Commentary
Immunosenescence and Cytomegalovirus: where do we stand after a decade?
1 Department of Internal Medicine II, University of Tübingen, Tübingen, Germany
2 Division of Infection and Immunity, Department of Immunology, University College, London, UK
3 Nuffield Dept. Medicine, University of Oxford, Oxford, UK
4 Department of Pathobiology and Medical and Forensic Biotechnologies, University of Palermo, Palermo, Italy
5 Research Center on Aging, Immunology Program, Geriatric Division, Faculty of Medicine, University of Sherbrooke, Sherbrooke, Canada
6 Centre for Virology, Department of Infection, University College, London, UK
7 Institute for Biomedical Aging Research, Austrian Academy of Sciences, Innsbruck, Austria
8 Department of Virology, University of Tübingen, Tübingen, Germany
9 Division of Medicine, Brighton and Sussex Medical School, Brighton, UK
10 Department of Experimental Immunology, Academic Medical Center, Amsterdam, The Netherlands
11 Department of Gerontology and Geriatrics, Leiden University Medical Center, Leiden, The Netherlands
12 Centre for Infection, St George's, University of London, UK
13 School of Cancer Sciences, University of Birmingham, Birmingham, UK
14 Sanofi Pasteur MSD, Lyon, France
15 Department of Natural Science and Biomedicine, Jönköping University, Jönköping, Sweden
16 Sanofi-Pasteur, Lyon, France
17 Department of Medicine, School of Clinical Medicine, University of Cambridge, Cambridge, UK
Immunity & Ageing 2010, 7:13 doi:10.1186/1742-4933-7-13
Published: 7 September 2010First paragraph (this article has no abstract)
Since Looney at al. published their seminal paper a decade ago [1] it has become clear that many of the differences in T cell immunological parameters observed between young and old people are related to the age-associated increasing prevalence of infection with the persistent β-herpesvirus HHV-5 (Cytomegalovirus). Ten years later, studies suggest that hallmark age-associated changes in peripheral blood T cell subset distribution may not occur at all in people who are not infected with this virus [[2]; Derhovanessian et al., in press]. Whether the observed changes are actually caused by CMV is an open question, but very similar, rapid changes observed in uninfected patients receiving CMV-infected kidney grafts are consistent with a causative role [3]. This meeting intensively discussed these and other questions related to the impact of CMV on human immune status and its relevance for immune function in later life.
