Enterovirus 71 pathogenicity in monkeys and cotton rats.

Enterovirus 71 (EV71) is a neurovirulent non-polio enterovirus that can cause severe central nervous system (CNS) infection in infants. Vervet monkeys infected intracerebrally or intramuscularly with EV71 isolates from the Bulgarian outbreak of 1975 developed clinical manifestations and pathological signs of encephalomyelitis and spinal poliomyelitis that were similar to EV71 neuroinfection in children. In addition, vervet monkeys with encephalomyelitis had severe alterations in the choroid plexus.

[Tick-borne encephalitis with fulminant course and lethal outcome in patients after plural vaccination].

In the Kurgan region, the Siberian subtype of the tick-borne encephalitis virus (TBEV) is dominant. The vaccines prepared from Far-Eastern TBEV subtype are used in this area. Among TBE patients in 2007-2011, 23.

[Morphological changes of brain choroid plexuses and ventricle induced by enterovirus infections in monkeys].

The morphological study of monkeys' brains, infected by the Bulgaria strain of enterovirus-71 (EV71), revealed specific for truncus cerebral encephalomyelitis, reactive and destructive changes in different areas of the brainstem and the spinal cord. For the first time viral cytopathology and destruction of choroid plexuses as an important secretory organ of the central nervous system, and ventricle of the brain infected by enterovirus have been studied. The specificity of this infection and the participation of neuroepithelium in reproduction of EV71 have been confirmed by identification of EV71 antigen in the choroid plexuses.

[Morphological changes and prion accumulation in the cerebellar cortex in Creutzfeldt-Jacob disease].

Histological sections of the cerebellar cortex taken from 5 patients with Creutzfeldt-Jacob disease (CJD), including 3 patients with sporadic form, were comparatively studied. The rate of pathological alterations as well as localization of prion protein (PrP) deposits greatly varied in these two groups of patients. The intensity of neural loss, damage of glial cells and accumulation of PrP increased in parallel to the duration of the disease.

[PRP(CJD) reproduction in the cerebral vascular plexus epitheliocytes in a new type of Creutzfeldt-Jakob disease].

The study of brain histological specimens from patients with Creutzfeldt-Jakob disease (CJD) revealed the active reproduction and accumulation of pathological prions in the epitheliocytes of cerebral vascular brain plexuses in a new variant of CJD. There was PrPCD accumulation on the cerebral ventricular ependymal cells and in the subpial superficial cortex parts of the cerebellum and brain to give rise to diffuse clusters, immature and kuru-plaques. Morphological changes in the blood-cerebrospinal fluid and cerebrospinal fluid-brain barriers are described and the possible pathways of intracerebral distribution of prions with cerebrospinal fluid considered.