ASPO Abstracts
Serological evidence of infections is associated with extent and intensity of intra-prostatic inflammation in men without prostate cancer or indication for biopsy in the placebo arm of the Prostate Cancer Prevention Trial
Category: Molecular Epidemiology & Environment
Conference Year: 2020
Abstract Body:
Purpose: Emerging evidence suggests that inflammation may contribute to prostate cancer risk and mortality.
However, the source of inflammation is unclear. Therefore, we examined cross-sectional associations between
selected infections [Human papillomavirus (HPV) 16, 18, and 31; Human herpes virus (HHV) 8, Cytomegalovirus
(CMV), and Trichomonas vaginalis] and histological inflammation in prostate tissue within the placebo arm of the
Prostate Cancer Prevention Trial (PCPT).
Methods: We measured infection history using serum IgG antibodies and visually assessed histological
inflammation from biopsied prostate samples of 247 men (92.7% non-clinically indicated) without evidence of
prostate cancer. Associations between infection serostatus and the prevalence, extent, and intensity of
inflammation were assessed, using linear and logistic regression and adjusting for age and race.
Results: Overall, 80% of men had at least one biopsy core (~3.3 evaluated per man) with histological
inflammation. Seroprevalences of HPV 16, 18, 31, CMV, HHV-8, were 19%, 4%, 17%, 64%, 10%, respectively,
while seroprevalence of T. vaginalis was 15% for high seropositivity and 41% for low seropositivity. 116 men (47%)
were seropositive for multiple infections and 46 (19%) were seronegative for all selected infections. Seronegative
men had the lowest prevalence of inflammation (67%) with 5% mean percentage of tissue area inflamed.
Comparing men seropositive for one infection to men seronegative for all infections, each seropositive group
(CMV, HPV, and T. vaginalis) was possibly positively associated with intraprostatic inflammation. However, after
adjustment for age and race only CMV and HPV seropositivity were significantly associated with inflammation as
evidenced by an increased mean percentage of tissue area inflamed (CMV=+8.3%, 95% CI: 2.3-14.4;
HPV=+10.6%, 95% CI: 1.9-19.2) compared to men seronegative for all infections. Similar findings were seen for
men seropositive for multiple infections or any infection compared with men overall seronegative for all infections.
Conclusions: These findings suggest that either a correlated, unmeasured infection or the cumulative burden of
infections influences intraprostatic inflammation, which may have implications for prostate cancer risk.
Keywords: inflammation, infection, prostate cancer,