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). 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: 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. 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.

Introduction: The research of biological properties of enteroviruses associated with ischemic stroke (IS) allows us to identify their intratypic differences. The aim: to identify genetic markers of strains of enteroviruses associated with IS. Materials and methods: 11 strains of enteroviruses isolated from the serum of patients with IS were identified in the virus neutralization test. Genetic markers of isolated strains (Abent, marker S, marker rct40) were determined. Results: Eleven strains of enteroviruses were isolated from the serum of patients with IS. Eight viruses: Coxsackie B viruses (serotypes 2, 3, 4) and ECHO viruses (serotypes 6, 9, 27 (two strains), 29) were identified in these strains. Other three strains of enteroviruses were unidentified. Different combinations of genetic markers were found. Seven strains of enteroviruses (Coxsackie B2, B3, ECHO 6, ECHO 9, ECHO 27 (two strains) and one unidentified virus) had virulence markers: Abent–, rct40+ and S−. Three strains (Coxsackie B4, ECHO 29, one unidentified virus) had markers: Abent–, rct40+, S+. Another one unidentified virus had markers: Abent+, rct40+, S –. Conclusions: All 11 isolates of enteroviruses associated with IS had rct40+ marker, 10 of the 11 isolates had marker Abent– and 8 of 11 isolates had marker S–. The research of genetic markers allows to perform typic and intratypic differentiation of strains of enteroviruses associated with the IS.

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The aim: To study the role of enteroviruses (EV) in the development of ischemic stroke and its outcome. Materials and methods: The main group (MG) included 72 patients with acute cerebrovascular disorders were examined using the National Institutes of Health Stroke Scale and Barthel Index. The comparison group (CG) included 35 patients without cerebrovascular disease. Viruses were isolated from patients’ sera and identified in neutralization test. EV genomes were detected in polymerase chain reaction (PCR). Serological diagnosis was performed by enzyme-linked immunosorbent assay. Results: EV genomes were more frequently detected in the patients’ sera in MG than in CG (23.6 ± 5.9% and 2.9 ± 2.8%, p <0.05). The greater level of neurological deficits was in patients with positive PCR test results comparatively with patients with negative PCR test results (11.76 ± 0.31 and 10.97 ± 0, 27, p = 0.040). The regression of neurological deficit during the treatment was a worse in patients with positive PCR test results and presence of specific IgG compared with patients with positive PCR test results and absence of specific IgG (11.2 ± 2.6% and 19.6 ± 2.4%, p = 0.031). Conclusions: The trigger role of EV in the development of IS is established. PCR is recommended for diagnosis of EV in patients with IS.

coronavirus infection, the causative agent of which is SARS-CoV-2, can cause a wide range of clinical manifestations. This infection is especially dangerous for patients with a predisposition to cardiovascular diseases, such as hypertension. Changes in vascular tone under conditions of increased blood pressure, as well as dysfunction of vascular walls under the influence of a viral infection, lead to irritation of the suprasegmental part of the autonomic nervous system, namely the posterior part of the hypothalamus, which provokes the development of sympathoadrenal attacks with panic attacks. This study aimed to demonstrate that comorbid disease of the cardiovascular system occurred after coronavirus infection worsens the course of the initial manifestations of cerebrovascular insufficiency. Patient T., who suffered from COVID-19 in October 2020, was examined in the neurological department of the State Institution «Head medical center of the Ministry of Internal Affairs of Ukraine» in December-January 2020-2021. During the examination of the patient's neurological status, positive pathological reflexes were found: proboscis and Marinescu-Radovichi reflex, foot pathological Strumpell extensor reflex on both sides, and lability of the autonomic nervous system in the form of acrohyperthermia, tremors of the eyelids and fingers of outstretched hands, slight unsteadiness in the Romberg pose. The patient underwent a general blood count, biochemical blood test, Doppler ultrasound of the main arteries of the head, ultrasound of the heart, and electrocardiography (ECG). Special attention should be paid to the results of the Doppler ultrasound of the main arteries of the head: the intima-media complex thickness of the left common carotid artery in the middle third is up to 0.91 mm, in the bifurcation it has a local thickening up to 1.27 mm, the right common carotid artery in the middle third is up to 0.85 mm (normal up to 1.0 mm), in the bifurcation up to 1.04 mm (normal up to 1.1 mm), with partially lost differentiation into layers, echogenicity is not changed. In consequence of the patient's treatment with statin drugs, scavenger-receptors of monocytes are blocked, the number of which on the surface of cells is stimulated by viruses in the presence of infection, and right to them LDL are attached. Blocking of the capture of LDL by phagocytes limits the formation of foam cells, which are the basis of atherosclerotic plaques, and leads to a decrease in the intima-media complex thickness. According to the results of the ultrasound of the main arteries of the head, after six months of treatment, the thickness of the intima-media complex of the left common carotid artery decreased from 0.91 mm to 0.76 mm, the right one - from 0.85 to 0.65 mm. Conclusions. Comorbid diseases occurring under the influence of coronavirus infection, namely arterial hypertension, worsen the course of such slowly progressive disorders of cerebral blood circulation, as the initial manifestations of cerebral blood circulation insufficiency with the development of sympathoadrenal paroxysms with panic attacks. Treatment with statins, anticoagulants, antihypertensive, nootropic, and sedative drugs helps to stabilize arterial hypertension and reduce the number of sympathoadrenal attacks with panic attacks in patients.