To define the development of herpes virus infection and morphological changes in the brain a upon a cerebrovascular accident. Methods. The experiments were performed on white mice weighing 18-20g. The animals were infected with type I HSV. Stroke was simulated after recovery and the rate of virus reactivation was determined. The rate of HSV production was evaluated by determination of viral antigens in Vero cell culture, PCR and dot-ELISA methods. The neurodegenerative process was confirmed by histological examination. Results. Reactivation of HSV-I was detected after the stroke. Histological study confirmed anincreased degree of neurodystrophic process around the hemorrhage, including hippocampus. A diagnostic value of the molecular methods has been proven in the detection of herpes infection in the biological samples (plasma, homogenates of animal organs). Conclusions. This study provided new data on the pathogenesis of herpes virus infection after acute stroke and its place in the development of complications. We have shown that the ischemic brain damage was a factor of type I HSV reactivation and it was characterized by a higher rate of neurodegenerative changes in hippocampus as compared to the isolated development of neuroinfection or impairment of cerebral circulation.

Background: Herpes simplex virus (HSV) is prevalent in today’s world population, and there is evidence of potential HSV reactivation in patients with immune deficiency induced by acute stroke. However, the data on the use of antivirals in the setting of stroke are scarce. The aim of this study was to evaluate the reactivation of HSV-1 in patients with stroke, using several methods, and to assess the efficacy of acyclovir in the treatment of experimental stroke. In the employed methodology, PCR and dot-ELISA were used to detect the occurrence of HSV-1 in patients with acute stroke. White mice were infected with HSV-1 and experimental stroke was simulated. The infected mice with stroke were subdivided into two groups: one of them received no treatment, while the other one was treated with acyclovir. The level of HSV-1 reactivation was determined by the methods used in human patients. The brain tissue of experimental animals was also subjected to morphological and morphometrical study. The results of such work reveal that, by the applied serological method, HSV-1 was found in all patients with stroke. Herein, the increased level of HSV-1 was seen in the brain tissue and blood in 100% of the experimental infected animals. However, the use of acyclovir suppressed reproduction of HSV-1. Hence, it can be concluded that clinical and laboratory studies have demonstrated the different sensitivity of Dot-Elisa and PCR, with the former being more sensitive. Moreover, the use of acyclovir in the experiment inhibited viral reproduction and further development of viral infection. Still, chemic lesions in the brain persisted.

Herpes simplex virus type I (HSV-I) is a latent neuroinfection which can cause focal brain lesion. The role of HSV-infection in nerve regeneration has not been studied so far. The aim of the work was to study sciatic nerve regeneration in the presence of HSV-infection and the influence of an antiviral drug. BALB/c line mice were divided into five groups. Group 1 animals were infected with HSV-I. After resolution of neuroinfection manifestations the sciatic nerve of these animals was crushed. Group 2 mice were administered acyclovir following the same procedures. Groups 3-5 mice served as controls. Thirty days after the operation distal nerve stumps and m.gastrocnemius were studied morphologically and biochemically. Ultrastructural organization of the sciatic nerve in control animals remained intact. Morphometric parameters of the nerves from the experimental groups have not reach control values. However, in the group 1 diameter of nerve fibers was significantly smaller than in the group 2. Both nerve regeneration and m.gastrocnemius reinnervation were confirmed. The muscle hypotrophy was found in groups 1, 2, and 3 (the muscle fibers diameter decreased). Metabolic changes in the muscles of the infected animals (groups 1 and 2) were more pronounced than in control groups 3 and 4. The levels of TBA-active products, conjugated dienes, carbonyl and SH-groups were reduced in m.gastrocnemius of the experimental groups, however no significant difference associated with acyclovir administration was found. HSV-infection is not limited to the local neurodegenerative changes in the CNS but affects regeneration of the injured sciatic nerve. Anat Rec, 301:1734-1744, 2018. © 2018 Wiley Periodicals, Inc.

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To investigate reactive changes of GFAP-positive astrocytes as a marker of brain response following hemorrhagic stroke and HSV-I. Methods. The experiments were performed on 110 Balb/c mice weighing 18-20 g. The animals were infected with HSV type I, on 30 day hemorrhagic stroke was simulated and changes in astrocytes were determined by immunohistochemistry. Gliosis was confirmed by changes in density and arborization of GFAP-positive astrocytes. Results. The results of immunohistochemical studies confirmed increased density of GFAP-positive astrocytes in the hippocampus of mice infected with HSV type I as well as the sharp increase in the density and hypertrophy of GFAP-positive astrocytes following stroke simulation in infected animals. Conclusions. The experiment has provided new evidence about the location and level of astrocytic gliosis following a stroke and herpes infection. GFAP can be studied as a marker of HSV type I reactivation against stroke.