Testicular atrophy is a common finding in autopsy series of patients infected with HIV (8-11). Histological examination of the testes reveals a spectrum of abnormalities, including hypospermatogenesis, spermatogenic arrest, and Sertoli cell-only pheno-types (11). In addition to the loss of germ cells and atrophy, the seminiferous tubules exhibit basement membrane thickening and peritubular fibrosis (8,9). Common abnormalities in semen include leukocytospermia, lower ejaculation volume and total sperm count, and lower percentage of rapidly progressive sperm in comparison to healthy controls (12,13); however, in the majority of HIV-infected patients, these values are within the normal adult male range.
The body mass index was the best predictor of testicular atrophy in a retrospective analysis (8); thus, underweight patients are at 3.5-fold higher risk for testicular atrophy than are normal weight patients. Surprisingly, in this small series, CD4+ T-lymphocyte count was not a significant predictor of testicular atrophy.
Opportunistic organisms may directly infect the testes in men with AIDS (10). The common pathogens involved in testicular infection include cytomegalovirus, Toxoplasma gondii, and Mycobacterium avium intracellular. In developing countries, infections of the reproductive tract by M. tuberculosis are relatively common. In addition, other sexually transmitted pathogens, such as trichomonas, chlamydia, gonococcus, and syphilis, often coexist in HIV-infected individuals because of common risk factors. The presence of Kaposi's sarcoma and some types of lymphoma in testis has also been reported.
The HIV virus is present in human semen (14), and sexual transmission is the major mode of HIV transmission; however, the exact source of HIV particles in the human semen is not known. The human testicular macrophages express cell surface markers CD45 and MAC387, and most also express CD4. These observations have led to the idea that macrophages in the testis may be infected by HIV and might be a site of early viral localization and a potential HIV reservoir (15). The presence of HIV-1 proviral DNA has been reported in the nuclei of germ cells at all stages of differentiation (16). In HIV-1-infected men who are receiving highly active antiretroviral therapy and who have undetectable viral RNA plasma levels, the virus may be still present in seminal cells and, therefore, may be transmitted by sexual contact.
HIV-related protein has been demonstrated in the prostate glands of infected individuals (17). Using in situ real-time polymerase chain reaction analysis of prostate and testis tissues, Paranjpe et al. (18) reported that T lymphocytes were the predominant cells infected with HIV-1 in both tissues. Because seminal plasma is derived mostly from the secretions of accessory sex organs, such as the prostate and seminal vesicles, and cells in the semen are derived mostly from the testis and the epididymis, the presence of HIV-1 in both the seminal plasma and cells in the semen led these investigators (18) to propose that the HIV in semen could originate from infection in either of these two compartments. Although this issue is controversial, there is no conclusive evidence to support HIV infection of spermatozoa.
Was this article helpful?