Nipah virus (Henipavirus nipahense) is a bat-borne, zoonotic virus that causes Nipah virus infection in humans and other animals, a disease with a very high case fatality rate (40–75%). Numerous disease outbreaks caused by the Nipah virus have occurred in India, Malaysia, and Singapore. Nipah virus belongs to the genus Henipavirus along with the Hendra virus, which has also caused disease outbreaks.
Virology Like other henipaviruses, the Nipah virus genome is a single (non-segmented) negative-sense, single-stranded RNA of over 18 kb, which is substantially longer than that of other paramyxoviruses. The enveloped virus particles are variable in shape, and can be filamentous or spherical; they contain a helical nucleocapsid. Six structural proteins are generated: N (nucleocapsid), P (phosphoprotein), M (matrix), F (fusion), G (glycoprotein) and L (RNA polymerase). The P open reading frame also encodes three nonstructural proteins, C, V and W.
There are two envelope glycoproteins. The G glycoprotein ectodomain assembles as a homotetramer to form the viral anti-receptor or attachment protein, which binds to the receptor on the host cell. Each strand in the ectodomain consists of four distinct regions: at the N-terminal and connecting to the viral surface is the helical stalk, followed by the beta-sandwich neck domain, the linker region, and finally, at the C-terminal, four heads which contain host cell receptor binding domains. Each head consists of a beta-propeller structure with six blades. There are three unique folding patterns of the heads, resulting in a 2-up/2-down configuration where two heads are positioned distal to the virus, and two heads are proximal. Due to the folding patterns and subsequent arrangement of the heads, only one of the four heads is positioned with its binding site accessible to associate with the host B2/B3 receptor. The G protein head domain is also highly antigenic, inducing head-specific antibodies in primate models. As such, it is a prime target for vaccine development as well as antibody therapy. One head-specific antibody, m102.4, has been used in compassionate use cases and has completed Phase 1 clinical trials. The F glycoprotein forms a trimer, which mediates membrane fusion.
Tropism Ephrins B2 and B3 have been identified as the main receptors for Nipah virus. Ephrin sub-types have a complex distribution of expression throughout the body, where the B3 is noted to have particularly high expression in some forebrain sub-regions.
Geographic distribution
Nipah virus has been isolated from Lyle's flying fox (Pteropus lylei) in Cambodia and its RNA has been detected in urine and saliva from P. lylei and Horsfield's roundleaf bat (Hipposideros larvatus) in Thailand. The virus has also been isolated from environmental samples of bat urine and partially eaten fruit in Malaysia. Antibodies to henipaviruses have also been found in fruit bats in Madagascar (Pteropus rufus, Eidolon dupreanum) and Ghana (Eidolon helvum), indicating a wide geographic distribution of the viruses. No infection of humans or other species has been observed in Cambodia, Thailand, or Africa as of May 2018. In September 2023, India reported at least five infections and two deaths. In July 2024, a new infection occurred and a 14-year-old boy died as a result of it. In January 2026, two Nipah cases were confirmed in the state of West Bengal in India.
Signs and symptoms
History
Emergence The first cases of Nipah virus infection were identified in 1998, when an outbreak of neurological and respiratory disease on pig farms in peninsular Malaysia caused 265 human cases, with 108 deaths. The virus was isolated in the following year of 1999. This outbreak resulted in the culling of one million pigs. In Singapore, 11 cases, including one death, occurred in slaughterhouse workers exposed to pigs imported from the affected Malaysian farms. The name "Nipah" refers to the place, Sungai Nipah (literally 'nipah river') in Port Dickson, Negeri Sembilan, the source of the human case from which Nipah virus was first isolated. The outbreak was originally mistaken for Japanese encephalitis, but physicians in the area noted that people who had been vaccinated against Japanese encephalitis were not protected in the epidemic, and the number of cases among adults was unusual. Although these observations were recorded in the first month of the outbreak, the Ministry of Health failed to take them into account, and launched a nationwide campaign to educate people on the dangers of Japanese encephalitis and its vector, Culex mosquitoes. Symptoms of infection from the Malaysian outbreak were primarily encephalitic in humans and respiratory in pigs. Later outbreaks have caused respiratory illness in humans, increasing the likelihood of human-to-human transmission and indicating the existence of more dangerous strains of the virus. During the 1999 outbreak of Nipah virus, which occurred among pig farmers, the majority of human infections stemmed from direct contact with sick pigs and the unprotected handling of secretions from the pigs. Based on seroprevalence data and virus isolations, the primary reservoir for Nipah virus was identified as pteropid fruit bats, including Pteropus vampyrus (large flying fox), and Pteropus hypomelanus (small flying fox), both found in Malaysia. The transmission of the Nipah virus from flying foxes to pigs is thought to be due to an increasing overlap between bat habitats and piggeries in peninsular Malaysia. In one outbreak, fruit orchards were in proximity to the piggery, allowing the spillage of urine, feces, and partially eaten fruit onto the pigs. Retrospective studies demonstrate that viral spillover into pigs may have been occurring, undetected, in Malaysia since 1996. During 1998, viral spread was aided by the transfer of infected pigs to other farms, where new outbreaks occurred.
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