The neurotropic herpes viruses: herpes simplex and varicella-zoster

Management of acute viral encephalitis in Brazil

“…The symptoms include fever, vomiting, and ataxia. This condition is considered benign and self limited and there is no evidence that antiviral therapy is useful [26,27]. VZV encephalitis is very rare and occurs more frequently in immunocompromised patients and children [28,29].…”

“…CT scan may be normal or show non-specific findings as well [29]. Diagnosis is based upon the history of VZV or herpes zoster rash, usually few weeks before encephalitic symptoms, and demonstration of specific antibodies, antigens, or nucleic acids of VZV by PCR in CSF samples [27,29].…”

Varicella and herpes zoster vaccine development: lessons learned

“…Its linear 125-kb double-stranded DNA genome encodes at least 71 unique open-reading frames (ORFs) [1], with approximately 40 conserved genes shared with other human herpesviruses [2]. The genome is located within an icosahedral capsid, surrounded by a protein tegument and encapsulated by a polyamine, lipid, and glycoprotein envelope [3]. Glycoproteins located within the envelope facilitate viral entry into cells [4].…”

“…During latency, the VZV genome is maintained in a nonintegrated circular concatemeric form, with a very restricted pattern of viral gene expression [3]. The absence of an animal model of VZV natural history has hampered understanding of the precise pattern of gene expression during latency, although low-level transcription of the immediate early gene ORF 63 has been repeatedly detected in human ganglia from autopsy samples taken as close to death as possible [15].…”

“…VZV-specific memory T cells, with a mixed central and effector phenotype, are important for maintaining VZV latency, with immunity boosted periodically by endogenous (subclinical) reactivation and exogenous reexposure to VZV [16]. Latent virus retains its ability to resume replication and cause recurrent clinical disease [3]. …”