Experimental study of the liver ultrastructure in the presence of infection with herpes simplex virus 1

Abstract

Introduction: Understanding of HSV-1liver infection pathogenesis is of great scientific, social and economic significance, since this is one of the main latent infections in population. However reactivation of this infection remains understudied. The aim: This experimental research aimed at studying the ultrastructure changes occurring in the liver in the presence of HSV-1infection. Materials and methods: Experiments were conducted on 12 BALB/c line mice weighing 18-20 g. They were divided into 2 groups: experimental, and control. Experimental animals were infected with the attenuated HSV-1. On day 40 the animals were withdrawn from the experiment by decapitation. Liver fragments were excised and studied ultramicroscopically. Results: Liver disorders were represented by the focal damage of hepatic lobuli cells. Ultrastructure changes were found both in the microvascular endothelium and hepatocytes. The vascular disorders included swelling of endotheliocytes, their demise and desquamation into the lumen, disruption of the basal lamina integrity and diapedesis of blood cells into the subendothelial space. Finding virions in the endotheliocytes allowed to explain the possible pathway of the infection into the interstitium and hepatocytes via systemic circulation from the primary source of infection. Electron microscopy has not revealed any virions in hepatocytes, with only the following changes: significant cytosole density of the osmiophylic granules, lisosomes and lamellar bodies found. These were considered to be the consequence of the infectious process. Findings of the experimental study enable understanding of the causal relationship between the acute infection and liver damage. Conclusions: Ultrastructure changes in the liver of mice infected with HSV-1 were focal, and more rarely diffuse in nature. Non-specific cytopathological changes (swelling of the cytoplasm and reduction of the endoplasmatic reticulum, and mitochondria) were found both in the endotheliocytes of the sinusoid capillaries and hepatocytes. Endotheliocytes of the sinusoid liver capillaries in mice infected with HSV-1 lose their barrier function, which leads to direct and indirect damage of hepatocytes and development of dystrophic changes in the liver.