Results
The prevalence of CMV seropositivity correlates inversely to cancer
incidence rates across a broad range of histology and worldwide
(Table 3; the top 3 malignancies with strongest correlations
are represented in Figs. 2-4 ). Correlations are obtained in
30/34 (88.2%) tumors and are highly significant over 25/34 (73.5%)
histology types. Also, an inverse association attains a significance if
annual incidence of new cancers of all histologic types was combined
(Spearman’s ρ = -0.732; p< 0.001, Fig.
1 ). These results favor a possible oncoprotection that CMV infection
provides to its host.
Conversely, CMV seroprevalence has a significant and co-incremental
relation with an incidence of malignancies of nasopharynx and the
gallbladder, suggesting a potential pro-oncogenic effect regarding these
malignancies.
Notably, country-specific prevalence of CMV did not correlate inversely
with an overall incidence of Kaposi’s sarcoma (Table 3 andFig. 5 , Spearman’s ρ = -0.007; p =0.953). This is
in line with a requirement of an operative T cell-mediated oncolytic
response as being critical for the expression a protective capacity of
CMV, supporting a hypothesis of specific T cell viral oncoprevention. We
propose that a severely disrupted T cell immunity in HIV/AIDS patients,
who comprise a vast majority of population with Kaposi’s sarcoma,
effectively precludes a CMV-associated anti-tumor response.
Table 1 exhibits comparative data on race/ethnic estimates of
the incidence of all cancers combined (both genders, all anatomical
sites, all ages) in the U.S, and the territorially matching prevalence
of CMV seropositivity. The estimate of cancer incidence for Mexico is
included as a contrasting population but was discarded from statistical
calculations. The aggregated results of studies mentioned therein
provide a clear representation of a higher CMV pervasiveness in the U.S.
minorities than in non-Hispanic Whites.
Table 2 represents a statistical analysis of the SEER data on
racial/ethnic rates of cancer (Henley et al. [44]) and the
corresponding prevalence of CMV. Also pointed in Table 2 is a
highly significant and inverse correlation (p <0.001;
mean: -0.674; SD=0.018; CI=-0.711) between the standardized cancer
incidence and the CMV seroprevalence in the U.S. An outlying group are
the Eskimos (AI/AN), perhaps because of an impaired T cell function
which distinguishes this ethnicity from the others [66,67].
Consequently, CMV-specific cytotoxic T cell oncolysis in Eskimos is not
an efficient suppressor of clonogenic processes (see Discussion ).
The results also support broad evidence (Figs. 1-4) suggesting a
tendency of CMV seropositivity to monotonically decrease as SES improves
across a range of developed and underdeveloped countries. This may
explain a higher incidence of malignancies in economically progressive
countries.