**5. Virus infection of spermatozoa**

Virus capsids morphologically identical to capsids of *Herpesviridae* family were detected in the nucleus and cytoplasmic droplet of infected spermatozoa by TEM (**Figure 8a**, **b**) (for the review see [99]). The structures shown in **Figure 8** (**8a**, **b**) are capsids of herpes simplex virus

**Figure 8.** (a) Longitudinal section of normal sperm; (b) section through the middle piece of the tail of sperm. VC, HSV capsids; M, mitochondria; A, acrosome; CH, chromatin; and C, centriole. The hexagonal structure of some capsids is visible. Phase-contrast microscopy (c) and IF (d) of infected sperm. HSV antigen (arrows) and DAPI stain for DNA (blue); (e) FISH with probes to DNA of HSV. Localization of HSV DNA in sperm heads (arrows).

(HSV), we proved this by immunofluorescence (IF) using the monoclonal antibodies to HSV1 and HSV2 (**Figure 8c**, **d**) and *in situ* hybridization (ISH) with biotinylated probes for HSV (**Figure 8e**). Infection was observed in both the total sperm fraction and the isolated fraction of motile spermatozoa. The persistence of the HSV genome in motile, morphologically normal sperms indicates that the virus may be transmitted vertically to the offspring via natural fertilization or various ARTs, including IVF or ICSI.

Herpetic infection of spermatozoa was significantly more common in infertile men and men whose spouses had a history of spontaneous miscarriage or ART failure as compared with fertile men. Specific antiherpetic treatment of men diagnosed with HSV infection of spermatozoa results in a substantial, almost fivefold increase in the rates of blastocyst formation after ICSI and clinical pregnancy after ART [100].
