Alphaherpesvirinae

Alphaherpesvirinae is a subfamily of viruses in the family Herpesviridae, primarily distinguished by reproducing more quickly than other subfamilies in the Herpesviridae. In animal virology the most important herpesviruses belong to the Alphaherpesvirinae. Pseudorabies virus is the causative agent of Aujeszky's disease in pigs and Bovine herpesvirus 1 is the causative agent of bovine infectious rhinotracheitis and pustular vulvovaginitis.[1][2] Mammals serve as natural hosts. There are currently 37 species in this subfamily, divided among 5 genera. Diseases associated with this subfamily include: HHV-1 and HHV-2: skin vesicles or mucosal ulcers, rarely encephalitis and meningitis, HHV-3: chickenpox (varicella) and shingles, GaHV-2: Marek's disease.[3][4]

Alphaherpesvirinae
Electron micrograph of a Human alphaherpesvirus 3 virion
Virus classification
(unranked): Virus
Phylum: incertae sedis
Class: incertae sedis
Order: Herpesvirales
Family: Herpesviridae
Subfamily: Alphaherpesvirinae
Genera

See text

Genera

Alphaherpesvirinae consists of the following five genera:[4]

Structure

Viruses in Alphaherpesvirinae are enveloped, with icosahedral, spherical to pleomorphic, and round geometries, and T=16 symmetry. The diameter is around 150-200 nm. Genomes are linear and non-segmented, around 120-180kb in length.[3]

GenusStructureSymmetryCapsidGenomic arrangementGenomic segmentation
IltovirusSpherical pleomorphicT=16EnvelopedLinearMonopartite
MardivirusSpherical pleomorphicT=16EnvelopedLinearMonopartite
SimplexvirusSpherical pleomorphicT=16EnvelopedLinearMonopartite
ScutavirusSpherical pleomorphicT=16EnvelopedLinearMonopartite
VaricellovirusSpherical pleomorphicT=16EnvelopedLinearMonopartite

Life cycle

Viral replication is nuclear, and is lysogenic. Entry into the host cell is achieved by attachment of the viral gB, gC, gD and gH proteins to host receptors, which mediates endocytosis. Replication follows the dsDNA bidirectional replication model. DNA-templated transcription, with some alternative splicing mechanism is the method of transcription. Translation takes place by leaky scanning. The virus exits the host cell by nuclear egress, budding, and microtubular outwards viral transport. Mammals serve as the natural host. Transmission routes are sexual, contact, body fluids, lesions, and respiratory.[3]

GenusHost detailsTissue tropismEntry detailsRelease detailsReplication siteAssembly siteTransmission
IltovirusBirds: galliform: psittacineNoneCell receptor endocytosisBuddingNucleusNucleusOral-fecal; aerosol
MardivirusChickens; turkeys; quailNoneCell receptor endocytosisBuddingNucleusNucleusAerosol
SimplexvirusHumans; mammalsEpithelial mucosaCell receptor endocytosisBuddingNucleusNucleusSaliva
ScutavirusSea turtlesNoneCell receptor endocytosisBuddingNucleusNucleusAerosol
VaricellovirusMammalsEpithelial mucosaGlycoproteinsBuddingNucleusNucleusAerosol

References
  1. Mettenleiter; et al. (2008). "Molecular Biology of Animal Herpesviruses". Animal Viruses: Molecular Biology. Caister Academic Press. ISBN 978-1-904455-22-6.
  2. Sandri-Goldin RM (editor). (2006). Alpha Herpesviruses: Molecular and Cellular Biology. Caister Academic Press. ISBN 978-1-904455-09-7.
  3. "Viral Zone". ExPASy. Retrieved 12 June 2015.
  4. ICTV. "Virus Taxonomy: 2014 Release". Retrieved 12 June 2015.

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