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HERPES SIMPLEX VIRUSES

MICROBIOLOGY AND PATHOGENESIS

The herpes simplex viruses HSV-1 and HSV-2 are linear, double-stranded DNA viruses that share ∼50% sequence homology. Exposure to HSV at mucosal surfaces or abraded skin sites permits viral entry and replication in cells of the epidermis and dermis prior to infection of neuronal cells and development of a latent infection in ganglia.

  • Reactivation occurs when normal viral gene expression resumes, with reappearance of the virus on mucosal surfaces.

  • Both antibody-mediated and cell-mediated immunity (including type-specific immunity) are clinically important.

EPIDEMIOLOGY

HSV-1 is acquired more frequently and at an earlier age than HSV-2. More than 90% of adults have antibodies to HSV-1 by the fifth decade of life. Antibodies to HSV-2 usually are not detected until adolescence and correlate with sexual activity. The seroprevalence of HSV-2 is higher in the developing than in the developed world; up to 60% of pregnant women in sub-Saharan Africa are seropositive.

  • HSV is transmitted by contact with active lesions or with virus shed from mucocutaneous surfaces by asymptomatic persons.

  • HSV reactivation is very common: HSV DNA can be detected on 20–30% of days by PCR, with most genital reactivation episodes lasting <6 h.

  • The large reservoir of unidentified carriers and the frequent asymptomatic reactivation of HSV-2 have fostered the continued spread of HSV throughout the world.

  • HSV-2 infection is associated with a two- to fourfold increase in HIV-1 acquisition; in fact, 33–50% of HIV-1 infections may be attributable to HSV-2 in men who have sex with men and in populations of sub-Saharan Africa.

CLINICAL MANIFESTATIONS

Both viral subtypes can cause indistinguishable genital and oral–facial infections. Overall, genital HSV-2 is twice as likely to reactivate as genital HSV-1, and HSV-2 infection recurs 8–10 times more often. In contrast, oral–labial HSV-1 infection recurs more frequently than oral–labial HSV-2 infection. The incubation period for primary infection with either virus is 1–26 days (median, 6–8 days).

Oral–Facial Infections

Primary HSV-1 infection results in gingivostomatitis, pharyngitis, and up to 2 weeks of fever, malaise, myalgia, inability to eat, and cervical adenopathy, with lesions on the palate, gingiva, tongue, lip, face, posterior pharynx, and/or tonsillar pillars and occasional exudative pharyngitis.

  • Reactivation of HSV from the trigeminal ganglia is associated with asymptomatic viral excretion in the saliva, intraoral mucosal ulcerations, or ulcers on the vermilion border of the lip or external facial skin.

    • – Approximately 50–70% of pts undergoing trigeminal nerve-root decompression and 10–15% of pts undergoing dental extraction develop oral–labial herpes a median of 3 days after the procedure.

    • – Reactivation of HSV-1 or VZV in the mandibular portion of the facial nerve causes flaccid paralysis (Bell’s palsy).

  • Immunosuppressed pts can have a severe infection that extends into the mucosa and skin, causing friability, necrosis, bleeding, pain, and inability to eat or drink.

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