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Details on Person Herpesviruses have a unique four-layered structure: a core c...
| Class:Id | Summation:9609654 |
|---|---|
| _displayName | Herpesviruses have a unique four-layered structure: a core c... |
| _timestamp | 2019-10-04 19:41:44 |
| created | [InstanceEdit:9609664] Gillespie, Marc E, 2018-05-29 |
| literatureReference | [LiteratureReference:9609651] Human cytomegalovirus: taking the strain [LiteratureReference:9609641] Human Cytomegalovirus (HCMV) - Revised |
| modified | [InstanceEdit:9663583] Gillespie, Marc E, 2019-10-04 |
| text | Herpesviruses have a unique four-layered structure: a core containing the large, double-stranded DNA genome is enclosed by an icosapentahedral capsid which is composed of capsomers. The capsid is surrounded by an amorphous protein coat called the tegument. It is encased in a glycoprotein-bearing lipid bilayer envelope. Herpesviruses are divided into three groups: alpha-herpesviruses, beta-herpesviruses, and gamma-herpesviruses. The beta herpesviruses have a restricted host range. Their reproductive life cycle is long (days), with infection progressing slowly in cell culture systems. These viruses cause their host cells to enlarge, as exemplified by a human cytomegalovirus (HCMV) infection. These viruses can establish latent infection in secretory glands, cells of the reticuloendothelial system, and the kidneys. Human Cytomegalovirus, or HCMV, is a common virus that infects people of all ages. In the United States, nearly one in three children are already infected with HCMV by age 5 years. Over half of adults by age 40 have been infected with HCMV. Once HCMV is in a person’s body, it stays there for life and can reactivate. Cytomegalovirus causes three clinical syndromes: (1) Congenital cytomegalovirus infection (when symptomatic) causes hepatosplenomegaly, retinitis, rash, and central nervous system involvement. (2) In about 10 per cent of older children and adults, primary cytomegalovirus infection causes a mononucleosis syndrome with fever, malaise, atypical lymphocytosis, and pharyngitis. (3) Immunocompromised hosts (transplant recipients and human immunodeficiency virus [HIV]-infected individuals) may develop life-threatening disseminated disease involving the lungs, gastrointestinal tract, liver, retina, and central nervous system. When propagated in human fibroblasts, HCMV clinical isolates acquire mutations in a manner that suggests a process of adaptation. Two strains of HCMV AD169 (grown from cultures of adenoid tissue taken from a 7-year-old girl) and Towne (developed as an attenuated vaccine by passaging 125 times in vitro) were initially used as the primary clinical strains. As only 26 % of HCMV canonical genes (45/171) are essential for viral replication in vitro it became important that a model strain be developed. The Merlin BAC was derived for this use. Produced using a bacterial artificial chromosome (BAC) cloning system (to avoid adaptation/degradation of the genome with each passage) the Merlin strain contains a complete HCMV genome that is thought to accurately to represent the original clinical agent from which it was derived. It is also a reproducible source of clonal virus (via transfection) and is capable of reconstituting phenotypically wild-type virus. The lifecycle represented here uses the Merlin strain where possible. |
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