Herpes Simplex Virus 2 (HSV2)
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Viruses - DNA Viruses
- Herpesvirus Overview
- Herpes Simplex Virus 1 (HSV1)
- Herpes Simplex Virus 2 (HSV2)
- Varicella-Zoster Virus (HHV3)
- Epstein-Barr Virus (HHV4)
- Cytomegalovirus (HHV5)
- Human Herpesviruses 6 and 7 (HHV6 and HHV7)
- Human Herpesviruses 8 (HHV8)
- Poxvirus
- Hepadnavirus
- Adenovirus
- Papillomavirus (HPV)
- Polyomavirus
- Parvovirus
Key Points
Herpes simplex virus 2 (HSV-2)
- Characteristics
- Member of Herpesvirus family
- Also known as human herpesvirus 2 (HHV-2)
- Enveloped DNA virus with double-stranded, linear DNA
- Herpesviruses are unique in that they get their envelope by budding from nuclear membrane of host cell
- Member of Herpesvirus family
- Transmission
- Contact with infected lesions
- Sexual transmission
- May be prevented with condom use
- Perinatal contact is also possible
- Sexual transmission
- Contact with infected lesions
- Pathophysiology and Presentation
- Viral infection manifests as grouped vesicles on erythematous base
- Can ulcerate, leading to lesions in various states of healing (vesicles, pustulations, ulcers, scabbing, etc.)
- Primary infection
- Herpes genitalis (genital ulcers)
- Associated with fever, dysuria (pain with urination), inguinal lymphadenopathy
- May occur in neonates
- From exposure to infected genitalia of mother
- Herpes genitalis (genital ulcers)
- Dormancy in sensory ganglia
- Enters sensory nerve and moves via retrograde transport from genitals
- Commonly in sacral ganglia
- Reactivation
- Replicates in ganglia with anterograde transport to epithelial cells, where virus continues to replicate
- Same symptoms as primary infection; but less severe
- Extragenital manifestations are rare
- Viral meningitis more common in HSV-2 than HSV-1
- Viral infection manifests as grouped vesicles on erythematous base
- Diagnosis
- PCR and viral culture is gold standard
- Tzank smear of lesions
- Epithelial cells scraped from lesion, prepared on Wright-Giemsa stain
- Multinuclear giant cells
- intranuclear inclusions (Cowdry type A bodies)
- Treatment
- Acyclovir and related drugs (famciclovir/valacyclovir)
- Guanosine analog that inhibit viral DNA polymerase (viral DNA synthesis)
- Requires herpes viral thymidine kinases (phosphorylation) for conversion into their active form
- Acyclovir and related drugs (famciclovir/valacyclovir)