ABSTRACT
To investigate the effect of Herpes Simplex virus (HSV) on spermatogenesis, HSV in ejaculate was detected by a rapid cultural method in 268 infertile males and 47 healthy ones. The number of mobile spermatozoa in HSV infected samples was less than in non-infected samples (21 mln/mlversus 40 mln/ml, p = 0.0001). The relative number of morphologically normal gametes was 13% versus 19% (p = 0.002), respectively. The quantitative karyological test discovered that males with HSV-infected ejaculate have more degenerating sex cells while in high virus contamination (more than 10 virus particles in 1 ml) the number of spermatides and spermatocytes of the 1 order at diploten stage is low. Organic testicular culture was used for more detailed study of pathogenetic mechanisms of HSV impact on spermatogenesis. Testicular explants infection was associated with reduction in the number of spermatogones, spermatocytes and spermatides on culturing week 2. The above findings reveal some pathogenetic mechanisms underling fertility disorders in males with HSV infection: a gametotoxic effect of the virus reducing populations of spermatogones, spermatocytes and spermatide; affected mobility and morphological characteristics of spermatozoa. Detection of the mechanisms of HSV action on spermatogenesis opens a perspective of antivirus drug administration in combined treatment of male infertility.
Subject(s)
Infertility, Male , Simplexvirus , Spermatids , Spermatocytes , Spermatogenesis , Aged , Cells, Cultured , Herpes Genitalis/metabolism , Herpes Genitalis/physiopathology , Humans , Infertility, Male/metabolism , Infertility, Male/physiopathology , Infertility, Male/virology , Male , Sperm Motility , Spermatids/metabolism , Spermatids/virology , Spermatocytes/metabolism , Spermatocytes/virologyABSTRACT
In an experiment using ten boars, the distribution of classical swine fever virus (CSFV) was determined in the male reproductive tract by in situ hybridization over a period of 120 days after intranasal inoculation. CSFV was detected in the testicular tissue of infected boars. Viral nucleic acid was localized to spermatogonia, spermatocytes and spermatids but was not detected in the epithelia of the prostate, epididymis or bulbourethral gland. Sections from control, CSFV-negative, pigs showed no hybridization signals for CSFV. The demonstration that CSFV infects the spermatogonia (and their progeny) suggests that this may serve as a primary reservoir for the venereal spread of CSFV.
