Betaherpesvirinae

Betaherpesvirinae is a subfamily of viruses in the order Herpesvirales and in the family Herpesviridae. Mammals serve as natural hosts. There are currently 25 species in this subfamily, divided among 4 genera with two species unassigned to a genus. Diseases associated with this subfamily include: human cytomegalovirus (HHV-5): congenital CMV infection; HHV-6: 'sixth disease' (also known as roseola infantum or exanthem subitum); HHV-7: symptoms analogous to the 'sixth disease'.[1][2]

Betaherpesvirinae
Virus classification
(unranked): Virus
Realm: Duplodnaviria
Kingdom: Heunggongvirae
Phylum: Peploviricota
Class: Herviviricetes
Order: Herpesvirales
Family: Herpesviridae
Subfamily: Betaherpesvirinae
Genera

See text

Genera

Betaherpesvirinae consists of the following four genera:[2]

Additionally, the following two species are unassigned to a genus:[2]

Structure

Viruses in Betaherpesvirinae 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 140-240kb in length.[1]

GenusStructureSymmetryCapsidGenomic arrangementGenomic segmentation
RoseolovirusSpherical pleomorphicT=16EnvelopedLinearMonopartite
CytomegalovirusSpherical pleomorphicT=16EnvelopedLinearMonopartite
ProboscivirusSpherical pleomorphicT=16EnvelopedLinearMonopartite
MuromegalovirusSpherical pleomorphicT=16EnvelopedLinearMonopartite

Life cycle

Viral replication is nuclear, and is lysogenic. Entry into the host cell is achieved by attachment of the viral glycoproteins 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, and budding. Mammals serve as the natural host. Transmission routes are transplancental, transplantation, blood transfusion, body fluids, urine, and saliva.[1]

Betaherpesvirinae establish latency (site where virus lies dormant until reactivated) in leukocytes. This is different from Alphaherpesvirinae, which establish latency in neurons, and Gammaherpesvirinae, which establish latency in cells of the immune system, such as B-cells. [3]

GenusHost detailsTissue tropismEntry detailsRelease detailsReplication siteAssembly siteTransmission
RoseolovirusHumansT-cells; B-cells; NK-cell; monocytes; macrophages; epithelialGlycoprotiensBuddingNucleusNucleusRespiratory contact
CytomegalovirusHumans; monkeysEpithelial mucosaGlycoprotiensBuddingNucleusNucleusUrine; saliva
ProboscivirusElephantsNoneGlycoprotiensBuddingNucleusNucleusContact
MuromegalovirusRodentsSalivary glandsGlycoprotiensBuddingNucleusNucleusContact

Human health

There are four known member species of the Betaherpesvirinae subfamily that are infectious for humans:

  • Human cytomegalovirus (HCMV), also known as Human herpesvirus 5 (HHV-5),
  • Human herpesvirus 6A and 6B (HHV-6A and HHV-6B), which were classified as distinct species in 2012,[3]
  • Human herpesvirus 7 (HHV-7)

Human cytomegalovirus (HCMV, HHV-5) "seems to have a large impact on immune parameters in later life and may contribute to increased morbidity and eventual mortality."[4] Human herpesvirus 6A (HHV-6A) has been described as more neurovirulent,[5] and as such is more frequently found in patients with neuroinflammatory diseases such as multiple sclerosis.[6] Both human herpesvirus 6B (HHV-6B) and human herpesvirus 7 (HHV-7), as well as other viruses, can cause a skin condition in infants known as exanthema subitum, roseola infantum (rose rash of infants) or the sixth disease.

gollark: Well, things which can cooperate with other things in common situations attain more points.
gollark: Mostly.
gollark: It is, yes.
gollark: The iterated version has them do it repeatedly, with knowledge of each other's previous moves.
gollark: Essentially, each round, each player either cooperates or defects.If both cooperate, they attain 2 points. If one cooperates and the other defects, the defector attains 3 points and the cooperator attains 0 points. If both defect, they attain 1 point. Different versions use different actual numbers but the concept is the same if the relative orderings are preserved.

References
  1. "Viral Zone". ExPASy. Retrieved 12 June 2015.
  2. "Virus Taxonomy: 2019 Release". talk.ictvonline.org. International Committee on Taxonomy of Viruses. Retrieved 9 May 2020.
  3. Adams, M. J.; Carstens, E. B. (2012). "Ratification vote on taxonomic proposals to the International Committee on Taxonomy of Viruses (2012)". Archives of Virology. 157 (7): 1411–22. doi:10.1007/s00705-012-1299-6. PMID 22481600.
  4. Caruso, Calogero; Buffa, Silvio; Candore, Giuseppina; Colonna-Romano, Giuseppina; Dunn-Walters, Deborah; Kipling, David; Pawelec, Graham (2009). "Mechanisms of immunosenescence". Immunity & Ageing. 6: 10. doi:10.1186/1742-4933-6-10. PMC 2723084. PMID 19624841.
  5. De Bolle, L.; Van Loon, J.; De Clercq, E.; Naesens, Lieve (2005). "Quantitative analysis of human herpesvirus 6 cell tropism". Journal of Medical Virology. 75 (1): 76–85. doi:10.1002/jmv.20240. PMID 15543581.
  6. Álvarez-Lafuente, Roberto; García-Montojo, Marta; De Las Heras, Virginia; Bartolomé, Manuel; Arroyo, Rafael (2006). "Clinical parameters and HHV-6 active replication in relapsing—remitting multiple sclerosis patients". Journal of Clinical Virology. 37: S24–6. doi:10.1016/S1386-6532(06)70007-5. PMID 17276363.
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