Herpesviridae

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Herpesviridae

Virus classification
Group: Group I (dsDNA)
Family: Herpesviridae
Genera

Subfamily Alphaherpesvirinae
   Simplexvirus
   Varicellovirus
   Mardivirus
   Iltovirus
Subfamily Betaherpesvirinae
   Cytomegalovirus
   Muromegalovirus
   Roseolovirus
Subfamily Gammaherpesvirinae
   Lymphocryptovirus
   Rhadinovirus
Unassigned
   Ictalurivirus

The Herpesviridae are a large family of DNA viruses that cause diseases in humans and animals.[1] [2] [3] The family name is derived from the Greek word herpein ("to creep"), referring to the latent, re-occurring infections typical of this group of viruses. Herpesviridae can cause latent or lytic infections.

Contents

There are eight distinct viruses in this family known to cause disease in humans.[4]

Human Herpesvirus (HHV) classification
Type Synonym Subfamily Pathophysiology
HHV-1 Herpes simplex virus-1 (HSV-1) α (Alpha) Oral and/or genital herpes (predominantly orofacial)
HHV-2 Herpes simplex virus-2 (HSV-2) α Oral and/or genital herpes (predominantly genital)
HHV-3 Varicella zoster virus (VZV) α Chickenpox and shingles
HHV-4 Epstein-Barr virus (EBV), lymphocryptovirus γ (Gamma) Infectious mononucleosis, Burkitt's lymphoma, CNS lymphoma in AIDS patients,
post-transplant lymphoproliferative syndrome (PTLD), nasopharyngeal carcinoma
HHV-5 Cytomegalovirus (CMV) β (Beta) Infectious mononucleosis-like syndrome,[5] retinitis, etc.
HHV-6, -7 Roseolovirus β Sixth disease (roseola infantum or exanthem subitum)
HHV-8 Kaposi's sarcoma-associated herpesvirus
(KSHV), a type of rhadinovirus		 γ Kaposi's sarcoma, primary effusion lymphoma, some types of multicentric Castleman's disease
References: [1][4]


Monkey B virus (Cercopithecine herpesvirus-1, Herpesvirus simiae) is a simplexvirus endemic in macaque monkeys. Human zoonotic infection typically results in fatal encephalomyelitis or severe neurologic impairment in untreated individuals.[6]

The human herpesviruses all share some common properties. One shared property is virus structure—all herpesviruses are composed of relatively large double-stranded, linear DNA genomes encoding 100-200 genes encased within an icosahedral protein cage called the capsid which is itself wrapped in a lipid bilayer membrane called the envelope. This particle is known as the virion.

Following binding of viral envelope glycoproteins to cell membrane receptors, the virion is internalized and dismantled, allowing viral DNA to migrate to the cell nucleus. Within the nucleus, replication of viral DNA and transcription of viral genes occurs. During symptomatic infection, infected cells transcribe lytic viral genes. In some host cells, a small number of viral genes termed latency associated transcript (LAT) accumulate instead. In this fashion the virus can persist in the cell (and thus the host) indefinitely. Reactivation of latent viruses has been implicated in a number of organic diseases. While primary infection is often accompanied by a self-limited period of clinical illness, long-term latency is symptom-free. Following activation, transcription of viral genes switches from LAT to multiple lytic genes that lead to enhanced replication and virus production. Often, lytic activation leads to cell death. Clinically, lytic activation is often accompanied by emergence of non-specific symptoms such as low grade fever, headache, sore throat, malaise, and rash as well as clinical signs such as swollen or tender lymph nodes and immunological findings such as reduced levels of natural killer cells.

In animal virology the most important herpesviruses belong to the Alphaherpesvirinae. Research on pseudorabies virus (PrV), the causative agent of Aujeszky's disease in pigs, has pioneered animal disease control with genetically modified vaccines. PrV is now extensively studied as a model for basic processes during lytic herpesvirus infection, and for unravelling molecular mechanisms of herpesvirus neurotropism, whereas bovine herpesvirus 1, the causative agent of bovine infectious rhinotracheitis and pustular vulvovaginitis, is analyzed to elucidate molecular mechanisms of latency. The avian infectious laryngotracheitis virus is phylogenetically distant from these two viruses and serves to underline similarity and diversity within the Alphaherpesvirinae.[2] [3]

The following genera are included here:

  1. ^ a b Ryan KJ; Ray CG (editors) (2004). Sherris Medical Microbiology, 4th ed., McGraw Hill. ISBN 0838585299. 
  2. ^ a b Mettenleiter et al (2008). "Molecular Biology of Animal Herpesviruses", Animal Viruses: Molecular Biology. Caister Academic Press. ISBN 978-1-904455-22-6. 
  3. ^ a b Sandri-Goldin RM (editor). (2006). Alpha Herpesviruses: Molecular and Cellular Biology. Caister Academic Press. ISBN 978-1-904455-09-7 . 
  4. ^ a b Whitley RJ (1996). Herpesviruses. in: Baron's Medical Microbiology (Baron S et al, eds.), 4th ed., Univ of Texas Medical Branch. ISBN 0-9631172-1-1. 
  5. ^ Bottieau E, Clerinx J, Van den Enden E, Van Esbroeck M, Colebunders R, Van Gompel A, Van den Ende J (2006). "Infectious mononucleosis-like syndromes in febrile travelers returning from the tropics.". J Travel Med 13 (4): 191-7. PMID 16884400. 
  6. ^ Huff J, Barry P (2003). "B-virus (Cercopithecine herpesvirus 1) infection in humans and macaques: potential for zoonotic disease". Emerg Infect Dis 9 (2): 246-50. PMID 12603998. 
  7. ^ Fenner, Frank J.; Gibbs, E. Paul J.; Murphy, Frederick A.; Rott, Rudolph; Studdert, Michael J.; White, David O. (1993). Veterinary Virology (2nd ed.). Academic Press, Inc. ISBN 0-12-253056-X. 

Retrieved from "http://en.wikipedia.org/wiki/Herpesviridae"
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