|Group:||Group I (dsDNA)|
Betaherpesvirinae is a subfamily of viruses in the order Herpesvirales, in the family Herpesviridae. Mammals serve as natural hosts. There are currently 18 species in this subfamily, divided among 4 genera. Diseases associated with this subfamily include: HHV-5: congenital CMV infection. HHV-6: 'sixth disease' (roseola infantum, exanthem subitum). HHV-7: symptoms analog to the 'sixth disease'.
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,
- 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." Human herpesvirus 6A (HHV-6A) has been described as more neurovirulent, and as such is more frequently found in patients with neuroinflammatory diseases such as multiple sclerosis. 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.
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.
|Genus||Structure||Symmetry||Capsid||Genomic Arrangement||Genomic Segmentation|
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.
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. 
|Genus||Host Details||Tissue Tropism||Entry Details||Release Details||Replication Site||Assembly Site||Transmission|
|Roseolovirus||Humans||T-cells; B-cells; NK-cell; monocytes; macrophages; epithelial||Glycoprotiens||Budding||Nucleus||Nucleus||Respiratory contact|
|Cytomegalovirus||Humans; monkeys||Epithelial mucosa||Glycoprotiens||Budding||Nucleus||Nucleus||Urine; saliva|
- Betaherpesvirinae at the US National Library of Medicine Medical Subject Headings (MeSH)
- Viralzone: Betaherpesvirinae
- "Viral Zone". ExPASy. Retrieved 12 June 2015.
- ICTV. "Virus Taxonomy: 2014 Release". Retrieved 12 June 2015.
- 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.
- 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 . PMID 19624841.
- 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.
- 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.