Cytomegalovirus and human immunosenescence
‘Immunosenescence’ is an imprecise term used to describe deleterious age‐associated changes to immune parameters observed in all mammals studied so far. Primarily anecdotal evidence implies that failing immunity is responsible for the increased incidence and severity of infectious disease in old peo...
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| Veröffentlicht in: | Reviews in medical virology Jg. 19; H. 1; S. 47 - 56 |
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| Hauptverfasser: | , , , , |
| Format: | Journal Article |
| Sprache: | Englisch |
| Veröffentlicht: |
Chichester, UK
John Wiley & Sons, Ltd
01.01.2009
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| ISSN: | 1052-9276, 1099-1654, 1099-1654 |
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| Abstract | ‘Immunosenescence’ is an imprecise term used to describe deleterious age‐associated changes to immune parameters observed in all mammals studied so far. Primarily anecdotal evidence implies that failing immunity is responsible for the increased incidence and severity of infectious disease in old people. However, there is a serious dearth of accurate hard data concerning the actual cause of death in the elderly and the contribution thereto of the multitude of age‐associated alterations measured in the immune system. Cross‐sectional studies comparing those currently young with those currently old reveal a large number of differences in the distribution of immune cell types in the blood, and to some extent the functional integrity of those cells. Many of these parameters differ markedly between individuals infected with CMV and uninfected people, regardless of infection with other persistent herpesviruses. The adaptive arm of immunity appears to be more seriously affected than the innate arm, particularly the T lymphocytes. However, cross‐sectional studies suffer the disadvantage that like is not being compared with like, because the conditions applied during the entire life course of the currently elderly were different from those applied now to the young. These differences in environment, nutrition, pathology and possibly genetics, rather than merely age, may be expected to influence the parameters studied. Moreover, pathogen exposure of the currently elderly was also different from contemporary exposure, probably including CMV. Some of the problems associated with cross‐sectional studies can be overcome by performing longitudinal studies, as pointed out in an earlier analysis of the Baltimore Longitudinal Ageing study looking at lymphocyte numbers. However, longitudinal studies are challenging in humans. Nonetheless, the pioneering Swedish OCTO/NONA studies of the very elderly which for the first time included a range of immune parameters, have identified a set of immune parameters predicting mortality at 2, 4 and 6 year follow‐up; CMV infection makes a material contribution to this so‐called ‘immune risk profile (IRP)’. Whether the IRP is informative in younger individuals and the mechanism of the CMV effect is discussed in this review. Copyright © 2008 John Wiley & Sons, Ltd. |
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| AbstractList | Immunosenescence is an imprecise term used to describe deleterious age-associated changes to immune parameters observed in all mammals studied so far. Primarily anecdotal evidence implies that failing immunity is responsible for the increased incidence and severity of infectious disease in old people. However, there is a serious dearth of accurate hard data concerning the actual cause of death in the elderly and the contribution thereto of the multitude of age-associated alterations measured in the immune system. Cross-sectional studies comparing those currently young with those currently old reveal a large number of differences in the distribution of immune cell types in the blood, and to some extent the functional integrity of those cells. Many of these parameters differ markedly between individuals infected with CMV and uninfected people, regardless of infection with other persistent herpesviruses. The adaptive arm of immunity appears to be more seriously affected than the innate arm, particularly the T lymphocytes. However, cross-sectional studies suffer the disadvantage that like is not being compared with like, because the conditions applied during the entire life course of the currently elderly were different from those applied now to the young. These differences in environment, nutrition, pathology and possibly genetics, rather than merely age, may be expected to influence the parameters studied. Moreover, pathogen exposure of the currently elderly was also different from contemporary exposure, probably including CMV. Some of the problems associated with cross-sectional studies can be overcome by performing longitudinal studies, as pointed out in an earlier analysis of the Baltimore Longitudinal Ageing study looking at lymphocyte numbers. However, longitudinal studies are challenging in humans. Nonetheless, the pioneering Swedish OCTO/NONA studies of the very elderly which for the first time included a range of immune parameters, have identified a set of immune parameters predicting mortality at 2, 4 and 6 year follow-up; CMV infection makes a material contribution to this so-called immune risk profile (IRP). Whether the IRP is informative in younger individuals and the mechanism of the CMV effect is discussed in this review. ‘Immunosenescence’ is an imprecise term used to describe deleterious age‐associated changes to immune parameters observed in all mammals studied so far. Primarily anecdotal evidence implies that failing immunity is responsible for the increased incidence and severity of infectious disease in old people. However, there is a serious dearth of accurate hard data concerning the actual cause of death in the elderly and the contribution thereto of the multitude of age‐associated alterations measured in the immune system. Cross‐sectional studies comparing those currently young with those currently old reveal a large number of differences in the distribution of immune cell types in the blood, and to some extent the functional integrity of those cells. Many of these parameters differ markedly between individuals infected with CMV and uninfected people, regardless of infection with other persistent herpesviruses. The adaptive arm of immunity appears to be more seriously affected than the innate arm, particularly the T lymphocytes. However, cross‐sectional studies suffer the disadvantage that like is not being compared with like, because the conditions applied during the entire life course of the currently elderly were different from those applied now to the young. These differences in environment, nutrition, pathology and possibly genetics, rather than merely age, may be expected to influence the parameters studied. Moreover, pathogen exposure of the currently elderly was also different from contemporary exposure, probably including CMV. Some of the problems associated with cross‐sectional studies can be overcome by performing longitudinal studies, as pointed out in an earlier analysis of the Baltimore Longitudinal Ageing study looking at lymphocyte numbers. However, longitudinal studies are challenging in humans. Nonetheless, the pioneering Swedish OCTO/NONA studies of the very elderly which for the first time included a range of immune parameters, have identified a set of immune parameters predicting mortality at 2, 4 and 6 year follow‐up; CMV infection makes a material contribution to this so‐called ‘immune risk profile (IRP)’. Whether the IRP is informative in younger individuals and the mechanism of the CMV effect is discussed in this review. Copyright © 2008 John Wiley & Sons, Ltd. 'Immunosenescence' is an imprecise term used to describe deleterious age-associated changes to immune parameters observed in all mammals studied so far. Primarily anecdotal evidence implies that failing immunity is responsible for the increased incidence and severity of infectious disease in old people. However, there is a serious dearth of accurate hard data concerning the actual cause of death in the elderly and the contribution thereto of the multitude of age-associated alterations measured in the immune system. Cross-sectional studies comparing those currently young with those currently old reveal a large number of differences in the distribution of immune cell types in the blood, and to some extent the functional integrity of those cells. Many of these parameters differ markedly between individuals infected with CMV and uninfected people, regardless of infection with other persistent herpesviruses. The adaptive arm of immunity appears to be more seriously affected than the innate arm, particularly the T lymphocytes. However, cross-sectional studies suffer the disadvantage that like is not being compared with like, because the conditions applied during the entire life course of the currently elderly were different from those applied now to the young. These differences in environment, nutrition, pathology and possibly genetics, rather than merely age, may be expected to influence the parameters studied. Moreover, pathogen exposure of the currently elderly was also different from contemporary exposure, probably including CMV. Some of the problems associated with cross-sectional studies can be overcome by performing longitudinal studies, as pointed out in an earlier analysis of the Baltimore Longitudinal Ageing study looking at lymphocyte numbers. However, longitudinal studies are challenging in humans. Nonetheless, the pioneering Swedish OCTO/NONA studies of the very elderly which for the first time included a range of immune parameters, have identified a set of immune parameters predicting mortality at 2, 4 and 6 year follow-up; CMV infection makes a material contribution to this so-called 'immune risk profile (IRP)'. Whether the IRP is informative in younger individuals and the mechanism of the CMV effect is discussed in this review.'Immunosenescence' is an imprecise term used to describe deleterious age-associated changes to immune parameters observed in all mammals studied so far. Primarily anecdotal evidence implies that failing immunity is responsible for the increased incidence and severity of infectious disease in old people. However, there is a serious dearth of accurate hard data concerning the actual cause of death in the elderly and the contribution thereto of the multitude of age-associated alterations measured in the immune system. Cross-sectional studies comparing those currently young with those currently old reveal a large number of differences in the distribution of immune cell types in the blood, and to some extent the functional integrity of those cells. Many of these parameters differ markedly between individuals infected with CMV and uninfected people, regardless of infection with other persistent herpesviruses. The adaptive arm of immunity appears to be more seriously affected than the innate arm, particularly the T lymphocytes. However, cross-sectional studies suffer the disadvantage that like is not being compared with like, because the conditions applied during the entire life course of the currently elderly were different from those applied now to the young. These differences in environment, nutrition, pathology and possibly genetics, rather than merely age, may be expected to influence the parameters studied. Moreover, pathogen exposure of the currently elderly was also different from contemporary exposure, probably including CMV. Some of the problems associated with cross-sectional studies can be overcome by performing longitudinal studies, as pointed out in an earlier analysis of the Baltimore Longitudinal Ageing study looking at lymphocyte numbers. However, longitudinal studies are challenging in humans. Nonetheless, the pioneering Swedish OCTO/NONA studies of the very elderly which for the first time included a range of immune parameters, have identified a set of immune parameters predicting mortality at 2, 4 and 6 year follow-up; CMV infection makes a material contribution to this so-called 'immune risk profile (IRP)'. Whether the IRP is informative in younger individuals and the mechanism of the CMV effect is discussed in this review. 'Immunosenescence' is an imprecise term used to describe deleterious age-associated changes to immune parameters observed in all mammals studied so far. Primarily anecdotal evidence implies that failing immunity is responsible for the increased incidence and severity of infectious disease in old people. However, there is a serious dearth of accurate hard data concerning the actual cause of death in the elderly and the contribution thereto of the multitude of age-associated alterations measured in the immune system. Cross-sectional studies comparing those currently young with those currently old reveal a large number of differences in the distribution of immune cell types in the blood, and to some extent the functional integrity of those cells. Many of these parameters differ markedly between individuals infected with CMV and uninfected people, regardless of infection with other persistent herpesviruses. The adaptive arm of immunity appears to be more seriously affected than the innate arm, particularly the T lymphocytes. However, cross-sectional studies suffer the disadvantage that like is not being compared with like, because the conditions applied during the entire life course of the currently elderly were different from those applied now to the young. These differences in environment, nutrition, pathology and possibly genetics, rather than merely age, may be expected to influence the parameters studied. Moreover, pathogen exposure of the currently elderly was also different from contemporary exposure, probably including CMV. Some of the problems associated with cross-sectional studies can be overcome by performing longitudinal studies, as pointed out in an earlier analysis of the Baltimore Longitudinal Ageing study looking at lymphocyte numbers. However, longitudinal studies are challenging in humans. Nonetheless, the pioneering Swedish OCTO/NONA studies of the very elderly which for the first time included a range of immune parameters, have identified a set of immune parameters predicting mortality at 2, 4 and 6 year follow-up; CMV infection makes a material contribution to this so-called 'immune risk profile (IRP)'. Whether the IRP is informative in younger individuals and the mechanism of the CMV effect is discussed in this review. 'Immunosenescence' is all imprecise term used to describe deleterious age-associated changes to immune parameters observed in all mammals studied so far. Primarily anecdotal evidence implies that failing immunity is responsible for the increased incidence and severity of infectious disease in old people. However, there is a serious dearth of accurate hard data concerning the actual cause of death in the elderly and the contribution thereto of the multitude of age-associated alterations measured in the immune system. Cross-sectional studies comparing those currently young With those currently old reveal a large number of differences in the distribution of immune cell types in the blood, and to some extent the functional integrity of those cells. Many of these parameters differ markedly between individuals infected with CMV and uninfected people, regardless of infection with other persistent herpesviruses. The adaptive arm of immunity appears to be more seriously affected than the innate arm, particularly the T lymphocytes. However, cross-sectional studies suffer the disadvantage that like is not being compared with like, because the conditions applied during the entire life course of the currently elderly were different from those applied now to the young. These differences in environment, nutrition, pathology and possibly genetics, rather than merely age, may be expected to influence the parameters studied. Moreover, pathogen exposure of the currently elderly was also different from contemporary exposure, probably including CMV. Some of the problems associated with cross-sectional studies can be overcome by performing longitudinal studies, as pointed out in an earlier analysis of the Baltimore Longitudinal Ageing study looking at lymphocyte numbers. However, longitudinal studies are challenging in humans. L Nonetheless, the pioneering Swedish OCTO/NONA studies of the very elderly which for the first time included a range of immune parameters, have identified a set of immune parameters predicting mortality at 2, 4 and 6 year follow-up; CMV infection makes a material contribution to this so-called immune risk profile (IRP)'. Whether the IRP is informative in younger individuals and the mechanism of the CMV effect is discussed in this review. |
| Author | Wikby, Anders Strindhall, Jan Pawelec, Graham Larbi, Anis Derhovanessian, Evelyna |
| Author_xml | – sequence: 1 givenname: Graham surname: Pawelec fullname: Pawelec, Graham email: graham.pawelec@uni-tuebingen.de organization: Center for Medical Research, University of Tübingen Medical School, Tübingen, Germany – sequence: 2 givenname: Evelyna surname: Derhovanessian fullname: Derhovanessian, Evelyna organization: Center for Medical Research, University of Tübingen Medical School, Tübingen, Germany – sequence: 3 givenname: Anis surname: Larbi fullname: Larbi, Anis organization: Center for Medical Research, University of Tübingen Medical School, Tübingen, Germany – sequence: 4 givenname: Jan surname: Strindhall fullname: Strindhall, Jan organization: Department of Natural Science and Biomedicine, School of Health Sciences, Jönköping University, Jönköping, Sweden – sequence: 5 givenname: Anders surname: Wikby fullname: Wikby, Anders organization: Department of Natural Science and Biomedicine, School of Health Sciences, Jönköping University, Jönköping, Sweden |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/19035529$$D View this record in MEDLINE/PubMed https://urn.kb.se/resolve?urn=urn:nbn:se:hj:diva-9294$$DView record from Swedish Publication Index (Högskolan i Jönköping) |
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I 2004; 200 1994; 179 2002; 59 2005; 174 2008; 9 2000; 95 2006; 176 2008; 8 2008; 5 1994; 29 2008; 3 2008; 300 2004; 1 2005; 22 2005; 23 1996; 31 1998; 16 2007; 178 2007; 179 2006; 24 2004; 39 2004; 173 2007; 9 1997; 18 1994; 77 2003; 4 2007; 7 2000; 121 1988; 41 2008; 63 2006; 127 2003; 124 1999; 90 2005; 79 1993; 133 2001; 122 2001; 124 2004; 86 2001; 72 2006; 439 2007; 128 2007; 447 2006; 12 2005; 114 2006; 16 2008 2003; 37 2003; 38 2006; 1067 2006; 3 2005; 83 2007; 52 2007; 56 2003; 31 2008; 180 1997; 160 2006; 43 2002; 23 2002; 24 2002; 169 2005; 205 1999; 34 2005; 53 2007; 81 2007; 41 2005; 50 2007; 42 2005; 17 2003; 21 2008; 172 2003; 23 1998; 8 Ataman S (e_1_2_1_21_2) 2007; 41 e_1_2_1_41_2 e_1_2_1_64_2 e_1_2_1_66_2 e_1_2_1_22_2 e_1_2_1_45_2 e_1_2_1_60_2 e_1_2_1_20_2 e_1_2_1_43_2 e_1_2_1_62_2 e_1_2_1_49_2 e_1_2_1_24_2 e_1_2_1_47_2 e_1_2_1_68_2 e_1_2_1_28_2 Carter D (e_1_2_1_30_2) 2006; 12 e_1_2_1_6_2 e_1_2_1_54_2 e_1_2_1_75_2 e_1_2_1_4_2 e_1_2_1_56_2 e_1_2_1_2_2 e_1_2_1_12_2 e_1_2_1_33_2 e_1_2_1_50_2 e_1_2_1_71_2 e_1_2_1_10_2 e_1_2_1_31_2 e_1_2_1_52_2 e_1_2_1_73_2 e_1_2_1_16_2 e_1_2_1_37_2 Qin W (e_1_2_1_77_2) 2004; 1 e_1_2_1_14_2 Stowe RP (e_1_2_1_34_2) 2001; 72 e_1_2_1_35_2 e_1_2_1_58_2 e_1_2_1_79_2 e_1_2_1_8_2 e_1_2_1_18_2 e_1_2_1_39_2 Just‐Nubling G (e_1_2_1_26_2) 2003; 31 e_1_2_1_80_2 e_1_2_1_40_2 e_1_2_1_65_2 e_1_2_1_67_2 e_1_2_1_23_2 e_1_2_1_44_2 e_1_2_1_61_2 e_1_2_1_42_2 e_1_2_1_63_2 e_1_2_1_27_2 e_1_2_1_48_2 e_1_2_1_25_2 e_1_2_1_46_2 e_1_2_1_69_2 e_1_2_1_29_2 e_1_2_1_70_2 Trzonkowski P (e_1_2_1_76_2) 2008 e_1_2_1_53_2 e_1_2_1_7_2 e_1_2_1_55_2 e_1_2_1_78_2 e_1_2_1_5_2 e_1_2_1_11_2 e_1_2_1_72_2 e_1_2_1_3_2 e_1_2_1_32_2 e_1_2_1_51_2 e_1_2_1_74_2 e_1_2_1_15_2 e_1_2_1_38_2 e_1_2_1_13_2 e_1_2_1_36_2 e_1_2_1_19_2 e_1_2_1_57_2 e_1_2_1_17_2 e_1_2_1_59_2 e_1_2_1_9_2 |
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| Snippet | ‘Immunosenescence’ is an imprecise term used to describe deleterious age‐associated changes to immune parameters observed in all mammals studied so far.... 'Immunosenescence' is an imprecise term used to describe deleterious age-associated changes to immune parameters observed in all mammals studied so far.... Immunosenescence is an imprecise term used to describe deleterious age-associated changes to immune parameters observed in all mammals studied so far.... 'Immunosenescence' is all imprecise term used to describe deleterious age-associated changes to immune parameters observed in all mammals studied so far.... |
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| SubjectTerms | Aged Aged, 80 and over Aging - immunology Animals Cross-Sectional Studies Cytomegalovirus Cytomegalovirus - immunology Cytomegalovirus Infections - immunology Human cytomegalovirus Humans Immunity - physiology Longitudinal Studies |
| Title | Cytomegalovirus and human immunosenescence |
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