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Nipah virus strain variation

Pulliam JR, Field HE, Olival KJ, Henipavirus Ecology Research Group

Emerg Infect Dis, 2005 Dec;11(12):1978-9; author reply 1979.
PMID: 16485499
Matched MeSH terms: Henipavirus Infections/virology*
Fulltext High Pathogenicity of Nipah Virus from Pteropus lylei Fruit Bats, Cambodia

Gaudino M, Aurine N, Dumont C, Fouret J, Ferren M, Mathieu C, et al.

Emerg Infect Dis, 2020 01;26(1):104-113.
PMID: 31855143 DOI: 10.3201/eid2601.191284

We conducted an in-depth characterization of the Nipah virus (NiV) isolate previously obtained from a Pteropus lylei bat in Cambodia in 2003 (CSUR381). We performed full-genome sequencing and phylogenetic analyses and confirmed CSUR381 is part of the NiV-Malaysia genotype. In vitro studies revealed similar cell permissiveness and replication of CSUR381 (compared with 2 other NiV isolates) in both bat and human cell lines. Sequence alignments indicated conservation of the ephrin-B2 and ephrin-B3 receptor binding sites, the glycosylation site on the G attachment protein, as well as the editing site in phosphoprotein, suggesting production of nonstructural proteins V and W, known to counteract the host innate immunity. In the hamster animal model, CSUR381 induced lethal infections. Altogether, these data suggest that the Cambodia bat-derived NiV isolate has high pathogenic potential and, thus, provide insight for further studies and better risk assessment for future NiV outbreaks in Southeast Asia.

Matched MeSH terms: Henipavirus Infections/virology
The pandemic potential of Nipah virus

Luby SP

Antiviral Res, 2013 Oct;100(1):38-43.
PMID: 23911335 DOI: 10.1016/j.antiviral.2013.07.011

Nipah virus, a paramyxovirus whose wildlife reservoir is Pteropus bats, was first discovered in a large outbreak of acute encephalitis in Malaysia in 1998 among persons who had contact with sick pigs. Apparently, one or more pigs was infected from bats, and the virus then spread efficiently from pig to pig, then from pigs to people. Nipah virus outbreaks have been recognized nearly every year in Bangladesh since 2001 and occasionally in neighboring India. Outbreaks in Bangladesh and India have been characterized by frequent person-to-person transmission and the death of over 70% of infected people. Characteristics of Nipah virus that increase its risk of becoming a global pandemic include: humans are already susceptible; many strains are capable of limited person-to-person transmission; as an RNA virus, it has an exceptionally high rate of mutation: and that if a human-adapted strain were to infect communities in South Asia, high population densities and global interconnectedness would rapidly spread the infection. Appropriate steps to estimate and manage this risk include studies to explore the molecular and genetic basis of respiratory transmission of henipaviruses, improved surveillance for human infections, support from high-income countries to reduce the risk of person-to-person transmission of infectious agents in low-income health care settings, and consideration of vaccination in communities at ongoing risk of exposure to the secretions and excretions of Pteropus bats.

Matched MeSH terms: Henipavirus Infections/virology
Bacterial infections in pigs experimentally infected with Nipah virus

Berhane Y, Weingartl HM, Lopez J, Neufeld J, Czub S, Embury-Hyatt C, et al.

Transbound Emerg Dis, 2008 May;55(3-4):165-74.
PMID: 18405339 DOI: 10.1111/j.1865-1682.2008.01021.x

Nipah virus (NiV; Paramyxoviridae) caused fatal encephalitis in humans during an outbreak in Malaysia in 1998/1999 after transmission from infected pigs. Our previous study demonstrated that the respiratory, lymphatic and central nervous systems are targets for virus replication in experimentally infected pigs. To continue the studies on pathogenesis of NiV in swine, six piglets were inoculated oronasally with 2.5 x 10(5) PFU per animal. Four pigs developed mild clinical signs, one exudative epidermitis, and one neurologic signs due to suppurative meningoencephalitis, and was euthanized at 11 days post-inoculation (dpi). Neutralizing antibodies reached in surviving animals titers around 1280 at 16 dpi. Nasal and oro-pharyngeal shedding of the NiV was detected between 2 and 17 dpi. Virus appeared to be cleared from the tissues of the infected animals by 23 dpi, with low amount of RNA detected in submandibular and bronchial lymph nodes of three pigs, and olfactory bulb of one animal. Despite the presence of neutralizing antibodies, virus was isolated from serum at 24 dpi, and the viral RNA was still detected in serum at 29 dpi. Our results indicate slower clearance of NiV from some of the infected pigs. Bacteria were detected in the cerebrospinal fluid of five NiV inoculated animals, with isolation of Streptococcus suis and Enterococcus faecalis. Staphylococcus hyicus was isolated from the skin lesions of the animal with exudative epidermitis. Along with the observed lymphoid depletion in the lymph nodes of all NiV-infected animals, and the demonstrated ability of NiV to infect porcine peripheral blood mononuclear cells in vitro, this finding warrants further investigation into a possible NiV-induced immunosuppression of the swine host.

Matched MeSH terms: Henipavirus Infections/virology
Molecular characteristics of the Nipah virus glycoproteins

Diederich S, Maisner A

Ann N Y Acad Sci, 2007 Apr;1102:39-50.
PMID: 17470910

Nipah virus (NiV) is a highly pathogenic paramyxovirus, which emerged in 1998 from fruit bats in Malaysia and caused an outbreak of severe respiratory disease in pigs and fatal encephalitis in humans with high mortality rates. In contrast to most paramyxoviruses, NiV can infect a large variety of mammalian species. Due to this broad host range, its zoonotic potential, its high pathogenicity for humans, and the lack of effective vaccines or therapeutics, NiV was classified as a biosafety level 4 pathogen. This article provides an overview of the molecular characteristics of NiV focusing on the structure, functions, and unique biological properties of the two NiV surface glycoproteins, the receptor-binding G protein, and the fusion protein F. Since viral glycoproteins are major determinants for cell tropism and virus spread, a detailed knowledge of these proteins can help to understand the molecular basis of viral pathogenicity.

Matched MeSH terms: Henipavirus Infections/virology
Fulltext Comparison of the pathogenicity of Nipah virus isolates from Bangladesh and Malaysia in the Syrian hamster

DeBuysscher BL, de Wit E, Munster VJ, Scott D, Feldmann H, Prescott J

PLoS Negl Trop Dis, 2013;7(1):e2024.
PMID: 23342177 DOI: 10.1371/journal.pntd.0002024

Nipah virus is a zoonotic pathogen that causes severe disease in humans. The mechanisms of pathogenesis are not well described. The first Nipah virus outbreak occurred in Malaysia, where human disease had a strong neurological component. Subsequent outbreaks have occurred in Bangladesh and India and transmission and disease processes in these outbreaks appear to be different from those of the Malaysian outbreak. Until this point, virtually all Nipah virus studies in vitro and in vivo, including vaccine and pathogenesis studies, have utilized a virus isolate from the original Malaysian outbreak (NiV-M). To investigate potential differences between NiV-M and a Nipah virus isolate from Bangladesh (NiV-B), we compared NiV-M and NiV-B infection in vitro and in vivo. In hamster kidney cells, NiV-M-infection resulted in extensive syncytia formation and cytopathic effects, whereas NiV-B-infection resulted in little to no morphological changes. In vivo, NiV-M-infected Syrian hamsters had accelerated virus replication, pathology and death when compared to NiV-B-infected animals. NiV-M infection also resulted in the activation of host immune response genes at an earlier time point. Pathogenicity was not only a result of direct effects of virus replication, but likely also had an immunopathogenic component. The differences observed between NiV-M and NiV-B pathogeneis in hamsters may relate to differences observed in human cases. Characterization of the hamster model for NiV-B infection allows for further research of the strain of Nipah virus responsible for the more recent outbreaks in humans. This model can be used to study NiV-B pathogenesis, transmission, and countermeasures that could be used to control outbreaks.

Matched MeSH terms: Henipavirus Infections/virology*
[Nipah virus infection]

Kaku Y

Uirusu, 2004 Dec;54(2):237-42.
PMID: 15745162

Nipah virus (NiV), emerged in Peninsular Malaysia, caused an outbreak of severe febrile encephalitis in humans and respiratory diseases in pigs between 1998 and 1999. By May of 1999, the death of 105 humans and the culling of about 1.1 million pigs were reported. Fruitbats of Pteropid species were identified as the natural reservoir hosts. The epidemiological studies suggested that NiV was introduced into pig farms by fruitbats, and was than transmitted to humans (mainly pig farmers) and other animals such as dogs, cats and horses. In 2004, NiV reappeared in Bangladesh with greater lethality. In contrast to the Malaysia case, epidemiologic characteristics of this outbreak suggested the possibility of fruitbats-to-person, or person-to-person transmission. In this article, the epidemiological comparison between two outbreaks in Malaysia and Bangladesh, and the new-trends of virological studies of NiV will be discussed.

Matched MeSH terms: Henipavirus Infections/virology
Origin and evolution of Nipah virus

Lo Presti A, Cella E, Giovanetti M, Lai A, Angeletti S, Zehender G, et al.

J Med Virol, 2016 Mar;88(3):380-8.
PMID: 26252523 DOI: 10.1002/jmv.24345

Nipah virus, member of the Paramyxoviridae family, is classified as a Biosafety Level-4 agent and category C priority pathogen. Nipah virus disease is endemic in south Asia and outbreaks have been reported in Malaysia, Singapore, India, and Bangladesh. Bats of the genus Pteropus appear to be the natural reservoir of this virus. The aim of this study was to investigate the genetic diversity of Nipah virus, to estimate the date of origin and the spread of the infection. The mean value of Nipah virus N gene evolutionary rate, was 6.5 × 10(-4) substitution/site/year (95% HPD: 2.3 × 10(-4)-1.18 × 10(-3)). The time-scaled phylogenetic analysis showed that the root of the tree originated in 1947 (95% HPD: 1888-1988) as the virus entered in south eastern Asiatic regions. The segregation of sequences in two main clades (I and II) indicating that Nipah virus had two different introductions: one in 1995 (95% HPD: 1985-2002) which correspond to clade I, and the other in 1985 (95% HPD: 1971-1996) which correspond to clade II. The phylogeographic reconstruction indicated that the epidemic followed two different routes spreading to the other locations. The trade of infected pigs may have played a role in the spread of the virus. Bats of the Pteropus genus, that are able to travel to long distances, may have contributed to the spread of the infection. Negatively selected sites, statistically supported, could reflect the stability of the viral N protein.

Matched MeSH terms: Henipavirus Infections/virology*
Fulltext Evidence of exposure to henipaviruses in domestic pigs in Uganda

Atherstone C, Diederich S, Weingartl HM, Fischer K, Balkema-Buschmann A, Grace D, et al.

Transbound Emerg Dis, 2019 Mar;66(2):921-928.
PMID: 30576076 DOI: 10.1111/tbed.13105

Hendra virus (HeV) and Nipah virus (NiV), belonging to the genus Henipavirus, are among the most pathogenic of viruses in humans. Old World fruit bats (family Pteropodidae) are the natural reservoir hosts. Molecular and serological studies found evidence of henipavirus infection in fruit bats from several African countries. However, little is known about the potential for spillover into domestic animals in East Africa, particularly pigs, which served as amplifying hosts during the first outbreak of NiV in Malaysia and Singapore. We collected sera from 661 pigs presented for slaughter in Uganda between December 2015 and October 2016. Using HeV G and NiV G indirect ELISAs, 14 pigs (2%) were seroreactive in at least one ELISA. Seroprevalence increased to 5.4% in October 2016, when pigs were 9.5 times more likely to be seroreactive than pigs sampled in December 2015 (p = 0.04). Eight of the 14 ELISA-positive samples reacted with HeV N antigen in Western blot. None of the sera neutralized HeV or NiV in plaque reduction neutralization tests. Although we did not detect neutralizing antibodies, our results suggest that pigs in Uganda are exposed to henipaviruses or henipa-like viruses. Pigs in this study were sourced from many farms throughout Uganda, suggesting multiple (albeit rare) introductions of henipaviruses into the pig population. We postulate that given the widespread distribution of Old World fruit bats in Africa, spillover of henipaviruses from fruit bats to pigs in Uganda could result in exposure of pigs at multiple locations. A higher risk of a spillover event at the end of the dry season might be explained by higher densities of bats and contact with pigs at this time of the year, exacerbated by nutritional stress in bat populations and their reproductive cycle. Future studies should prioritize determining the risk of spillover of henipaviruses from pigs to people, so that potential risks can be mitigated.

Matched MeSH terms: Henipavirus Infections/virology
Hendra and Nipah viruses: pathogenesis and therapeutics

Eaton BT, Broder CC, Wang LF

Curr Mol Med, 2005 Dec;5(8):805-16.
PMID: 16375714

Within the past decade a number of new zoonotic paramyxoviruses emerged from flying foxes to cause serious disease outbreaks in man and livestock. Hendra virus was the cause of fatal infections of horses and man in Australia in 1994, 1999 and 2004. Nipah virus caused encephalitis in humans both in Malaysia in 1998/99, following silent spread of the virus in the pig population, and in Bangladesh from 2001 to 2004 probably as a result of direct bat to human transmission and spread within the human population. Hendra and Nipah viruses are highly pathogenic in humans with case fatality rates of 40% to 70%. Their genetic constitution, virulence and wide host range make them unique paramyxoviruses and they have been given Biosecurity Level 4 status in a new genus Henipavirus within the family Paramyxoviridae. Recent studies on the virulence, host range and cell tropisms of henipaviruses provide insights into the unique biological properties of these emerging human pathogens and suggest approaches for vaccine development and therapeutic countermeasures.

Matched MeSH terms: Henipavirus Infections/virology*
Phylogenetic and genetic analyses of the emerging Nipah virus from bats to humans

Shi J, Sun J, Hu N, Hu Y

Infect Genet Evol, 2020 11;85:104442.
PMID: 32622923 DOI: 10.1016/j.meegid.2020.104442

Little is known about the genetic features of Nipah virus (NiV) associated with virulence and transmission. Herein, phylogenetic and genetic analyses for all available NiV strains revealed sequence variations between the two genetic lineages of NiV with pathogenic differences, as well as among different strains within Bangladesh lineage. A total of 143 conserved amino acid differences, distributed among viral nucleocapsid (N), phosphoprotein (P), matrix protein (M), fusion protein (F) and glycoprotein (G), were revealed. Structural modeling revealed one key substitution (S3554N) in the viral G protein that might mediate a 12-amino-acid structural change from a loop into a β sheet. Multiple key amino acids substitutions in viral G protein were observed, which may alter viral fitness and transmissibility from bats to humans.

Matched MeSH terms: Henipavirus Infections/virology*
Nipah virus: epidemiology, pathology, immunobiology and advances in diagnosis, vaccine designing and control strategies - a comprehensive review

Singh RK, Dhama K, Chakraborty S, Tiwari R, Natesan S, Khandia R, et al.

Vet Q, 2019 Dec;39(1):26-55.
PMID: 31006350

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.

Matched MeSH terms: Henipavirus Infections/virology
Hendra and Nipah viruses: different and dangerous

Eaton BT, Broder CC, Middleton D, Wang LF

Nat Rev Microbiol, 2006 Jan;4(1):23-35.
PMID: 16357858

Hendra virus and Nipah virus are highly pathogenic paramyxoviruses that have recently emerged from flying foxes to cause serious disease outbreaks in humans and livestock in Australia, Malaysia, Singapore and Bangladesh. Their unique genetic constitution, high virulence and wide host range set them apart from other paramyxoviruses. These features led to their classification into the new genus Henipavirus within the family Paramyxoviridae and to their designation as Biosafety Level 4 pathogens. This review provides an overview of henipaviruses and the types of infection they cause, and describes how studies on the structure and function of henipavirus proteins expressed from cloned genes have provided insights into the unique biological properties of these emerging human pathogens.

Matched MeSH terms: Henipavirus Infections/virology
Establishment of a Nipah virus rescue system

Yoneda M, Guillaume V, Ikeda F, Sakuma Y, Sato H, Wild TF, et al.

Proc Natl Acad Sci U S A, 2006 Oct 31;103(44):16508-13.
PMID: 17053073

Nipah virus (NiV), a paramyxovirus, was first discovered in Malaysia in 1998 in an outbreak of infection in pigs and humans and incurred a high fatality rate in humans. Fruit bats, living in vast areas extending from India to the western Pacific, were identified as the natural reservoir of the virus. However, the mechanisms that resulted in severe pathogenicity in humans (up to 70% mortality) and that enabled crossing the species barrier were not known. In this study, we established a system that enabled the rescue of replicating NiVs from a cloned DNA by cotransfection of a constructed full-length cDNA clone and supporting plasmids coding virus nucleoprotein, phosphoprotein, and polymerase with the infection of the recombinant vaccinia virus, MVAGKT7, expressing T7 RNA polymerase. The rescued NiV (rNiV), by using the newly developed reverse genetics system, showed properties in vitro that were similar to the parent virus and retained the severe pathogenicity in a previously established animal model by experimental infection. A recombinant NiV was also developed, expressing enhanced green fluorescent protein (rNiV-EGFP). Using the virus, permissibility of NiV was compared with the presence of a known cellular receptor, ephrin B2, in a number of cell lines of different origins. Interestingly, two cell lines expressing ephrin B2 were not susceptible for rNiV-EGFP, indicating that additional factors are clearly required for full NiV replication. The reverse genetics for NiV will provide a powerful tool for the analysis of the molecular mechanisms of pathogenicity and cross-species infection.

Matched MeSH terms: Henipavirus Infections/virology*
Purification and characterization of Nipah virus nucleocapsid protein produced in insect cells

Eshaghi M, Tan WS, Ong ST, Yusoff K

J Clin Microbiol, 2005 Jul;43(7):3172-7.
PMID: 16000431

The nucleocapsid (N) protein of Nipah virus (NiV) is a major constituent of the viral proteins which play a role in encapsidation, regulating the transcription and replication of the viral genome. To investigate the use of a fusion system to aid the purification of the recombinant N protein for structural studies and potential use as a diagnostic reagent, the NiV N gene was cloned into the pFastBacHT vector and the His-tagged fusion protein was expressed in Sf9 insect cells by recombinant baculovirus. Western blot analysis of the recombinant fusion protein with anti-NiV antibodies produced a band of approximately 62 kDa. A time course study showed that the highest level of expression was achieved after 3 days of incubation. Electron microscopic analysis of the NiV recombinant N fusion protein purified on a nickel-nitrilotriacetic acid resin column revealed different types of structures, including spherical, ring-like, and herringbone-like particles. The light-scattering measurements of the recombinant N protein also confirmed the polydispersity of the sample with hyrdrodynamic radii of small and large types. The optical density spectra of the purified recombinant fusion protein revealed a high A(260)/A(280) ratio, indicating the presence of nucleic acids. Western blotting and enzyme-linked immunosorbent assay results showed that the recombinant N protein exhibited the antigenic sites and conformation necessary for specific antigen-antibody recognition.

Matched MeSH terms: Henipavirus Infections/virology
Fulltext Nipah virus infection in dogs, Malaysia, 1999

Mills JN, Alim AN, Bunning ML, Lee OB, Wagoner KD, Amman BR, et al.

Emerg Infect Dis, 2009 Jun;15(6):950-2.
PMID: 19523300 DOI: 10.3201/eid1506.080453

The 1999 outbreak of Nipah virus encephalitis in humans and pigs in Peninsular Malaysia ended with the evacuation of humans and culling of pigs in the epidemic area. Serologic screening showed that, in the absence of infected pigs, dogs were not a secondary reservoir for Nipah virus.

Matched MeSH terms: Henipavirus Infections/virology*
Fulltext Risk Factors for Nipah virus infection among pteropid bats, Peninsular Malaysia

Rahman SA, Hassan L, Epstein JH, Mamat ZC, Yatim AM, Hassan SS, et al.

Emerg Infect Dis, 2013 Jan;19(1):51-60.
PMID: 23261015 DOI: 10.3201/eid1901.120221

We conducted cross-sectional and longitudinal studies to determine the distribution of and risk factors for seropositivity to Nipah virus (NiV) among Pteropus vampyrus and P. hypomelanus bats in Peninsular Malaysia. Neutralizing antibodies against NiV were detected at most locations surveyed. We observed a consistently higher NiV risk (odds ratio 3.9) and seroprevalence (32.8%) for P. vampyrus than P. hypomelanus (11.1%) bats. A 3-year longitudinal study of P. hypomelanus bats indicated nonseasonal temporal variation in seroprevalence, evidence for viral circulation within the study period, and an overall NiV seroprevalence of 9.8%. The seroprevalence fluctuated over the study duration between 1% and 20% and generally decreased during 2004-2006. Adult bats, particularly pregnant, with dependent pup and lactating bats, had a higher prevalence of NiV antibodies than juveniles. Antibodies in juveniles 6 months-2 years of age suggested viral circulation within the study period.

Matched MeSH terms: Henipavirus Infections/virology
Genetic characterization of Nipah virus, Bangladesh, 2004

Harcourt BH, Lowe L, Tamin A, Liu X, Bankamp B, Bowden N, et al.

Emerg Infect Dis, 2005 Oct;11(10):1594-7.
PMID: 16318702

Until 2004, identification of Nipah virus (NV)-like outbreaks in Bangladesh was based on serology. We describe the genetic characterization of a new strain of NV isolated during outbreaks in Bangladesh (NV-B) in 2004, which confirms that NV was the etiologic agent responsible for these outbreaks.

Matched MeSH terms: Henipavirus Infections/virology*
Fulltext The Nature of Exposure Drives Transmission of Nipah Viruses from Malaysia and Bangladesh in Ferrets

Clayton BA, Middleton D, Arkinstall R, Frazer L, Wang LF, Marsh GA

PLoS Negl Trop Dis, 2016 06;10(6):e0004775.
PMID: 27341030 DOI: 10.1371/journal.pntd.0004775

Person-to-person transmission is a key feature of human Nipah virus outbreaks in Bangladesh. In contrast, in an outbreak of Nipah virus in Malaysia, people acquired infections from pigs. It is not known whether this important epidemiological difference is driven primarily by differences between NiV Bangladesh (NiV-BD) and Malaysia (NiV-MY) at a virus level, or by environmental or host factors. In a time course study, ferrets were oronasally exposed to equivalent doses of NiV-BD or NiV-MY. More rapid onset of productive infection and higher levels of virus replication in respiratory tract tissues were seen for NiV-BD compared to NiV-MY, corroborating our previous report of increased oral shedding of NiV-BD in ferrets and suggesting a contributory mechanism for increased NiV-BD transmission between people compared to NiV-MY. However, we recognize that transmission occurs within a social and environmental framework that may have an important and differentiating role in NiV transmission rates. With this in mind, ferret-to-ferret transmission of NiV-BD and NiV-MY was assessed under differing viral exposure conditions. Transmission was not identified for either virus when naïve ferrets were cohoused with experimentally-infected animals. In contrast, all naïve ferrets developed acute infection following assisted and direct exposure to oronasal fluid from animals that were shedding either NiV-BD or NiV-MY. Our findings for ferrets indicate that, although NiV-BD may be shed at higher levels than NiV-MY, transmission risk may be equivalently low under exposure conditions provided by cohabitation alone. In contrast, active transfer of infected bodily fluids consistently results in transmission, regardless of the virus strain. These observations suggest that the risk of NiV transmission is underpinned by social and environmental factors, and will have practical implications for managing transmission risk during outbreaks of human disease.

Matched MeSH terms: Henipavirus Infections/virology
Fulltext Serological evidence of henipavirus exposure in cattle, goats and pigs in Bangladesh

Chowdhury S, Khan SU, Crameri G, Epstein JH, Broder CC, Islam A, et al.

PLoS Negl Trop Dis, 2014 Nov;8(11):e3302.
PMID: 25412358 DOI: 10.1371/journal.pntd.0003302

BACKGROUND: Nipah virus (NiV) is an emerging disease that causes severe encephalitis and respiratory illness in humans. Pigs were identified as an intermediate host for NiV transmission in Malaysia. In Bangladesh, NiV has caused recognized human outbreaks since 2001 and three outbreak investigations identified an epidemiological association between close contact with sick or dead animals and human illness.
METHODOLOGY: We examined cattle and goats reared around Pteropus bat roosts in human NiV outbreak areas. We also tested pig sera collected under another study focused on Japanese encephalitis.
PRINCIPAL FINDINGS: We detected antibodies against NiV glycoprotein in 26 (6.5%) cattle, 17 (4.3%) goats and 138 (44.2%) pigs by a Luminex-based multiplexed microsphere assay; however, these antibodies did not neutralize NiV. Cattle and goats with NiVsG antibodies were more likely to have a history of feeding on fruits partially eaten by bats or birds (PR=3.1, 95% CI 1.6-5.7) and drinking palmyra palm juice (PR=3.9, 95% CI 1.5-10.2).
CONCLUSIONS: This difference in test results may be due to the exposure of animals to one or more novel viruses with antigenic similarity to NiV. Further research may identify a novel organism of public health importance.

Matched MeSH terms: Henipavirus Infections/virology

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