Roberts et al. Respond to "Human CMV, Inflammation, and Mortality"

Abstract

We thank Dr. Crumpacker (1) for his discussion of the mechanisms by which cytomegalovirus (CMV) infection and inflammation may impact cardiovascular disease and mortality as a context for supporting our population-based study findings (2). We fully agree with Dr. Crumpacker’s call for further research on CMV and cardiovascular disease. Chief among these research goals will be defining the cellular immune parameters of CMV infection. To this end, our research group is currently analyzing the relation between CMV immunoglobulin G antibody titers and measures of immune function in a multiethnic population-based cohort. Furthermore, characterizing the genes that control the specific functions of CMV will likely aid in the development of improved antiviral drugs and an effective vaccine, which would be extremely beneficial for immunosuppressed patients and neonates. From a population health perspective, we also advocate future research on life course and sociologic studies of CMV infection as a means of elucidating the pathways and mechanisms by which CMV may ultimately influence later-life health outcomes. It is known that CMV infection is patterned by race/ethnicity and socioeconomic status (3). It is also well established that exposure to stress reactivates latent herpesvirus infections including CMV (4), leading to an increase in antibody titers (5). Others have shown that high antibody titers are related to loss of immune control over the virus (6). Therefore, we propose that immune system alterations resulting from the interaction of CMV and exposure to stress over the life course may be an important mechanism explaining the patterning of chronic disease morbidity and mortality in the United States (7, 8). In addition to vaccine development, future research should therefore focus on ways to reduce exposure to CMV in the community setting; reduce immune susceptibility to CMV; and begin to address racial/ethnic, socioeconomic, and psychosocial disparities in primary CMV infection and life course reactivation of this persistent virus.