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      Herpes simplex virus type 1 epidemiology in Latin America and the Caribbean: Systematic review and meta-analytics

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          Abstract

          Objectives

          To investigate the epidemiology of herpes simplex virus type 1 (HSV-1) in Latin America and the Caribbean.

          Methods

          Systematic review and meta-analytics guided by the Cochrane Collaboration Handbook and reported following the PRISMA guidelines.

          Results

          Thirty-three relevant reports were identified including 35 overall (and 95 stratified) seroprevalence measures, and five and nine proportions of virus isolation in genital ulcer disease (GUD) and in genital herpes, respectively. Pooled mean seroprevalence was 57.2% (95% CI: 49.7–64.6%) among children and 88.4% (95% CI: 85.2–91.2%) among adults. Pooled mean seroprevalence was lowest at 49.7% (95% CI: 42.8–56.6%) in those aged ≤10, followed by 77.8% (95% CI: 67.9–84.8%) in those aged 10–20, 82.8% (95% CI: 73.1–90.8%) in those aged 20–30, 92.5% (95% CI: 89.4–95.1%) in those aged 30–40, and 94.2% (95% CI: 92.7–95.5%) in those aged ≥40. Age was the strongest source of heterogeneity in seroprevalence, explaining 54% of variation. Evidence was found for seroprevalence decline over time. Pooled mean proportion of HSV-1 isolation was 0.9% (95% CI: 0.0–3.6%) in GUD and 10.9% (95% CI: 4.4–19.4%) in genital herpes.

          Conclusions

          HSV-1 is a widely prevalent infection in this region, but its epidemiology may be slowly transitioning, with still limited contribution for HSV-1 in genital herpes.

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          Most cited references56

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          Global and Regional Estimates of Prevalent and Incident Herpes Simplex Virus Type 1 Infections in 2012

          Background Herpes simplex virus type 1 (HSV-1) commonly causes orolabial ulcers, while HSV-2 commonly causes genital ulcers. However, HSV-1 is an increasing cause of genital infection. Previously, the World Health Organization estimated the global burden of HSV-2 for 2003 and for 2012. The global burden of HSV-1 has not been estimated. Methods We fitted a constant-incidence model to pooled HSV-1 prevalence data from literature searches for 6 World Health Organization regions and used 2012 population data to derive global numbers of 0-49-year-olds with prevalent and incident HSV-1 infection. To estimate genital HSV-1, we applied values for the proportion of incident infections that are genital. Findings We estimated that 3709 million people (range: 3440–3878 million) aged 0–49 years had prevalent HSV-1 infection in 2012 (67%), with highest prevalence in Africa, South-East Asia and Western Pacific. Assuming 50% of incident infections among 15-49-year-olds are genital, an estimated 140 million (range: 67–212 million) people had prevalent genital HSV-1 infection, most of which occurred in the Americas, Europe and Western Pacific. Conclusions The global burden of HSV-1 infection is huge. Genital HSV-1 burden can be substantial but varies widely by region. Future control efforts, including development of HSV vaccines, should consider the epidemiology of HSV-1 in addition to HSV-2, and especially the relative contribution of HSV-1 to genital infection.
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            Age-specific prevalence of infection with herpes simplex virus types 2 and 1: a global review.

            Information on age- and sex-specific prevalence of herpes simplex virus (HSV) types 2 and 1 infections is essential to optimize genital herpes control strategies, which increase in importance because accumulating data indicate that HSV-2 infection may increase acquisition and transmission of human immunodeficiency virus. This review summarizes data from peer-reviewed publications of type-specific HSV seroepidemiologic surveys. HSV-2 prevalence is, in general, highest in Africa and the Americas, lower in western and southern Europe than in northern Europe and North America, and lowest in Asia. HSV-2 and -1 prevalence, overall and by age, varies markedly by country, region within country, and population subgroup. Age-specific HSV-2 prevalence is usually higher in women than men and in populations with higher risk sexual behavior. HSV-2 prevalence has increased in the United States but national data from other countries are unavailable. HSV-1 infection is acquired during childhood and adolescence and is markedly more widespread than HSV-2 infection. Further studies are needed in many geographic areas.
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              Trends in herpes simplex virus type 1 and type 2 seroprevalence in the United States.

              Herpes simplex virus type 1 (HSV-1) and type 2 are common infections worldwide. Herpes simplex virus type 2 (HSV-2) is the cause of most genital herpes and is almost always sexually transmitted. In contrast, HSV-1 is usually transmitted during childhood via nonsexual contacts. Preexisting HSV-1 antibodies can alleviate clinical manifestations of subsequently acquired HSV-2. Furthermore, HSV-1 has become an important cause of genital herpes in some developed countries. To examine trends in HSV-1 and HSV-2 seroprevalence in the United States in 1999-2004 compared with 1988-1994. Cross-sectional, nationally representative surveys (US National Health and Nutrition Examination Surveys [NHANES]), were used to compare national seroprevalence estimates from 1999-2004 with those from 1988-1994, and changes in HSV-1 and HSV-2 seroprevalence since 1976-1980 were reviewed. Persons aged 14 to 49 years were included in these analyses. Seroprevalence of HSV-1 and HSV-2 antibodies based on results from type-specific immunodot assays; diagnosis of genital herpes. The overall age-adjusted HSV-2 seroprevalence was 17.0% (95% confidence interval [CI], 15.8%-18.3%) in 1999-2004 and 21.0% (95% CI, 19.1%-23.1%) in 1988-1994, a relative decrease of 19.0% between the 2 surveys (95% CI, -28.6% to -9.5%; P<.001). Decreases in HSV-2 seroprevalence were especially concentrated in persons aged 14 to 19 years between 1988 and 2004. In adolescents aged 17 to 19 years and young adults, the decreases in HSV-2 seroprevalence were significant even after adjusting for changes in sexual behaviors. Among those infected with HSV-2, the percentage who reported having been diagnosed with genital herpes was statistically different (14.3% in 1999-2004 and 9.9% in 1988-1994; P = .02). Seroprevalence of HSV-1 decreased from 62.0% (95% CI, 59.6%-64.6%) in 1988-1994 to 57.7% (95% CI, 55.9%-59.5%) in 1999-2004, a relative decrease of 6.9% between the 2 surveys (95% CI, -11.6% to -2.3%; P = .006). Among persons infected with HSV-1 but not with HSV-2, a higher percentage reported having been diagnosed with genital herpes in 1999-2004 compared with 1988-1994 (1.8% vs 0.4%, respectively; P<.001). These data show declines in HSV-2 seroprevalence, suggesting that the trajectory of increasing HSV-2 seroprevalence in the United States has been reversed. Seroprevalence of HSV-1 decreased but the incidence of genital herpes caused by HSV-1 may be increasing.
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                Author and article information

                Contributors
                Role: Data curationRole: Formal analysisRole: InvestigationRole: MethodologyRole: ValidationRole: VisualizationRole: Writing – original draftRole: Writing – review & editing
                Role: Data curationRole: Formal analysisRole: InvestigationRole: MethodologyRole: ValidationRole: VisualizationRole: Writing – original draftRole: Writing – review & editing
                Role: Data curationRole: Formal analysisRole: InvestigationRole: MethodologyRole: ValidationRole: VisualizationRole: Writing – original draftRole: Writing – review & editing
                Role: ConceptualizationRole: Formal analysisRole: Funding acquisitionRole: InvestigationRole: MethodologyRole: Project administrationRole: ResourcesRole: SoftwareRole: SupervisionRole: ValidationRole: VisualizationRole: Writing – original draftRole: Writing – review & editing
                Role: Editor
                Journal
                PLoS One
                PLoS ONE
                plos
                plosone
                PLoS ONE
                Public Library of Science (San Francisco, CA USA )
                1932-6203
                22 April 2019
                2019
                : 14
                : 4
                : e0215487
                Affiliations
                [1 ] Infectious Disease Epidemiology Group, Weill Cornell Medicine-Qatar, Cornell University, Qatar Foundation—Education City, Doha, Qatar
                [2 ] Department of Health Sciences, Qatar University, Doha, Qatar
                [3 ] Department of Healthcare Policy and Research, Weill Cornell Medicine, Cornell University, New York, New York, United States of America
                [4 ] College of Health and Life Sciences, Hamad bin Khalifa University, Doha, Qatar
                University of Pretoria, SOUTH AFRICA
                Author notes

                Competing Interests: The authors have declared that no competing interests exist.

                Author information
                http://orcid.org/0000-0003-0790-0506
                Article
                PONE-D-18-36888
                10.1371/journal.pone.0215487
                6476500
                31009486
                e298c146-c1a3-4c0a-98c9-c7af0aba82b7
                © 2019 Sukik et al

                This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

                History
                : 27 December 2018
                : 2 April 2019
                Page count
                Figures: 2, Tables: 5, Pages: 20
                Funding
                Funded by: funder-id http://dx.doi.org/10.13039/100008982, Qatar National Research Fund;
                Award ID: NPRP grant number 9-040-3-008
                Award Recipient :
                Funded by: Weill Cornell Medical College in Qatar
                Award ID: Biomedical Research Program Pilot Funding
                Award Recipient :
                This publication was made possible by NPRP grant number 9-040-3-008 from the Qatar National Research Fund (a member of Qatar Foundation) to LJA-R. The statements made herein are solely the responsibility of the authors. The authors are also grateful for pilot funding provided by the Biomedical Research Program and infrastructure support provided by the Biostatistics, Epidemiology, and Biomathematics Research Core, both at Weill Cornell Medicine in Qatar to LJA-R.
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