Difference between revisions of "Category:Herpesviridae"

This article is still under construction.

Introduction

Herpes viruses are some of the more difficult viruses to combat as they quite contentedly go latent for long periods of time. They often produce an initial respiratory response but go subclinical until the animal becomes immunosuppressed. Protection against herpes is challenging, as immunity relies on stimulating a CD8+ T-cell response, which is difficult to provoke by conventional vaccination.

Morphology

• Double stranded DNA that becomes a closed circle in the host nucleus
• Remains unintegrated while latent

Virulence and Pathogenesis

• Three types of genes involved in replication:
  • Immediate early genes (IE genes): strong promoter of the expression of adjacent viral genes
  • Early genes: stimulate viral DN replication; potential cause of lymphoproliferation and tumors in the absence of cell lysis
  • Late genes: encode viral structural proteins
    • Cause large intranuclear inclusion bodies typical of herpes viruses as capsid proteins are assembled
    • Envelope buds through nuclear membrane, containing spike glycoproteins (gA to gE)
    • Masses of virus then either lyse or fuse cells, causing ulceration, etc.
• Initial replication in respiratory tract
• Spread determines pathogenicity:
  • Cell-associated spread means that virus is spread by cell fusion
  • Can target crucial tissues: brain, placenta, etc
• All become latent and reactivate under stress
• Reactivation is associated with the presence of thymidine kinadse (tk) gene (which is deleted in GE vaccines)
  • Accelerates DNA synthesis

Research

• Some herpes and pox viruses express non-structural proteins known as virokines
• Virokines appear to help the virus evade the Th-1 response by altering the inflammatory response

Virus by Species