Two of the most common viruses, herpes simplex virus-1 (HSV-1) and herpes simplex virus-2 (HSV-2), are steadily declining in the U.S. population. From 1999-2000 to 2015-2016, prevalence of both types of HSV decreased (HSV-1, 59.4% to 48.1%, and HSV-2, 18.0% to 12.1%).
- Both HSV-1 and HSV-2 cause human diseases ranging from very painful oral cold sores and genital lesions, to eye conditions that can lead to blindness. People infected with HSV also have an increased risk of acquiring or transmitting HIV.
- Randomized trials have indicated that three antiviral medications provide clinical benefit for genital herpes: acyclovir, valacyclovir, and famciclovir. While these medications may provide symptomatic relief from outbreaks, they do not cure HSV infection.
Two of the most common viruses, herpes simplex virus-1 (HSV-1) and herpes simplex virus-2 (HSV-2), are steadily declining in the U.S population. For both virus types, a decrease in prevalence over time was seen in all race and Hispanic-origin subpopulations, according to national data.1
Both HSV-1 and HSV-2 cause human diseases ranging from very painful oral cold sores and genital lesions, to eye conditions that can lead to blindness. Infants infected with HSV may develop neurological and developmental problems. People infected with HSV also have an increased risk of acquiring or transmitting HIV.
Both viruses cause infections in which patients who present with symptoms have painful blisters or sores at the site of infection. Both viruses are transmitted through contact with an infected person’s lesion, mucosal surface, or genital or oral secretions. There is no cure for infections caused by such viruses; once a person has been infected, the virus can remain latent for long periods of time before periodically reactivating to cause recurrent disease.
Take a Closer Look
While questions about HSV-1 and -2 testing have been included since 1999 in the National Health and Nutrition Examination Survey, a large national survey, researchers had not examined prevalence data since 2010, notes Geraldine McQuillan, PhD, an infectious disease epidemiologist at the National Center for Health Statistics.2 To gain a better perspective of trends over time, analysts looked at the data since the initial report.
What does the analysis reveal? During 2015-2016, the prevalence of herpes simplex virus type 1 was 47.8%, and the prevalence of herpes simplex virus type 2 was 11.9%. In closer inspection, data indicate:
- Prevalence of both HSV-1 and HSV-2 increased with age.
- Prevalence of both HSV-1 and HSV-2 was higher among females than males.
- Prevalence of HSV-1 was highest among Mexican-Americans and lowest among non-Hispanic white persons. The analysis indicates that HSV-2 prevalence was highest among non-Hispanic black persons and lowest among non-Hispanic Asian persons.
- From 1999-2000 to 2015-2016, prevalence of both types of HSV decreased (HSV-1, 59.4% to 48.1%, and HSV-2, 18.0% to 12.1%).1
Symptomatic Relief, but No Cure
Randomized trials have indicated that three antiviral medications provide clinical benefit for genital herpes: acyclovir, valacyclovir, and famciclovir.3-6 Although these medications may provide symptomatic relief from outbreaks, they do not cure HSV infection. These systemic antiviral drugs can partially control the signs and symptoms of genital herpes when used to treat first clinical and recurrent episodes or when used as daily suppressive therapy, but neither eradicates latent virus nor affects the risk, frequency, or severity of recurrences after the drug is discontinued. German drug maker AiCuris received fast track status in August 2017 from the Food and Drug Administration to determine the safety and efficacy of oral pritelivir, the company’s lead candidate for the treatment of acyclovir-resistant mucocutaneous herpes simplex virus infections in immunocompromised adults. (Contraceptive Technology Update reported on pritelivir in its March 2017 article, “Task Force Recommends Against Genital Herpes Screening,” available at .)
Researchers at the National Institutes of Health’s National Institute of Allergy and Infectious Diseases are making progress in unraveling the role of cellular protein HCF-1 in initiating HSV infection and reactivation. This protein and associated proteins are recruited to the viral genome, enabling the virus to replicate and spread. Working with fellow scientists from Princeton University, the researchers have now published data that identifies new HCF-1 protein complexes that play additional roles in initiating viral infection and reactivation. By using a mouse model, investigators discovered they could reactivate latent HSV using compounds that turn on components of HCF-1 protein complexes.7
- McQuillan G, Kruszon-Moran D, Flagg EW, Paulose-Ram R. Prevalence of herpes simplex virus type 1 and type 2 in persons aged 14-49: United States, 2015-2016. NCHS Data Brief 2018;(304):1-8.
- Bradley H, Markowitz LE, Gibson T, McQuillan GM. Seroprevalence of herpes simplex virus types 1 and 2 — United States, 1999-2010. J Infect Dis 2014;209:325-333.
- Diaz-Mitoma F, Sibbald RG, Shafran SD, et al; Collaborative Famciclovir Genital Herpes Research Group. Oral famciclovir for the suppression of recurrent genital herpes: A randomized controlled trial. JAMA 1998;280:887-892.
- Mertz GJ, Loveless MO, Levin MJ, et al; Collaborative Famciclovir Genital Herpes Research Group. Oral famciclovir for suppression of recurrent genital herpes simplex virus infection in women: A multicenter, double-blind, placebo-controlled trial. Arch Intern Med 1997;157:343-349.
- Reitano M, Tyring S, Lang W, et al; International Valaciclovir HSV Study Group. Valaciclovir for the suppression of recurrent genital herpes simplex virus infection: A large-scale dose range-finding study. J Infect Dis 1998;178:603-610.
- Romanowski B, Marina RB, Roberts JN; Valtrex HS230017 Study Group. Patients’ preference of valacyclovir once-daily suppressive therapy versus twice-daily episodic therapy for recurrent genital herpes: A randomized study. Sex Transm Dis 2003;30:226-231.
- Alfonso-Dunn R, Turner AW, Jean Beltran PM, et al. Transcriptional elongation of HSV immediate early genes by the super elongation complex drives lytic infection and reactivation from latency. Cell Host Microbe 2017;21:507-517.