Human endogenous retrovirus K10 (HERV-K10) env and gag expression has been detected in placenta, embryonic tissue, and cell lines. By transfection, these sequences have been expressed in insect cells and developed into serological assays, revealing HERV-K10
antibodies in patients with
testicular cancer. Patients with
AIDS are at an increased risk for
testicular cancer and frequently reactivate
latent infections. We postulated that HERV-K10 seroprevalence might be increased with
HIV infection or
AIDS. Stored, frozen serum samples from 52 patients with
testicular cancer (8 patients with HIV and 30 patients with samples near the time of diagnosis) and 84 controls (40 patients with HIV) were diluted 1:40 and tested by immunofluorescence against SF158 cells transfected with HERV-K10 env [ENV1.9(+)] or gag (pACGAG). Seroprevalence rates were compared cross-sectionally in cases and controls, excluding those with indeterminate results (3 of 30 cases and 7 of 84 controls), and also were examined longitudinally in the cases before or after diagnosis of
testicular cancer. Seroprevalence to HERV-K10 Env or Gag was 17 of 27
testicular cancer patients (63%) around the time of diagnosis, compared to 4 of 77 controls (5%; P < 0.0001). Seroprevalence was similar (50% to 60%) with
seminoma,
teratocarcinoma, or
embryonal carcinoma, and it was not increased with
HIV infection in either cases (33%) or controls (3%). HERV-K10
antibodies were detected in 12 of 19 cases (63%) more than 6 months before
seminoma diagnosis, as well as in four cases with residual or recurrent
malignancy more than 1 month after initial diagnosis. Thus, HERV-K10
antibodies are detected frequently with
testicular cancer and seem to resolve rapidly with effective
therapy of the
malignancy. Antibody reactivity also occurs in approximately 5% of controls, perhaps because of nonspecific or cross-reactive
epitopes. HIV and
AIDS were not associated with HERV-K10
antibodies, thus, leaving their higher risk of
testicular cancer unexplained.