[Analysis of germ cell populations in ejaculate of men infected with herpes simplex virus].

Cytological and molecular genetics methods were used to study sperm from patients with sperm infected with herpes simplex virus (HSV) as indicated by virological and immunocytochemical tests. The following methods were used: (1) sperm analysis to evaluate the morphology and functional properties of sperm; (2) fluorescence in situ hybridization (FISH) with DNA probes specific for chromosomes 1, X, and Y to evaluate nondisjunction frequencies of these chromosomes in sperm; and (3) quantitative analysis of immature germ cells in the ejaculate to identify spermatogenic abnormalities. The total sperm count and the count of sperm with normal motility proved similar to the norm. FISH analysis demonstrated no difference in the nondisjunction frequency of chromosomes 1, X, and Y between infertile patients with HSV-infected sperm and fertile donors. Comparative quantitative analysis of immature germ cells from the ejaculate has demonstrated a significant and considerable (threefold) increase in the number of spermatocytes I at the prepachytene stages of prophase I (preleptotene, leptotene, and zygotene) in HSV patients compared to normal donors. At the same time, HSV patients demonstrated a significant decrease in the number of spermatocytes I, a decrease in the proportion of spermatocytes II and spermatids, and a twofold increase in the number of unidentifiable immature germ cells. The data obtained indicate a partial spermatogenic arrest at the early stages of meiotic prophase I in HSV patients, which prompts further research into the cellular mechanisms of abnormal spermatogenesis after viral infection in humans.

[Herpetic infection of spermatozoa in failure of reproductive technologies and spontaneous abortion].

Herpes simplex virus (HSV) was studied in ejaculate of 36 men whose wives had the history of spontaneous abortions, or failure of artificial insemination (AI), or extracorporeal fertilization (ECF). The control group consisted of 222 patients examined prophylactically after urogenital inflammation or for primary infertility. HSV was detected with immunofluorescence (IF) reaction with monoclonal antibodies to HSV antigens, rapid culture method (RCM) and transmission electronic microscopy. HSV antigens were detected in fraction of mobile spermatozoa in 13 (65%) of 20 samples from patients of the study group. HSV detectability in the study group was significantly higher than in the controls (p = 0.003). Intragametic capsides of HSV were detected at ultrastructural investigation in 13 of 19 (68%) ejaculate samples from patients of the study group in whom IF and/ or RCM results were positive. The study of 6 ejaculate samples of this group in which HSV was not detected by IF or RCM and 24 control samples HSV capsides were not detected. The following conclusions can be made: mobile spermatozoa of normal morphology can be infected with HSV; as shown morphologically, samples of ejaculate from men whose wives had spontaneous abortions contained intragametic HSV capsides; intragametic HSV infection of spermatozoa had a negative effect on the course of pregnancy and/or embryon vitality.

Detection of type 2 herpes simplex virus in cells of spermatogenic epithelium in infected testes of guinea pigs.

We developed a model of herpetic orchitis in guinea pigs. Intratesticular inoculation of type 2 herpes simplex virus suspension results in infection of the testicular spermatocytes and spermatides. The possibility of viral infection dissemination from infected into intact testis is proven.