Herpes simplex virus 1 infection induces morphological changes in brain and liver in BALB/c mice

Introduction: Herpes simplex virus type I (HSV-I) is quite prevalent in the general population. HSV-I exists in a latent form in the nervous system. The effects on other organs, particularly the liver, are not studied enough. The aim of the current work is to study morphological features of systemic or­gan injury caused by HSV-I.Materials and methods: Experiments were conducted on BALB/c line mice weighing 18-20g. The an­imals were infected with mouse-adapted HSV-I in the Institute of Epidemiology and Infectious Dis­eases (Kyiv, Ukraine). On day 30 histological studies of the brain and liver were conducted. The virus in blood serum, brain and liver was assessed by polymerase chain reaction (PCR) and dot enzyme-linked immunosorbent assay (dot-ELISA).Results: Using PCR, dot-ELISA and histological methods the presence of HSV-I and organ damage was confirmed in 100% of samples. Focal infiltration of lymphocytes and monocytes in mice brains was observed in the corpus callosum, brain cortex and hippocampus. The inflammation caused neu­rodegenerative changes leading to reduction of neurons in the studied areas. Herpes infection in liv­er was marked by hyperaemia of hemocapillaries and central veins and local hemorrhages. Some por­tal tracts demonstrated focal accumulation of neutrophils and monocytes. Cytopathological changes (cell dystrophy, hypertrophic nuclei) of hepatocytes were focal or diffuse. The patterns of herpetic liv­er infection are characterized by the absence of tissue basophil response and their absence in the stro­ma as well as by the delayed process of fibrosis.Conclusions: The experimental data showed that HSV-infection is not limited to the neurodegenera­tive changes in the nervous system and can cause systemic damage of organs. Our study demonstrat­ed features of systemic organ damage due to HSV-I viremia. This data also suggests a spread and pen­etration of the infection into the organs following viral damage of the blood vessel wall