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The results of an analysis of international scientific literature on the epizootic situation of the emerging zoonotic disease Nipah virus disease are presented. The virological, serological, and molecular-genetic characteristics of Nipah virus (NiV), which belongs to the family Paramyxoviridae, subfamily Orthoparamyxovirinae, genus Henipavirus, are described. The structure of its genome is outlined; it consists of six genes (N, P, M, F, G, and L) encoding the nucleoprotein (NP), phosphoprotein (P), matrix protein (M), fusion protein (F), glycoprotein (G), and large RNA-dependent RNA polymerase (L), respectively. The pathogen is shown to replicate efficiently in various primary and continuous mammalian cell cultures. In Vero cell culture, a cytopathic effect (CPE) is observed on days 3–6 of the first passage; after prior viral adaptation, CPE appears within 24–48 hours. The main natural reservoir hosts of the virus are fruit bats of the genus Pteropus, including Pteropus vampyrus, Pteropus hypomelanus, Pteropus medius (formerly P. giganteus), and Pteropus lylei; Pteropus poliocephalus has been infected experimentally. The virus is capable of infecting pigs, humans, cattle, goats, cats, dogs, and horses. Under natural conditions, pigs are most commonly infected, and transmission to humans primarily occurs from infected pigs. Transmission from bats to other hosts occurs through viral shedding in saliva and urine; contamination of food and water sources creates conditions for infection of other animals and humans. Fewer than 10% of patients are capable of transmitting the virus to other individuals; most cases of person-to-person transmission occur in the later stages of the disease, particularly in patients with respiratory symptoms. The case fatality rate during major outbreaks has ranged from 38% to approximately 75%. The development of vasculitis indicates that endothelial cells of blood vessels are the primary target cells; the central nervous system, lungs, and kidneys are severely affected. Histopathological findings include hemorrhagic or necrotizing alveolitis, pulmonary edema, aspiration pneumonia, intra-alveolar inflammatory cells, and occasionally multinucleated giant cells. Diagnosis is based on epidemiological data, clinical signs, pathological findings, and laboratory methods (virological, serological, and molecular-genetic assays). Based on global experience, measures for control, prevention, and surveillance of this disease are substantiated.
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Korniienko et al. (2026) studied this question.
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