Introduction
Human cytomegalovirus (CMV) is a ubiquitous β-herpesvirus typically causing an asymptomatic to mild infection in healthy children and adults. In the immunocompromised patient and the unprotected fetus CMV can present as a significant cause of morbidity and mortality. After primary contact, the virus persists within the host as a lifelong infection awakening at times from dormancy and leading to reactivation and virion shedding. Over millennia of evolutionary time, CMV had interlocked in a complex interplay with the immune system of its human host, with growing evidence pointing to T lymphocytes as being galvanized by CMV and directed against specific cancer cells. Recently, we drew attention to an inversely correlated incidence of human B lymphocyte malignancies and CMV seroprevalence in a single-center clinical setting and in humans across races/ethnicities the world over (Spearman’s coefficient ρ = −0.625, p < 0.001) [13]. This hinted at a possible oncopreventive faculty of the virus (Fig. 1 ). Similar findings were described in animal in vitro tissue models [6-8] covering several oncological diseases [9-11,12]. This indicates that CMV infection may bestow a capacity on its host to resist carcinogenesis somewhat more effectively than does a normal immunity in an uninfected subject. In effect, CMV and cancer may be profoundly connected. Virus/host interaction has not been investigated in a racial/ethnic background or across the globe. Inquiring into this association we used the wealth of data derived from authorized literature based on the U.S. registries and global publications (World Health Association [WHO]).
An intriguing disparity in overall health status between Whites, Blacks, and Hispanics and the CMV seroprevalence patterns by race and ethnicity in the U.S. evades a full explanation by factors of family size, household income level, education, marital status, census region, area of residence, country of birth or type of medical insurance. Differential exposure to CMV might partially explain these incongruities in health status, though [5,14,15].
The U.S. Hispano-Americans (Latinos) have significantly better health and mortality outcomes than the average population [16], contradicting their low socioeconomic status (SES). Medical experts have known for some time that Latinos living in the U.S. have on average a better life expectancy than non-Hispanic Whites. The so-called “Hispanic paradox” was recently supported by new data from the U.S. Centers for Disease Control and Prevention (CDC) [17-20]. Of note, the “paradox” seems not to hold true for follicular lymphoma (FL) and chronic lymphocytic leukemia (CLL) [21].
In this work we correlated age-adjusted incidence rates of all primary invasive cancers combined with the age-adjusted CMV seropositivity estimates among races and minorities in the U.S. The presentation of the reports used (Table 1 ) shows that, comparatively, CMV seropositivity is higher in the U.S. minorities than in non-Hispanic Whites. The significance of this observation is confirmed by statistical analysis. Moreover, we show that this effect is global, predominating across nations, societies, and histological types of malignant tumors (Figs. 1-4 and Table 3 ).