Nipah virus

Not to be confused with Nepovirus.
Nipah virus
False-color electron micrograph showing a Nipah virus particle (purple) by an infected Vero cell (brown)
Virus classification e
(unranked): Virus
Realm: Riboviria
Kingdom: Orthornavirae
Phylum: Negarnaviricota
Class: Monjiviricetes
Order: Mononegavirales
Family: Paramyxoviridae
Genus: Henipavirus
Species:
Nipah virus

Nipah virus is a bat-borne virus that causes Nipah virus infection in humans and other animals.[1]

The disease with a high mortality rate. Numerous disease outbreaks caused by Nipah virus have occurred in South and Southeast Asia. Nipah virus belongs to the genus Henipavirus along with the Hendra virus, which has also caused disease outbreaks.[2]

It was reported on September 14, 2023, that five cases, including two deaths, were confirmed in Kozhikode district in Kerala, India. With some 700 people linked to the two deaths[3][4]

Virology

Like other henipaviruses, the Nipah virus genome is a single (nonsegmented) negative-sense, single-stranded RNA of over 18 kb, which is substantially longer than that of other paramyxoviruses.[5][6] The enveloped virus particles are variable in shape, and can be filamentous or spherical; they contain a helical nucleocapsid.[5] 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.[7][8]

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.[9] Each head consists of a beta-propellor 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.[9] 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.[10] The F glycoprotein forms a trimer, which mediates membrane fusion.[5][6]

  • Transmission electron micrograph of mature extracellular Nipah Virus particles (yellow) near the periphery of an infected VERO cell
    Transmission electron micrograph of mature extracellular Nipah Virus particles (yellow) near the periphery of an infected VERO cell
  • Nipah virus particles
    Nipah virus particles
  • Transmission electron micrograph depicted a number of Nipah virus virions
    Transmission electron micrograph depicted a number of Nipah virus virions

Tropism

Ephrins B2 and B3 have been identified as the main receptors for Nipah virus.[5][6][11] Ephrin subtypes have a complex distribution of expression throughout the body, where the B3 is noted to have particularly high expression in some forebrain subregions.[12]

Mechanism

In terms of the mechanism of this infection we find that entry is via the oro-nasal route. The site of initial replication has not been determined (however lymphoid and respiratory tissues could be probable sites), secondary replication occurs in the endothelium. We later find that the glycoprotein G of NiV binds to the cellular receptor Ephrin-B2.[13]

The CNS is overtaken via the haematogenous route. The virus is highly lethal due to its ability to elude the human immune defence; the P gene inhibit interferon activity, interferons are signaling proteins released in response to the presence of a virus[14][13]

Transmission

Pteropus vampyrus (large flying fox),natural reservoir of Nipah virus

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.[15]

The transmission of Nipah virus from flying foxes to pigs is thought to be due to an increasing overlap between bat habitats and piggeries in peninsular Malaysia. At the index farm, fruit orchards were in close proximity to the piggery, allowing the spillage of urine, faeces and partially eaten fruit onto the pigs.[16]

Retrospective studies demonstrate that viral spillover into pigs may have been occurring, undetected, in Malaysia since 1996.[17]

During 1998, viral spread was aided by the transfer of infected pigs to other farms, where new outbreaks occurred.[18]

The risk of exposure is high for hospital workers and caretakers of those infected with the virus. In Malaysia and Singapore, Nipah virus infection occurred in those with close contact to infected pigs. In Bangladesh and India, the disease has been linked to consumption of raw date palm sap (toddy) and eating of fruits partially consumed by bats and using water from wells inhabited by bats.[19][20][21]

Geographic distribution

Nipah virus has been isolated from Lyle's flying fox (Pteropus lylei) in Cambodia[22] and viral RNA found in urine and saliva from P. lylei and Horsfield's roundleaf bat (Hipposideros larvatus) in Thailand.[23]

Infective virus has also been isolated from environmental samples of bat urine and partially eaten fruit in Malaysia.[24]

Antibodies to henipaviruses have also been found in fruit bats in Madagascar (Pteropus rufus, Eidolon dupreanum)[25] and Ghana (Eidolon helvum)[26]indicating a wide geographic distribution of the viruses.

No infection of humans or other species have been observed in Cambodia, Thailand or Africa as of 2018.[27]

Disease

Further information: Nipah virus infection

Presentation

Symptoms of infection from an outbreak in Malaysia were primarily encephalitic in humans .[28] Other 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.[7][29]

The signs and symptoms usually present as:[30][31]

These symptoms can be followed by more serious conditions including:[32]

Diagnosis

Laboratory diagnosis of Nipah virus infection is made by:ARN detection can be done using reverse transcriptase polymerase chain reaction (RT-PCR) from throat swabs, cerebrospinal fluid, urine and blood analysis during acute and convalescent stages of the disease.[33] IgG and IgM antibody detection can be done after recovery to confirm Nipah virus infection. Immunohistochemistry on tissues collected during autopsy also confirms the disease.[33]

Treatment

Currently there is no specific treatment for Nipah virus infection as of 2020.[34] The mainstay of treatment is supportive care.[35][34] Standard infection control practices and proper barrier nursing techniques are recommended to avoid the spread of the infection from person to person,[35] all suspected cases of Nipah virus infection should be isolated.[36] While tentative evidence supports the use of ribavirin, it has not yet been studied in people with the disease.[35]

Epidemiology

Outbreaks

Main article: Nipah virus infection § Outbreaks

Nipah virus infection outbreaks have been reported in Malaysia, Singapore, Bangladesh and India. The highest mortality due to Nipah virus infection has occurred in Bangladesh, where outbreaks are typically seen in winter.[37] Nipah virus first appeared in 1998, in peninsular Malaysia in pigs and pig farmers. By mid-1999, more than 265 human cases of encephalitis, including 105 deaths, had been reported in Malaysia, and 11 cases of either encephalitis or respiratory illness with one fatality were reported in Singapore.[38] In 2001, Nipah virus was reported from Meherpur District, Bangladesh[39][40] and Siliguri, India.[39] The outbreak again appeared in 2003, 2004 and 2005 in Naogaon District, Manikganj District, Rajbari District, Faridpur District and Tangail District.[40] In Bangladesh there were also outbreaks in subsequent years.[41] In September 2021, Nipah virus resurfaced in Kerala, India claiming the life of a 12-year-old boy.[42]

In 2023 we have seen several outbreaks. On 4 January 2023 , 11 cases (10 confirmed and one probable) including eight deaths (Case Fatality Rate (CFR) 73%) have been reported in Bangladesh. WHO assesed the risk as high at the national level.[43] Then in September we saw India have as of 14 September 2023, five cases, including two deaths, being confirmed in Kozhikode district in Kerala. The government has prepared a contact list of over 700 people linked to the two deaths, of whom two family members and a healthcare worker tested positive for the virus.[3][44]

  • Locations of henipavirus outbreaks (red stars–Hendra virus; blue stars–Nipah virus) and distribution of henipavirus flying fox reservoirs (red shading–Hendra virus; blue shading–Nipah virus)
    Locations of henipavirus outbreaks (red stars–Hendra virus; blue stars–Nipah virus) and distribution of henipavirus flying fox reservoirs (red shading–Hendra virus; blue shading–Nipah virus)

History

Peninsula Malaysia

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.[4][17][45][46] The virus itself was isolated the following year in 1999.[33] This outbreak resulted in the culling of one million pigs. In Singapore, 11 cases, including one death, occurred in abattoir workers exposed to pigs imported from the affected Malaysian farms. The Nipah virus has been classified by the Centers for Disease Control and Prevention as a Category C agent.[47]

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.[48][49] Nipah virus is one of several viruses identified by WHO as a likely cause of a future epidemic in a new plan developed after the Ebola epidemic for urgent research and development before and during an epidemic toward new diagnostic tests, vaccines and medicines.[50][51]

The outbreak was originally mistaken for Japanese encephalitis, but physicians in the area noted that persons who had been vaccinated against Japanese encephalitis were not protected in the epidemic, and the number of cases among adults was unusual.[52] 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.[53][54]

Evolution

The most likely origin of the Nipah virus was in 1947 (95% credible interval: 1888–1988).[55]

There are two clades of this virus—one with its origin in 1995 (95% credible interval: 1985–2002) and a second with its origin in 1985 (95% credible interval: 1971–1996). The mutation rate was estimated to be 6.5 × 10−4 substitution/site/year (95% credible interval: 2.3 × 10−4 –1.18 × 10−3).[56][57]

See also

References

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