Cytomegalovirus infection: a driving force in human T cell immunosenescence
- PMID: 17986574
- DOI: 10.1196/annals.1396.043
Cytomegalovirus infection: a driving force in human T cell immunosenescence
Abstract
The human immune system evolved to defend the organism against pathogens, but is clearly less well able to do so in the elderly, resulting in greater morbidity and mortality due to infectious disease in old people, and higher healthcare costs. Many age-associated immune alterations have been reported over the years, of which probably the changes in T cell immunity, often manifested dramatically as large clonal expansions of cells of limited antigen specificity together with a marked shrinkage of the T cell antigen receptor repertoire, are the most notable. It has recently emerged that the common herpesvirus, cytomegalovirus (CMV), which establishes persistent, life-long infection, usually asymptomatically, may well be the driving force behind clonal expansions and altered phenotypes and functions of CD8 cells seen in most old people. In those few who are not CMV-infected, another even more common herpesvirus, the Epstein-Barr virus, appears to have the same effect. These virus-driven changes are less marked in "successfully aged" centenarians, but most marked in people whom longitudinal studies have shown to be at higher risk of death, that is, those possessing an "immune risk profile" (IRP) characterized by an inverted CD4:8 ratio (caused by the accumulation primarily of CD8(+) CD28(-) cells). These findings support the hypothesis that persistent herpesviruses, especially CMV, act as chronic antigenic stressors and play a major causative role in immunosenescence and associated mortality.
Similar articles
-
The immune system in extreme longevity.Exp Gerontol. 2008 Feb;43(2):61-5. doi: 10.1016/j.exger.2007.06.008. Epub 2007 Jul 4. Exp Gerontol. 2008. PMID: 17870272 Review.
-
Impact of CMV and EBV seropositivity on CD8 T lymphocytes in an old population from West-Sicily.Exp Gerontol. 2007 Oct;42(10):995-1002. doi: 10.1016/j.exger.2007.05.006. Epub 2007 May 23. Exp Gerontol. 2007. PMID: 17611062
-
Human immunosenescence: does it have an infectious component?Ann N Y Acad Sci. 2006 May;1067:56-65. doi: 10.1196/annals.1354.009. Ann N Y Acad Sci. 2006. PMID: 16803971 Review.
-
Human cytomegalovirus infection and T cell immunosenescence: a mini review.Mech Ageing Dev. 2006 Jun;127(6):538-43. doi: 10.1016/j.mad.2006.01.011. Epub 2006 Mar 2. Mech Ageing Dev. 2006. PMID: 16513159 Review.
-
Human immunosenescence: is it infectious?Immunol Rev. 2005 Jun;205:257-68. doi: 10.1111/j.0105-2896.2005.00271.x. Immunol Rev. 2005. PMID: 15882359 Review.
Cited by
-
Characterization of the genetic determinants of context-specific DNA methylation in primary monocytes.Cell Genom. 2024 May 8;4(5):100541. doi: 10.1016/j.xgen.2024.100541. Epub 2024 Apr 24. Cell Genom. 2024. PMID: 38663408 Free PMC article.
-
Excess of body weight is associated with accelerated T-cell senescence in hospitalized COVID-19 patients.Immun Ageing. 2024 Mar 8;21(1):17. doi: 10.1186/s12979-024-00423-6. Immun Ageing. 2024. PMID: 38454515 Free PMC article.
-
How to manage drug-virus interplay underlying skin eruptions in children.World Allergy Organ J. 2024 Feb 8;17(3):100877. doi: 10.1016/j.waojou.2024.100877. eCollection 2024 Mar. World Allergy Organ J. 2024. PMID: 38361746 Free PMC article. Review.
-
Cytomegalovirus IgG is Associated With Physical Function But Not Muscle Density in People With HIV.J Acquir Immune Defic Syndr. 2024 Apr 15;95(5):470-478. doi: 10.1097/QAI.0000000000003377. J Acquir Immune Defic Syndr. 2024. PMID: 38180893 Clinical Trial.
-
Cytomegalovirus Infection Facilitates the Costimulation of CD57+CD28- CD8 T Cells in HIV Infection and Atherosclerosis via the CD2-LFA-3 Axis.J Immunol. 2024 Jan 15;212(2):245-257. doi: 10.4049/jimmunol.2300267. J Immunol. 2024. PMID: 38047900
Publication types
MeSH terms
LinkOut - more resources
Full Text Sources
Other Literature Sources
Medical
Research Materials