Herpes simplex virus

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Revision as of 15:32, 16 October 2019 by Aidan (talk | contribs) (Initial completion of background section)
  • Comprises herpes simplex virus 1 (HSV-1) and HSV-2, which are members of the Human herpesvirus family
  • Cause typical painful vesicular lesions on labia or external genitals
  • Occasionally cause a viral encephalitis

Background

Microbiology

  • Enveloped, double-stranded DNA virus
  • HSV-1 and HSV-2 are morphologically and genetically distinct viruses
  • Can be infected with both

Epidemiology

  • Worldwide distribution, and only found in humans
  • Most common cause of genital lesions
  • Spread through person-to-person contact with skin or mucosa; not spread via fomits
  • HSV-1 is more common, with 90% of adults having antibodies by age 40
    • Often acquired in childhood in Asia and Africa
    • More common in lower SES populations
  • HSV-2 has seroprevalence of 15-20% in US
    • More common in women than men, in HIV-infected people, and in MSM
    • May be subclinical if already infected with HSV-1

Pathophysiology

  • Fusion of envelope and cell membrane is mediated by viral glycoproteins B, C, and D and host cell proteins cellular heparin sulfate, TNF receptors, and immunoglobulins
  • Internal capsid is released, which makes its way to the nucleus
  • Viral DNA polymerase enzyme and viral DNA helicase are targets of antivirals
  • Viral DNA may remain latent in about 10% of nearby neurons, characterized by latency-associated transcripts (LATs)
    • Despite being latent, virus can still be shed in mucosa anywhere from 1/10 to 3/4 of days
  • HSV-1 prefers trigeminal ganglia as well as cervical ganglia, or sacral nerve root ganglia if genital

Clinical Presentation

  • Incubation period usually within 5 days for primary infection

Diagnosis

Management