Abstract
Background Positive serology for cytomegalovirus (CMV) has been associated with all-cause mortality risk but its role in COPD mortality is unknown. The objective of the present study was to assess the relationship between CMV serology and COPD mortality.
Methods We analysed data from 806 participants in the Tucson Epidemiological Study of Airway Obstructive Disease who, at enrolment, were aged 28–70 years and had completed lung function tests. We tested CMV serology in sera from enrolment and defined “high CMV serology” as being in the highest tertile. Vital status, date and cause of death were assessed through death certificates and/or linkage with the National Death Index up to January 2017. The association of CMV serology with all-cause and cause-specific mortality risk was tested in Cox models adjusted for age, sex, level of education, body mass index, smoking status and pack-years.
Results High CMV serology was marginally associated with all-cause mortality (p=0.071) but the effect was inversely dependent on age, with the association being much stronger among participants <55 years than among participants ≥55 years at enrolment (p-value for CMV-by-age interaction <0.001). Compared with low CMV serology, high CMV serology was associated with mortality from COPD among all subjects (adjusted hazard ratio (HR) 2.38, 95% CI 1.11–5.08; p=0.025) and particularly in subjects <55 years old at enrolment (HR 5.40, 95% CI 1.73–16.9; p=0.004). Consistent with these results, high CMV serology also predicted mortality risk among subjects who already had airflow limitation at enrolment (HR 2.10, 95% CI 1.20–3.68; p=0.009).
Conclusions We report a strong relationship between CMV serology and the risk of dying from COPD, and thus identify a novel risk factor for COPD mortality.
Abstract
Using a 45-year longitudinal population-based cohort, it was demonstrated for the first time that high CMV serology predicts COPD mortality risk, particularly in younger subjects, identifying a novel and early risk factor for COPD mortality http://bit.ly/32odP0Q
Footnotes
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Author contributions: R. Nenna, F.D. Martinez, M. Halonen and S. Guerra contributed to the study concept and design. S. Guerra, F.D. Martinez and M. Halonen obtained funding. A. Spangenberg and M. Halonen performed the assays. R. Nenna, J. Zhai, D.L. Sherrill and S. Guerra performed the statistical analysis. J. Zhai and S.E. Packard aided in collection of and provided access to data for analysis. R. Nenna and S. Guerra wrote the manuscript with input from all authors. R. Nenna, J. Zhai, S.E. Packard, A. Spangenberg, D.L. Sherrill, F.D. Martinez, M. Halonen and S. Guerra reviewed the manuscript.
Support statement: This work was supported by grant awards P50 HL107188 and R01 HL095021 from the National Heart, Lung, and Blood Institute. Funding information for this article has been deposited with the Crossref Funder Registry.
Conflict of interest: R. Nenna has nothing to disclose.
Conflict of interest: J. Zhai has nothing to disclose.
Conflict of interest: S.E. Packard reports grants from the NIH during the conduct of the study.
Conflict of interest: A. Spangenberg has nothing to disclose.
Conflict of interest: D.L. Sherrill has nothing to disclose.
Conflict of interest: F.D. Martinez reports grants HL139054, HL132523, HL091889, HL130045, HL098112 and HL056177 from NIH/NHLBI, grant ES006614 from NIH/NIEHS, grant AI126614 from NIH/NIAID, grant OD023282 from NIH/Office of Director, grant UA009253-0001 from Johnson & Johnson, and personal fees for consultancy from Copeval and Commense Inc., outside the submitted work.
Conflict of interest: M. Halonen reports grants from the NIH during the conduct of the study.
Conflict of interest: S. Guerra reports grants from the NIH during the conduct of the study.
- Received February 10, 2020.
- Accepted February 18, 2020.
- Copyright ©ERS 2020
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