The herpes simplex virus (HSV)-infected mouse model was used to correlate histopathological lesions in adrenal glands and ovaries with the localisation of viral nucleic acids and viral antigens, employing in situ hybridization and immunohistochemistry. In the adrenals, the lesions were mainly restricted to the zona fasciculata and the zona reticularis, sometimes extending to the medulla. In the ovaries, lesions were detected in follicles and in the stroma. During the course of infection, HSV nucleic acids could be detected earlier than HSV proteins. Next to the center of necrotic foci mainly HSV proteins were detected, whereas peripheral cells were found to contain viral nucleic acids. In situ hybridization revealed no proof of HSV latency in either organ. Among HSV-1 and HSV-2 strains of different neurovirulence, only HSV-2 variant ER− failed to replicate in adrenal glands and ovaries, whereas the neuroinvasive variant ER+ showed the same patterns as the HSV-1 strains used.

The herpes simplex virus (HSV)-infected mouse model was used to correlate histopathological lesions in adrenal glands and ovaries with the localisation of viral nucleic acids and viral antigens, employing in situ hybridization and immunohistochemistry. In the adrenals, the lesions were mainly restricted to the zona fasciculata and the zona reticularis, sometimes extending to the medulla. In the ovaries, lesions were detected in follicles and in the stroma. During the course of infection, HSV nucleic acids could be detected earlier than HSV proteins. Next to the center of necrotic foci mainly HSV proteins were detected, whereas peripheral cells were found to contain viral nucleic acids. In situ hybridization revealed no proof of HSV latency in either organ. Among HSV-1 and HSV-2 strains of different neurovirulence, only HSV-2 variant ER- failed to replicate in adrenal glands and ovaries, whereas the neuroinvasive variant ER+ showed the same patterns as the HSV-1 strains used.