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 ).