Herpesviridae

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Herpesviridae

Image:Herpesviridae EM PHIL 2171 lores.jpg

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

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Overview

The Herpesviridae are a large family of DNA viruses that cause diseases in humans and animals.[1] 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.

Human herpesviridae

There are eight distinct viruses in this family known to cause disease in humans.[1]

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,[1] 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][1]


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.[1]

Viral structure

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, viral DNA limited replication and transcription of viral genes. 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.

Animal herpesviridae

Taxonomy

The following genera are included here:

References

External links

cs:Herpes viry da:Herpesviridae de:Herpesvirenfr:Herpesviridae it:Herpesviridae nl:Herpesvirussen ja:ヘルペスウイルス科fi:Herpesvirukset sv:Herpesvirus

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Acknowledgement and Attribution Regarding Sources of Content

Some of the initial content on this page may be incorporated in part from copyleft sources in the public domain including wikis such as Wikipedia and AskDrWiki. Drug information for patients came from the The National Library of Medicine. Infectious disease information may have come from the Centers for Disease Control (CDC). Differential Diagnoses are drawn from clinicians as well as an amalgamation of 3 sources: 1.The Disease Database; 2. Kahan, Scott, Smith, Ellen G. In A Page: Signs and Symptoms. Malden, Massachusetts: Blackwell Publishing, 2004:3; 3. Sailer, Christian, Wasner, Susanne. Differential Diagnosis Pocket. Hermosa Beach, CA: Borm Bruckmeir Publishing LLC, 2002:7 .

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