Seroprevalence of Herpes Simplex Virus Types 1 and 2--United States, 1999-2010.
ABSTRACT Background. Herpes simplex virus types 1 and 2 (HSV-1 and HSV-2) are common infections with serious sequelae. HSV-1 is an increasingly important cause of genital herpes in industrialized countries.Methods. Using nationally representative data from the National Health and Nutrition Examination Survey (NHANES), we examined HSV-1 and HSV-2 seroprevalence among 14- to 49-year-olds in the United States. We estimated seroprevalence in 1999-2004 and 2005-2010, stratified by sociodemographic characteristics and sexual behaviors. We also reviewed HSV-1 and HSV-2 seroprevalence from 1976-1980 to 2005-2010.Results. In 2005-2010, the seroprevalence of HSV-1 was 53.9%, and the seroprevalence of HSV-2 was 15.7%. From 1999-2004 to 2005-2010, HSV-1 seroprevalence declined by nearly 7% (P < .01), but HSV-2 seroprevalence did not change significantly. The largest decline in HSV-1 seroprevalence from 1999-2004 to 2005-2010 was observed among adolescents aged 14-19 years, among whom seroprevalence declined by nearly 23%, from 39.0% to 30.1% (P < .01). In this age group, HSV-1 seroprevalence declined >29% from 1976-1980 to 2005-2010 (P < .01).Conclusions. An increasing number of adolescents lack HSV-1 antibodies at sexual debut. In the absence of declines in HSV-2 infections, the prevalence of genital herpes may increase.
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ABSTRACT: Herpes simplex virus type 2 (HSV-2) is a common sexually transmitted disease, but there is limited data on its epidemiology among urban populations. The urban Emergency Department (ED) is a potential venue for surveillance as it predominantly serves an inner city minority population. We evaluate the seroprevalence and factors associated with HSV-2 infection among patients attending the Johns Hopkins Hospital Adult Emergency Department (JHH ED).PLoS ONE 01/2014; 9(7):e102422. · 3.53 Impact Factor
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ABSTRACT: Disseminated herpes simplex virus (HSV) infection during pregnancy is a rare, but potentially fatal condition. We present a case where prompt treatment with intravenous acyclovir resulted in a successful outcome for both mother and baby.Qatar Medical Journal 06/2014; 2014(1):61-4.
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ABSTRACT: Herpes Simplex Virus type-1 (HSV-1) and type-2 (HSV-2) establish life-long infections and cause significant orofacial and genital infections in humans. HSV-1 is the leading cause of infectious blindness in the western world. Currently, there are no available vaccines to protect against herpes simplex infections. Recently, we showed that a single intramuscular immunization with an HSV-1(F) mutant virus lacking expression of the viral glycoprotein K (gK), which prevents the virus from entering into distal axons of ganglionic neurons, conferred significant protection against either virulent HSV-1(McKrae) or HSV-2(G) intravaginal challenge in mice. Specifically, 90% of the mice were protected against HSV-1(McKrae) challenge, while 70% of the mice were protected against HSV-2(G) challenge. We constructed the recombinant virus VC2 that contains specific mutations in gK and the membrane protein UL20 preventing virus entry into axonal compartments of neurons, while allowing efficient replication in cell culture, unlike the gK-null virus, which has a major defect in virus replication and spread. Intramuscular injection of mice with 10 7 VC2 plaque forming units did not cause any significant clinical disease in mice. A single intramuscular immunization with the VC2 virus protected 100% of mice against lethal intravaginal challenge with either HSV-1(McKrae) or HSV-2(G) viruses. Importantly, vaccination with VC2 produced robust cross protective humoral and cellular immunity that fully protected vaccinated mice against lethal disease. Quantitative PCR did not detect any viral DNA in ganglionic tissues of vaccinated mice, while unvaccinated mice contained high levels of viral DNA. The VC2 virus may serve as an efficient vaccine against both HSV-1 and HSV-2 infections, as well as a safe vector for the production of vaccines against other viral and bacterial pathogens. Copyright: ß 2014 Stanfield 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. Data Availability: The authors confirm that all data underlying the findings are fully available without restriction. All relevant data are within the paper and its Supporting Information file. Funding: This work was funded by the Louisiana Board of Regents Biotechnology Initiative grant to KGK. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. Competing Interests: The authors have declared that no competing interests exist.PLoS ONE 10/2014; · 3.53 Impact Factor