Varicella-zoster virus (VZV) is distinguished from herpes simplex virus type 1 (HSV-1) by the fact that cell-to-cell fusion and syncytium formation require only gH and gL within a transient-expression system. For herpesviruses, this event is governed by the multiprotein core complex of conserved glycoproteins (g)B and gH/gL. VZV lacks a gD homologous protein. In addition, electron microscopy shows that very little virus is present on the surfaces of cells infected with VZV gB-36, while cells infected with native VZV exhibit abundant virions on the cell surface. Conversely, the promoters of ORF 36 (thymidine kinase) and ORF 14 (glycoprotein C), genes expressed during lytic but not latent infection, were not enriched in the fraction of latently infected ganglia that bound to anti-H3K9(Ac) antibody. In immunogold electron microscopic studies, VZV gK was in enveloped virions and was evenly distributed in the cytoplasm in infected cells. The very low levels of IE62 in ROka66S virions indicate that ORF66 protein mediates the redistribution of IE62 to sites of tegument assembly.
Thus, directed mutagenesis of the VZV genome is providing new insights into viral pathogenesis and may provide new candidate vaccines. (B) Varicella zoster virus (VZV) vasculopathy: proton-density brain MRI scan shows multiple areas of infarction in both hemispheres, particularly involving white matter (thin arrow) and extending to gray white-matter junctions (thick arrow). Smialek, and S.E. In this case, tyrosine phosphorylation occurred on a previously unrecognized and underglycosylated VZV gE dimeric product. Links to PubMed are also available for Selected References. -Incidence rises with age and declining cellular immunity. The DNA genomes of VZV and HSV show more difference at the sequence level.
In contrast, our understanding of VZV latency is restricted by a lack of animal models and further complicated by the lower levels of latent VZV in human cadaver ganglionic tissues. Human herpesvirus 6 (HHV-6) is the common collective name for Human herpesvirus 6A (HHV-6A) and Human herpesvirus 6B (HHV-6B). This process was first reported for the herpes simplex virus. Age distribution of latent herpes simplex virus 1 and varicella-zoster virus genome in human nervous tissue. Herpes simplex viruses types 1 and 2 (HSV1 and HSV2) and varicella-zoster virus (VZV) establish latent infection in dorsal root ganglia for the entire life of the host. Although the viruses vary in the clinical disorders they cause and in their molecular structure, they share several features that affect the course of infection of the human nervous system. Liedtke W, Opalka B, Zimmermann CW, Lignitz E: Age distribution of latent herpes simplex virus.
1 and varicella-zoster virus genome in human nervous tissue. I have had 24 years of seeing the healing Cineraria stimulates, and it continues to impress me. An outstanding property – the ability to establish latent infections, to persist indefinitely in infected hosts, and to periodically become reactivated. ORF4 protein interacts with VZV ORF62 protein, the TATA binding protein, transcription factor IIB, and NF-κB subunits p50 and p65 (11, 34). Similar to other herpesviruses, VZV entry into host cells is presumed to be initiated by virion attachment to the cell surface, followed by fusion between the virus envelope and the plasma membrane of the target cell. After chickenpox resolves, the virus becomes latent in neurons of cranial and spinal ganglia of nearly all individuals. Varicella-zoster virus (VZV), an alpha herpesvirus found exclusively in humans, can cause a wide spectrum of disorders throughout the lifetime of the individual.
). The herpesvirus particle has a very complex structure:. Reactivation of latent virus leads to recurrent disease – virus travels back down sensory nerves to surface of body and replicates, causing tissue damage:. Varicella-zoster virus (VZV/HHV-3). Herpesviruses can establish latent infections after cellular replication and covalent integration of viral DNA into the host genome. Each index score is expressed as an age-adjusted standard score with a mean of approximately 100 and an SD of approximately 15 based on a group of 540 healthy subjects who ranged in age from 20 to 89 years and were matched to US census data by sex, ethnicity, and level of education. Liedtke WOpalka BZimmermann CWLignitz E Age distribution of latent herpes simplex virus 1 and varicella-zoster virus genome in human nervous tissue.
Herpes simplex virus type 2 (HSV-2) infection is responsible for significant neurological morbidity, perhaps more than any other virus. Herpes simplex virus type 2 associated neurological disease may result from primary infection or reactivation of latent HSV-2. HSV-2 latency in ganglia throughout the central nervous system (CNS) axis, albeit at significantly lower frequencies than in the sacral ganglia. Typically, this sight-threatening disorder has a bimodal age distribution, with varicella zoster virus and HSV-1 infections affecting older patients and HSV-2 infection affecting patients with a median age of 20 years. 6Deatly, A.M., Haase, A.T., Fewster, P.H., Lewis, E., Ball, M.J. Human herpes virus infections and Alzheimer’s disease. Presence of herpes simplex DNA in surgical tissue from human epileptic seizure foci detected by polymerase chain reaction: Preliminary study.
Lignitz, E. Age distribution of latent herpes simplex virus 1 and varicella-zoster virus genome in human nervous tissue. HSV-1 genomic DNA has also been detected in the central nervous system of a significant percentage of humans 18, 26, 27. Herpes viruses are a leading cause of human viral disease, second only to influenza and cold viruses. Herpes viruses infect most of the human population and persons living past middle age usually have antibodies to most of the above herpes viruses with the exception of HHV-8. Herpes Virus Structure – General. Table 1 Cadaver Information and Positivity for Herpes Simplex Virus.