Herpes Simplex and Varicella Zoster Flashcards
Herpes Viruses
HSV1 HSV2 VZV EBV CMV HHV6 HHV7
Common characteristics of herpes viruses
Large, enveloped dsDNA viruses, very ubiquitous, chronic/latent infection follows acute infection, reactivations are common, mostly transmitted during asymptomatic shedding, mostly transmitted by close contact
Which herpes virus isn’t transmitted via close contact and asymptomatic shedding?
Varicella
Herpes Viruses Mechanisms of Injury
Direct Cell damage, immune reactions, malignant transformation, immunosuppression and opportunistic infections
Life cycle of the herpes viruses
Attachment and penetration by fusion, immediate early protein synthesis regulates viral replication, early protein synthesis replicates the genome, late protein synthesis mediates the assembly of viral particles, release, cell to cell spread.
Acyclovir
Herpes DNA polymerase inhibitor that requires phosphorylation by a viral thymidine kinase.
HSV 1 and 2 pathogenesis
Enters via abraded skin and mucosa, create lesions at the site of entry and remain latent in the sensory ganglia (geniculate and dorsal root). Reactivates with intercurrent illness, UV light, stress and immunosuppression.
HSV pathology
Giant cells with intranuclear inclusions: Tzanck Test
What infections are associated with HSV-1/HSV-2?
HSV-1 more commonly associated with oral infection, HSV-2 more commonly associated with genital infeciton
How does HSV spread?
Close contact
What does HSV cause?
Crops of painful small blisters and ulcers. Asymptomatic shedding
HSV esophagitis
Happens, so does HSV encephalitis
Diagnosis of HSV
Viral culture (but not good for CSF), DFA of skin lesions, PCR for CSF, Tzanck smear (older test)
What is better than oral acyclovir?
Valacyclovir (prodrug that is converted to acyclovir) is absorbed more efficiently.
Adverse effects of acyclovir?
Rare kidney dysfunction, resistance due to mutations in viral thymidine kinase or DNA polymerase
