Regulation of Cellular Genes by Cytomegalovirus

Abstract

Cytomegaloviruses (CMVs) are members of the betaherpesviruses with the prototype of this classification group being human CMV. Animal CMVs, such as simian, guinea pig, rat, and murine CMV, have also been used to study betaherpesvirus replication and pathogenesis. Human and animal CMVs have many genes in common. For example, murine CMV, the most widely used model for CMV pathogenesis, has 78 open reading frames (ORFs) in common with the greater than 200 ORFs of human CMV. Two human viruses that are also genetically related to human CMV are human herpesvirus-6 (HHV-6) and HHV-7 which are associated with a disseminated infection in children called roseola.Depending on location and economic status, between 40 and 90% of the population is infected with human CMV. The virus is the leading cause of congenital birth defects which include brain damage and sight and hearing defects. The virus also establishes disseminated infections in immunosuppressed individuals that can result in pneumonitis, retinitis, hepatitis, and gastroenteritis (Alford and Britt, 1990;Ho, 1991). The stromal and epithelial tissues are frequently damaged by CMV infection. In addition, both human and animal CMVs infect vascular endothelial and smooth muscle cells. CMV DNAs are detectable in lesions of the blood vessel (Melnick et al., 1994). A correlation between CMV infection of smooth muscle cells and migration of these cells has been shown, and it is

Manipulation of the cell cycle by human cytomegalovirus

“…As mentioned above, infection with HCMV leads to a cellular response similar to, yet distinct from mitogenic stimulation (reviewed in 11,50,51). HCMV infection induces the transcription of the oncogenes fos, jun and myc, but not others such as ras, myb or mos (52,53).…”

Effect of the human cytomegalovirus IE86 protein on expression of E2F-responsive genes: A DNA microarray analysis

“…HCMV infection induces the progression of quiescent cells toward the G 1 ͞S transition point (reviewed in ref. 1) and activates cellular genes required for DNA replication such as thymidine kinase (TK) (2), dihydrofolate reductase (DHFR) (3), cyclin E (4), and DNA polymerase ␣ (5). Mouse CMV induces the expression of ribonucleotide reductase (RR) (6) and thymidylate synthetase (TS) (7).…”