Herpes Simplex Virus

Abstract

Human infections with herpes simplex virus type 1 (HSV-1) and type 2 (HSV-2) are common throughout the world. HSV infection can cause a variety of illnesses depending on the anatomic site infected, whether it is a primary or recurrent infection, and the immune status of the person infected. Persons at risk for serious or prolonged active HSV infection are those with eczema, severe burns, or immunosuppressive conditions, such as organ transplant patients or HIV-infected persons. Primary infection occurs in individuals who have not previously been infected with either HSV-1 or HSV-2. Primary infections may be subclinical or mild enough to be unrecognized in a majority of cases, whereas clinically apparent infections comprise a wide array of presentations, ranging from mild pharyngitis or cutaneous infections to severe generalized disease and, on rare occasions, death (1). HSV-1 has a greater propensity to cause oral infections and is typically acquired during childhood. The most frequent manifestation of primary HSV-1 infection in children is gingivostomatitis. Primary HSV-1 infection in adolescents and adults usually manifests as pharyngitis or tonsillitis. Conjunctivitis, keratitis, vesicular eruptions of the skin, herpes whitlow, and encephalitis occur much less frequently. While the most common manifestation of sexually acquired HSV-2 is genital disease, both HSV-2 and HSV-1 can cause genital infection. HSV is the most common cause of genital ulcer disease in developed countries. In recent years, HSV-1 has been more frequently implicated as the etiologic agent (1). Complications of HSV-2 infection include aseptic meningitis and other neurological complications, extragenital lesions, and disseminated infection. Neonatal herpes is caused by mother-to-child transmission of HSV-1 or HSV-2 in utero, during the birth process, or during the neonatal period. Infants infected during delivery or postpartum present in one of three ways: (i) disease localized to the skin, eyes, or mouth; (ii) central nervous system disease with or without skin, eye, or mouth disease; or (iii) disseminated infection. HSV-1 seroprevalence in the United States declined about 7% from 1999 to 2004 and from 2005 to 2010, with roughly 60% of persons being HSV-1 seropositive among 40- to 49-year-olds (2). HSV-2 seroprevalence in the United States increased by more than 50% between the mid-1970s and the mid-1990s but then began to decline; in 2005 to 2010, the estimated seroprevalence was 25% in 40- to 49-year-olds (2).