Skip to Main Content

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; in the United States, 15–20% of the population has antibody to HSV-2.

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

  • HSV reactivation is very common: HSV-2 is shed on a median of 25% of days by infected pts, with 29% of 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.

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.

    • – 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.

  • Pts with atopic dermatitis may also develop severe oral-facial HSV infection (eczema herpeticum), with extensive skin lesions and occasional visceral dissemination.

  • HSV infection is the precipitating event in ∼75% of cases of erythema multiforme.

Genital Infections

First-episode primary genital herpes is characterized by ...

Pop-up div Successfully Displayed

This div only appears when the trigger link is hovered over. Otherwise it is hidden from view.