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Review
, 39 (1), 26-55

Nipah Virus: Epidemiology, Pathology, Immunobiology and Advances in Diagnosis, Vaccine Designing and Control Strategies - A Comprehensive Review

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Review

Nipah Virus: Epidemiology, Pathology, Immunobiology and Advances in Diagnosis, Vaccine Designing and Control Strategies - A Comprehensive Review

Raj Kumar Singh et al. Vet Q.

Abstract

Nipah (Nee-pa) viral disease is a zoonotic infection caused by Nipah virus (NiV), a paramyxovirus belonging to the genus Henipavirus of the family Paramyxoviridae. It is a biosafety level-4 pathogen, which is transmitted by specific types of fruit bats, mainly Pteropus spp. which are natural reservoir host. The disease was reported for the first time from the Kampung Sungai Nipah village of Malaysia in 1998. Human-to-human transmission also occurs. Outbreaks have been reported also from other countries in South and Southeast Asia. Phylogenetic analysis affirmed the circulation of two major clades of NiV as based on currently available complete N and G gene sequences. NiV isolates from Malaysia and Cambodia clustered together in NiV-MY clade, whereas isolates from Bangladesh and India clusterered within NiV-BD clade. NiV isolates from Thailand harboured mixed population of sequences. In humans, the virus is responsible for causing rapidly progressing severe illness which might be characterized by severe respiratory illness and/or deadly encephalitis. In pigs below six months of age, respiratory illness along with nervous symptoms may develop. Different types of enzyme-linked immunosorbent assays along with molecular methods based on polymerase chain reaction have been developed for diagnostic purposes. Due to the expensive nature of the antibody drugs, identification of broad-spectrum antivirals is essential along with focusing on small interfering RNAs (siRNAs). High pathogenicity of NiV in humans, and lack of vaccines or therapeutics to counter this disease have attracted attention of researchers worldwide for developing effective NiV vaccine and treatment regimens.

Keywords: Nipah virus (NiV); bats; control; diagnosis; encephalitis; epidemiology; pathology; prevention; therapeutics; vaccines; zoonosis.

Conflict of interest statement

All authors declare that there exist no commercial or financial relationships that could in any way lead to a potential conflict of interest.

Figures

Figure 1.
Figure 1.
Structure of Nipah virus.
Figure 2.
Figure 2.
Transmission of the Nipah virus. 1. Fruit bats acts as natural reservoir of Nipah viruses. Fruit bats with NiV feeds on date palm sap. Virus can survive in solutions that are rich in sugar, viz., fruit pulp. 2. Virus transmitted to human through the consumption of date palm sap. 3. Fruit bats of Pteropus spp. which are NiV reservoirs visited such fruit trees and got opportunity to naturally spill the drop containing virus in the farm to contaminate the farm soil and fruits. 4. Contaminated fruits are consumed by pigs and other animals. Pigs act as intermediate as well as amplifying host. Combination of close surroundings of fruiting trees, fruits-like date palm, fruit bats, pigs and human altogether form the basis of emergence and spread of new deadly zoonotic virus infection like Nipah. 5. Pork meat infected with NiV are exported to other parts. 6. Consumption of infected pork can act as a source of infection to human. 7. Close contact with NiV affected human can lead to spread of NiV to other persons.
Figure 3.
Figure 3.
Phylogenetic analyses of sequences of Nipah Virus (NiV) strains from different countries (Bangladesh, Cambodia, India, Malaysia, and Thailand). (A) Phyloanalysis based on complete G gene (1809 bp) and (B) Phyloanalysis based on complete N gene (1599 bp). Tree created with maximum likelihood method with 1,000 bootstrap replicates. Scale bars indicate number of sequence changes corresponding to illustrated branch length. Major two NiV clades are mentioned in the side bar as BD (Bangladesh) and MY (Malaysia).
Figure 4.
Figure 4.
Pathogenesis of NiV. 1. NiV can be seen in the epithelial cells of the bronchiole in the initial stage of infection. 2. NiV antigen can be detected in bronchi and alveoli. 3. Inflammatory mediators are activated as a result of infection to the airway epithelium. 4. Virus is disseminated to the endothelial cells of the lungs in the later stage of the disease. 5, 6. Virus enter the blood stream followed by dissemination, either freely or in host leukocyte bound form, reach brain, spleen and kidneys. 7. Two pathways are involved in the process of viral entry into the central nervous system (CNS), via hematogenous route and anterogradely via olfactory nerve nerves. 8. The blood brain barrier (BBB) is disrupted and IL-1β along with tumor necrosis factor (TNF)-α are expressed due to infection of the CNS by the virus which ultimately leads to development of neurological signs. Red font shows the symptoms in human.
Figure 5.
Figure 5.
Vaccine platforms for NiV. 1. Recombinant measles virus (rMV) vaccine that expresses envelope glycoprotein of NiV has been found to be effective vaccine candidate. 2. A recombinant vaccine based on vesicular stomatitis virus (replication-competent) has been developed in recent years encoding a glycoprotein of NiV. 3. Nipah virus-like particles (NiV-VLPs) composed of three NiV proteins G, F and M derived from mammalian cells have been produced and validated as vaccine in BALB/c mice. 4. Immunoinformatic advances have been utilized for developing peptide-based NiV vaccine by prediction and modeling of T-cell epitopes of NiV antigenic proteins.

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