Herpes simplex virus infection is common and has multiple clinical manifestations.
The classic clinical presentation of vesicles progressing to painful ulcers is unusual; atypical and mild symptoms are common, and most people have unrecognized disease.
Symptoms of oral herpes (herpes labialis) include tingling and burning followed by development of vesicular then ulcerative lesions involving the oropharynx and perioral mucosa.
Symptoms of genital herpes range from asymptomatic to tingling and burning without lesions, to recurrent genital ulcerations.
Acyclovir, famciclovir, and valacyclovir are effective at shortening the duration and severity of an outbreak.
Daily suppressive therapy reduces recurrences by 80% and reduces transmission risk by approximately 50%.
Glycoprotein G-based type-specific serology testing is used to diagnose infection with or without lesions and distinguish between type 1 and 2.
The major clinical manifestations of infection with herpes simplex virus (HSV) type 1 (HSV-1) or HSV type 2 (HSV-2) are oral, genital, and ocular ulcers. Less commonly, primary or recurrent HSV infections may also present at other sites with neurologic, hepatic, or respiratory complications. The primary episode occurs during initial infection with HSV, in which the host lacks an antibody response.
Herpes labialis is infection of the mouth area and lips, most commonly with HSV-1.
Genital herpes is caused by infection with either HSV-1 or HSV-2. The first clinical episode of genital ulceration may represent either new acquisition of the virus or newly recognized disease with remote acquisition of the virus.
For both HSV-1 and HSV-2, asymptomatic shedding may occur in the absence of lesions; transmission of the virus may occur during asymptomatic shedding. HSV establishes latency in neuronal ganglia and periodically reactivates. Most reactivations are asymptomatic but can result in transmission of the virus.
For details of management of ophthalmic HSV infection, please refer to the Uveitis and Keratitis topics. For details of management of suspected HSV encephalitis, please refer to the Encephalitis topic.
History and exam
- HIV infection (risk factor for clinical disease)
- immunosuppressive medications (risk factor for clinical disease)
- female sex (risk factor for seropositivity)
- black race (risk factor for seropositivity)
- increasing age (risk factor for seropositivity)
- high-risk sexual behavior (risk factor for seropositivity)
- lack of condom use (risk factor for seropositivity)
Benjamin D. Lorenz, MD
Division of Hospital Medicine
MedStar Georgetown University Hospital
BDL declares that he has no competing interests.
Dr Benjamin D. Lorenz would like to gratefully acknowledge Dr Christine Johnson and Dr Anna Wald, previous contributors to this topic.
CJ reports funding from AiCuris; grants from Agenus, Gilead, Genocea, Sanofi, and Vical to conduct clinical research studies; and royalties from Up To Date. AW reports grants from Agenus, Gilead, Genocea, Sanofi, and Vical to conduct clinical research studies. AW receives royalties from Up To Date. AW is an NIH grant recipient (NIH AI30731 and AI071113) and a consultant for Aicuris, Eisai, and Amgen.
Giuseppe Pizzo, DDS
Department of Surgical, Oncological and Oral Sciences
School of Dentistry
University of Palermo
GP declares that he has no competing interests.
Peter Leone, MD
Professor of Medicine
University of North Carolina at Chapel Hill
PL declares that he has no competing interests.
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