Silent Threat of Nipah Virus (NIV) as a Re-Emerging zoonosis: Overview on Evolution and Impact, Pathogenesis, Transmission, and Molecular Mechanisms of NIV Entry and Replication

Abstract

Nipah virus (NiV) is one of the emerging and deadly zoonotic virus threats to animal health, livestock production and ecological stability because of its complicated modes of transmission and serious disease consequences. Studies on animals have determined Pteropus bats to be natural reservoirs in which the virus is held in an asymptomatic manner allowing the virus to persist and be shed into the environment, and pigs which are critical amplifying hosts allowing the virus to be easily spread in densely populated livestock systems. Hamsters and ferrets have been useful experimental animal models that show the relationship to disease progression, such as intense respiratory disease, neurological dysfunction, and extensive vascular destruction that is indicative of systemic infection. NiV uses cellular entry via special host receptors ephrin-B2 ephrin-B3, which is mediated by concerted activity of viral glycoproteins, after which efficient replication and cell-to-cell transmission causes widespread tissue damage. Moreover, the virus demonstrates high immune evasion mechanisms and disrupts host interferon activation, the adaptive immune system, and increases its virulence. Nevertheless, the presence of interspecies variation, insufficient knowledge of immune tolerance in reservoir hosts, as well as restrictions related to recreating natural ecological conditions are still the challenges of importance. This review summarizes animal experimental data on the evolution, spread, pathogenesis, and molecular pathogenesis of NiV, its effects on animal systems, and the necessity to have better surveillance, advanced biosecurity frameworks, and develop effective vaccinations and therapeutic interventions.