Neurotropic Herpesviruses Flashcards
Describe the structure, capsid, and genomes of herpesviruses.
Describe their lytic and latent lifestyles.
All herpesviruses are enveloped, icosahedral viruses with dsDNA (Type I)
Lytic infection is typical; hijack host transcriptional machinery in the nucleus to produce alpha>beta>gamma gene products, assemble in cytosol and bud. Latent infection involves episomal maintenance and low viral expression until reactivation.
How are Herpesvirsues usually treated? Provide mechanisms.
How are herpesviruses usually diagnosed?
Most herpes treatments target DNA proteins produced by the virus. Acyclovir is phosphorylated by viral and cellular kinases to resemble dGTP and break chain elongation.
Diagnosis usually by examination (vesicles), culture, immunofluorescence, PCR and/or serology.
Herpes Simplex
How is it transmitted?
How widespread is it?
Describe its pathogenesis.
Herpes Simplex
Direct contact (skin/genitals/mucosae/saliva/tears, plus perinatal/intrauterine). HSV-1 mostly orally spread, HSV-2 more from genitals.
HSV-1 is widespread. HSV-2 found in 1/4 females, 1/8 males.
Travels along sensory neurons to go latent in their cell bodies (Trigem/Sacral; uses LATs to repress expression). Reactivates robustly.
Which herpesviruses cause genital disease?
Which cause oral-facial infections?
What is the name for recurrent facial infections? Are antivirals indicated?
HSV-1 and HSV-2 can affect the genitals.
Only HSV-1 causes pharyngitis/gingivostomatotitis.
Herpes labialis: antivirals are not necessary, but can reduce scarring and improve cosmesis.
How does neonatal herpes originate?
What are its clinical symptoms?
How can it be avoided?
Inoculation in utero, or more likely during birth.
Viral dissemination, affecting the CNS and causing high mortality and disability.
Treat the virus in the pregnant mother.
What illnesses can Herpes simplex cause besides primary genital, oralfacial, and neonatal illness?
Herpes encephalitis
Herpes keratitis/conjunctivitis
Herpes gladiatorium (athletes)
Herpes whitlow (healthcare workers)
Varicella Zoster
How is it transmitted?
Describe its pathogenesis.
Varicella Zoster
Through person-person contact, especially by aerosolization and inhalation, but also by skin lesions.
During a 2-3week incubation period, the virus replicates in T cells as well as endothelium/epitthelium. Ganglia are latently infected (note: higher level of activity than herpes simplex).
Varicella Zoster
What are its clinical symptoms?
Are antivirals indicated?
What is this illness also called?
Varicella Zoster
Blisters, malaise, fever and itching. Worse in adults (pneumonia and skin infections), and potentially fatal in the immunosuppressed.
Usually only for neonatal and disseminated infection.
Chickenpox!
Herpes Zoster
Describe its pathogenesis and symptoms.
What are some late sequelae of this illness?
What is this disease also called?
Herpes Zoster
Reactivation of varicella zoster originally latent in a sensory ganglion. Presents with skin lesions following the nerve’s somatotome. Visually impairing if in trigeminal ganglion.
Postherpetic neuralgia can result–pain without apparent cause in the region of the lesion.
Shingles.
What are some differential diagnoses for varicella zoster?
Describe the VSV vaccine. What are its risks?
Bacterial/enteroviral infections, dermatitis, and disseminated HSV.
VSV vaccine is a live-attenuated Oka VSV. Given in two doses to reduce severity of future infections. However, can itself reactivate (mildly), and can be transmitted to immunocompromised.
