Ultrastructural features of herpesvirus-induced aortic intima damage in mice fed the high-fat diet.

OBJECTIVE: The aim: To study the effect of a high-fat diet (HFD) on the structural changes in the aortic intima in intact and HSV-1-infected mice using Scanning electron microscopy (SEM) and Transmission electron microscopy (TEM). PATIENTS AND METHODS: Materials and methods: In experiments Balb/c mice were infected with the HVS-1 and fed high-fat diet and 12 weeks later aortic ultrastructure was examined by SEM and TEM methods. The animals were subdivided into four experimental groups: 1st group - HSV-1-infected animals; 2nd - animals consuming high-fat diet (HFD); 3rd - infected animals that were subsequently consuming a high-fat diet (HSV / HFD); 4th - animals consuming a high-fat diet that were subsequently infected with HSV-1 (HFD / HSV) (n = 6); and control group - intact animals. RESULTS: Results: HVS-1 impaired ultrastructural changes in aorta greater than high-fat diet and HVS-1 alone (higher density of lipid inclusions in the subendothelial space, necrosis of endothelial cells), and infection of mice after high-fat diet ended 100% mortality. The formation of atheroma in the aortic wall during HFD was not detected, but the initiative manifestations of atherogenesis have been identified and restricted in the aortic intima. These structural changes included lipid inclusions in the subendothelial space, cell damage and destruction, which lead to an increase cellular detritus in the 3rd (HSV / HFD) group. CONCLUSION: Conclusions: HSV infection potentiates the accumulation of lipid inclusions in the aortic intima during a HFD, facilitates infection and contributes to the development of acute infection.

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

OBJECTIVE: 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. PATIENTS AND METHODS: 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: 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. CONCLUSION: 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.

The study of leukocyte phagocytic activity in the presence of herpetic infection and stroke.

OBJECTIVE: Inrtoduction: Post-stroke complications are one of the urgent and insufficiently resolved problems. According to different literature data 23% to 65% of patients suffer from the post-stroke development of an infectious process. Herpes simplex virus type 1 and 2 can also be etiological factors of stroke development, however their reactivation is seldom mentioned in clinical observations. The development of immune suppression is considered to be the cause of these complications. The aim: The current study aims at determining post-stroke changes in leukocyte component of the immunity and in the presence of concomitant herpetic infection as well as at finding changes in phagocytosis parameters during antiviral treatment. PATIENTS AND METHODS: Materials and methods: The experiments were carried out on mice of the Balb/с line. The animals were infected with the herpes simplex virus type I, and 30 days later hemorrhagic stroke was simulated by administering 0.1 ml of autoblood into the right hemisphere. Following the acute stroke some animals were given acyclovir, proteflazid or altabor. From the animals' blood leukocytes were obtained and phagocytic activity and production of reactive oxygen species of granulocytes and agranulocytes in relation to fluorescent E.coli bacteria were studied by flow cytometry. RESULTS: Results: The experiment revealed significant changes in the redistribution between two major types of leukocytes in mice with stroke (an increased number of agranulocytes by 19.9%) and decreased phagocytosis activity, in the animals infected with herpes simplex virus type І in particular. Ischemic brain damage had an immunosuppressive effect on blood leukocytes. For comparison a significant increase in phagocyte count in leukocytes was found in the case of viral infection. The use of drugs with antiviral effects did not affect the activity of granulocytes / agranulocytes. CONCLUSION: Conclusion: Stroke can be the cause of latent herpes virus infection reactivation and has essential negative effect on immune characteristics of leukocytes that remain unchanged with the use of antiviral agents.