Science and Clinical PracticeLatency and Reactivation of Human Cytomegalovirus
References (38)
- et al.
Reactivation of latent human cytomegalovirus by allogeneic stimulation of blood cells from healthy donors
Cell
(1997) Coronary heart disease, Helicobacter pylori, dental disease, Chlamydia pneumoniae, and cytomegalovirus: meta-analyses of prospective studies
Am Heart J
(1999)Exploitation of cellular signaling and regulatory pathways by human cytomegalovirus
Trends Microbiol
(2000)- et al.
Unlocking the mechanisms of transcription factor YY1: are chromatin modifying enzymes the key?
Gene
(1999) - et al.
Latency-associated sense transcripts are expressed during in vitro human cytomegalovirus productive infection
Virology
(2000) The immunogenicity of human and murine cytomegaloviruses
Curr Opin Immunol
(2000)Cytomegaloviruses use multiple mechanisms to elude the host immune response
Immunol Lett
(1997)- et al.
Latent and persistent infections of monocytes and macrophages
Intervirology
(1996) Detection of endogenous human cytomegalovirus in CD34+ bone marrow progenitors
J Gen Virol
(1996)Monocytes are a major site of persistence of human cytomegalovirus in peripheral blood mononuclear cells
J Gen Virol
(1991)
Cytomegalovirus remains latent in a common precursor of dendritic and myeloid cells
Proc Natl Acad Sci U.S.A.
Human cytomegalovirus latent infection of granulocyte-macrophage progenitors
Proc Natl Acad Sci U.S.A.
Induction of endogenous human cytomegalovirus gene expression after differentiation of monocytes from healthy carriers
J Virol
Reactivation of latent human cytomegalovirus in CD14(+) monocytes is differentiation dependent
J Virol
Human cytomegalovirus latency-associated protein pORF94 is dispensable for productive and latent infection
J Virol
Polymorphonuclear cells are not sites of persistence of human cytomegalovirus in healthy individuals
J Gen Virol
Tissue macrophages are infected by human cytomegalovirus
in vivo. J Infect Dis
Circulating cytomegalovirus (CMV)-infected endothelial cells in patients with an active CMV infection
J Infect Dis
Modification of human cytomegalovirus tropism through propagation in vitro is associated with changes in the viral genome
J Gen Virol
Cited by (88)
CRISPR based genome editing and removal of human viruses
2021, Progress in Molecular Biology and Translational ScienceCitation Excerpt :The virus is able to reactivate from dormancy to start lytic (active, acute, productive) infection to produce tremendous amount of virus progeny in hosts and thereby cause hosts' illness. Two types of viral latency are described as follows8–12: (1) Proviral latency: A provirus is a viral genome which integrates into the host genome, for example, Retrovirus family, such as human immunodeficiency virus (HIV). In this type, viral DNA replicates synchronously with the host genome instead of lysing the host cell and viruses reside in their hosts for long-term. (
Significant IFNγ responses of CD8+ T cells in CMV-seropositive individuals with autoimmune arthritis
2016, Journal of Clinical VirologyCitation Excerpt :Cytomegalovirus (CMV) is a human lymphotropic beta-herpes virus usually causing asymptomatic infection in immunocompetent hosts. Latent CMV infection carries the risk of reactivation in patients with insufficient T-cell immune responses due to immunodeficiency or pharmacological immunosuppression [1]. CMV is controlled by the generation of CMV-specific T-cells to the immunodominant proteins, immediate-early protein IE-1 and the phosphoprotein 65 (pp65) [2,3].
Structural basis for clonal diversity of the public T cell response to a dominant human cytomegalovirus epitope
2015, Journal of Biological ChemistryCitation Excerpt :root mean square difference. Although CMV infections are usually kept in check by the immune system of immunocompetent individuals, they can cause life-threatening diseases in immunocompromised patients and are a major health concern in patients undergoing bone marrow transplantation (1, 2). In addition, congenital CMV infection is the most common cause of infectious complications in newborns, resulting in deafness and other developmental abnormalities (3).
Maintenance and replication of the human cytomegalovirus genome during latency
2014, Cell Host and MicrobeCitation Excerpt :Human cytomegalovirus (HCMV) can cause significant disease and mortality in immune-compromised individuals. It is well established and accepted that HCMV latent infection occurs primarily in CD34 (+) hematopoietic progenitor cells (HPCs) or CD14 (+) monocytes (Goodrum et al., 2002; Maciejewski et al., 1992; Mendelson et al., 1996; Reeves et al., 2005; Sinclair and Sissons, 1996; Sissons et al., 2002; Söderberg-Nauclér et al., 1997; Taylor-Wiedeman et al., 1991; Zhuravskaya et al., 1997). Although latency has been studied in a variety of natural and experimental systems, the mechanisms involved in HCMV genome maintenance are poorly understood.
- f1
Please address all correspondence to: Professor J. G. P. Sissons, University of Cambridge School of Clinical Medicine, Department of Medicine, Level 5, Addenbrooke's Hospital, Hills Road, Cambridge CB2 2QQ, UK.