (gB), D (gD), G (gG), thymidine kinase (TK), and DNA polymerase (POL) HSV-2 genes. Sequence alignments and phylogenetic trees were performed. No significant differences were found in terms of replication capacity. The interstrain nucleotide identities of the 3 glycoprotein genes (gB, gC, and gG) ranged from 99.5% to 100% among the 24 HSV-2 strains. The phylogenetic analysis showed no clustering of HSV-2 strains when correlating to the HIV status of the patients. A lower variability was observed for the functional proteins TK and DNA polymerase (98.9% to 100% identity). Genetic analysis of TK evidenced mutations related to acyclovir-resistance in two HSV-2 strains. No specific differences regarding replication capacity and gene sequence were found when comparing HSV-2 strains isolated from patients infected with HIV-1 and HIV-negative patients, suggesting that the virological properties of HSV-2 infection are not influenced by HIV-1 infection among co-infected patients. J. Med. Virol. 9999: XX–XX, 2014. © 2014 Wiley Periodicals, Inc.
    Journal of Medical Virology 08/2014; 87(3). DOI:10.1002/jmv.24061 · 2.35 Impact Factor
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