Displaying publications 1 - 20 of 42 in total

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  1. Chang LY, Ali AR, Hassan SS, AbuBakar S
    J Med Virol, 2006 Aug;78(8):1105-12.
    PMID: 16789019
    Nipah virus infection of porcine stable kidney cells (PS), human neuronal cells (SK-N-MC), human lung fibroblasts cells (MRC-5), and human monocytes (THP-1) were examined. Rapid progression of cytopathic effects (CPE) and cell death were noted in PS cell cultures treated with Nipah virus, followed by MRC-5, SK-N-MC, and THP-1 cell cultures, in descending order of rapidity. Significant increase in the intracellular Nipah virus RNA occurred beginning at 24 hr PI in all the infected cells. Whereas, the extracellular release of Nipah virus RNA increased significantly beginning at 48 and 72 hr PI for the infected MRC-5 cells and PS cells, respectively. No significant release of extracellular Nipah virus RNA was detected from the Nipah virus-infected SK-N-MC and THP-1 cells. At its peak, approximately 6.6 log PFU/microl of extracellular Nipah virus RNA was released from the Nipah virus-infected PS cells, with at least a 100-fold less virus RNA was recorded in the Nipah virus-infected SK-N-MC and THP-1. Approximately 15.2% (+/-0.1%) of the released virus from the infected PS cell cultures was infectious in contrast to approximately 5.5% (+/-0.7%) from the infected SK-N-MC cells. The findings suggest that there are no differences in the capacity to support Nipah virus replication between pigs and humans in fully susceptible PS and MRC-5 cells. However, there are differences between these cells and human neuronal cells and monocytes in the ability to support Nipah virus replication and virus release.
    Matched MeSH terms: Nipah Virus/genetics*
  2. Chang LY, Ali AR, Hassan SS, AbuBakar S
    Virol J, 2006;3:47.
    PMID: 16784519
    Nipah virus is a zoonotic virus isolated from an outbreak in Malaysia in 1998. The virus causes infections in humans, pigs, and several other domestic animals. It has also been isolated from fruit bats. The pathogenesis of Nipah virus infection is still not well described. In the present study, Nipah virus replication kinetics were estimated from infection of African green monkey kidney cells (Vero) using the one-step SYBR Green I-based quantitative real-time reverse transcriptase-polymerase chain reaction (qRT-PCR) assay.
    Matched MeSH terms: Nipah Virus/genetics
  3. Thakur N, Bailey D
    Microbes Infect, 2019;21(7):278-286.
    PMID: 30817995 DOI: 10.1016/j.micinf.2019.02.002
    Nipah virus is an emerging zoonotic paramyxovirus that causes severe and often fatal respiratory and neurological disease in humans. The virus was first discovered after an outbreak of encephalitis in pig farmers in Malaysia and Singapore with subsequent outbreaks in Bangladesh or India occurring almost annually. Due to the highly pathogenic nature of NiV, its pandemic potential, and the lack of licensed vaccines or therapeutics, there is a requirement for research and development into highly sensitive and specific diagnostic tools as well as antivirals and vaccines to help prevent and control future outbreak situations.
    Matched MeSH terms: Nipah Virus/genetics
  4. 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: Nipah Virus/genetics*
  5. Weingartl HM, Berhane Y, Caswell JL, Loosmore S, Audonnet JC, Roth JA, et al.
    J Virol, 2006 Aug;80(16):7929-38.
    PMID: 16873250
    Nipah virus (NiV), of the family Paramyxoviridae, was isolated in 1999 in Malaysia from a human fatality in an outbreak of severe human encephalitis, when human infections were linked to transmission of the virus from pigs. Consequently, a swine vaccine able to abolish virus shedding is of veterinary and human health interest. Canarypox virus-based vaccine vectors carrying the gene for NiV glycoprotein (ALVAC-G) or the fusion protein (ALVAC-F) were used to intramuscularly immunize four pigs per group, either with 10(8) PFU each or in combination. Pigs were boosted 14 days postvaccination and challenged with 2.5 x 10(5) PFU of NiV two weeks later. The combined ALVAC-F/G vaccine induced the highest levels of neutralization antibodies (2,560); despite the low neutralizing antibody levels in the F vaccinees (160), all vaccinated animals appeared to be protected against challenge. Virus was not isolated from the tissues of any of the vaccinated pigs postchallenge, and a real-time reverse transcription (RT)-PCR assay detected only small amounts of viral RNA in several samples. In challenge control pigs, virus was isolated from a number of tissues (10(4.4) PFU/g) or detected by real-time RT-PCR. Vaccination of the ALVAC-F/G vaccinees appeared to stimulate both type 1 and type 2 cytokine responses. Histopathological findings indicated that there was no enhancement of lesions in the vaccinees. No virus shedding was detected in vaccinated animals, in contrast to challenge control pigs, from which virus was isolated from the throat and nose (10(2.9) PFU/ml). Based on the data presented, the combined ALVAC-F/G vaccine appears to be a very promising vaccine candidate for swine.
    Matched MeSH terms: Nipah Virus/genetics
  6. Epstein JH, Anthony SJ, Islam A, Kilpatrick AM, Ali Khan S, Balkey MD, et al.
    Proc Natl Acad Sci U S A, 2020 11 17;117(46):29190-29201.
    PMID: 33139552 DOI: 10.1073/pnas.2000429117
    Nipah virus (NiV) is an emerging bat-borne zoonotic virus that causes near-annual outbreaks of fatal encephalitis in South Asia-one of the most populous regions on Earth. In Bangladesh, infection occurs when people drink date-palm sap contaminated with bat excreta. Outbreaks are sporadic, and the influence of viral dynamics in bats on their temporal and spatial distribution is poorly understood. We analyzed data on host ecology, molecular epidemiology, serological dynamics, and viral genetics to characterize spatiotemporal patterns of NiV dynamics in its wildlife reservoir, Pteropus medius bats, in Bangladesh. We found that NiV transmission occurred throughout the country and throughout the year. Model results indicated that local transmission dynamics were modulated by density-dependent transmission, acquired immunity that is lost over time, and recrudescence. Increased transmission followed multiyear periods of declining seroprevalence due to bat-population turnover and individual loss of humoral immunity. Individual bats had smaller host ranges than other Pteropus species (spp.), although movement data and the discovery of a Malaysia-clade NiV strain in eastern Bangladesh suggest connectivity with bats east of Bangladesh. These data suggest that discrete multiannual local epizootics in bat populations contribute to the sporadic nature of NiV outbreaks in South Asia. At the same time, the broad spatial and temporal extent of NiV transmission, including the recent outbreak in Kerala, India, highlights the continued risk of spillover to humans wherever they may interact with pteropid bats and the importance of limiting opportunities for spillover throughout Pteropus's range.
    Matched MeSH terms: Nipah Virus/genetics*
  7. Guillaume V, Lefeuvre A, Faure C, Marianneau P, Buckland R, Lam SK, et al.
    J Virol Methods, 2004 Sep 15;120(2):229-37.
    PMID: 15288966
    Nipah and Hendra viruses belong to the novel Henipavirus genus of the Paramyxoviridae family. Its zoonotic circulation in bats and recent emergence in Malaysia with fatal consequences for humans that were in close contact with infected pigs, has made the reinforcement of epidemiological and clinical surveillance systems a priority. In this study, TaqMan RT-PCR of the Nipah nucleoprotein has been developed so that Nipah virus RNA in field specimens or laboratory material can be characterized rapidly and specifically and quantitated. The linearity of the standard curve allowed quantification of 10(3) to 10(9) RNA transcripts. The sensitivity of the test was close to 1 pfu. The kinetics of Nipah virus production in Vero cells was monitored by the determination of infectious virus particles in the supernatant fluid and by quantitation of the viral RNA. Approximately, 1000 RNA molecules were detected per virion, suggesting the presence of many non-infectious particles, similar to other RNA viruses. TaqMan real-time RT-PCR failed to detect Hendra virus DNA. Importantly, the method was able to detect virus despite a similar ratio in viremic sera from hamsters infected with Nipah virus. This standardized technique is sensitive and reliable and allows rapid detection and quantitation of Nipah RNA in both field and experimental materials used for the surveillance and specific diagnosis of Nipah virus.
    Matched MeSH terms: Nipah Virus/genetics
  8. Pasha F, Alatawi A, Amir M, Faridi U
    Pak J Biol Sci, 2020 Jan;23(8):1086-1095.
    PMID: 32700860 DOI: 10.3923/pjbs.2020.1086.1095
    BACKGROUND AND OBJECTIVE: The epidemiology of Nipah virus (NiV) was shortly seen in many Asian countries like Malaysia, Bangladesh and India most recently. Nipah virus also synonym as bat born virus is transmitted primarily by fruit bats. The 2 different strains transmitted are Hendra (highly pathogenic) and Cedar (non-pathogenic). The present study was attempt to develop recombinant protein based reagents for molecular diagnosis of Nipah.

    MATERIALS AND METHODS: The different primer sets were developed using bioinformatics software DNASTAR. The E. coli cells were used for recombinant protein expression.

    RESULTS: The NiV 'G' region primers were designed and amplified for 1 kb fragment and cloned. The NiV 'G' fragments were sub-cloned in pET-28(+) B and pGEX-5x-1. Recombinant protein thus obtained in soluble form in both the cases was essayed using western blot. The result showed the protein expression yield was more in pET-28(+) B with low stability and vice versa for pGEX-5x-1.

    CONCLUSION: The antibodies raised from the protein can be used as diagnostic reagent for detection of NiV. Thus, a new diagnostic technique can be industrialized.

    Matched MeSH terms: Nipah Virus/genetics
  9. Mire CE, Versteeg KM, Cross RW, Agans KN, Fenton KA, Whitt MA, et al.
    Virol J, 2013 Dec 13;10:353.
    PMID: 24330654 DOI: 10.1186/1743-422X-10-353
    BACKGROUND: Nipah virus (NiV) is a highly pathogenic zoonotic agent in the family Paramyxoviridae that is maintained in nature by bats. Outbreaks have occurred in Malaysia, Singapore, India, and Bangladesh and have been associated with 40 to 75% case fatality rates. There are currently no vaccines or postexposure treatments licensed for combating human NiV infection.

    METHODS AND RESULTS: Four groups of ferrets received a single vaccination with different recombinant vesicular stomatitis virus vectors expressing: Group 1, control with no glycoprotein; Group 2, the NiV fusion protein (F); Group 3, the NiV attachment protein (G); and Group 4, a combination of the NiV F and G proteins. Animals were challenged intranasally with NiV 28 days after vaccination. Control ferrets in Group 1 showed characteristic clinical signs of NiV disease including respiratory distress, neurological disorders, viral load in blood and tissues, and gross lesions and antigen in target tissues; all animals in this group succumbed to infection by day 8. Importantly, all specifically vaccinated ferrets in Groups 2-4 showed no evidence of clinical illness and survived challenged. All animals in these groups developed anti-NiV F and/or G IgG and neutralizing antibody titers. While NiV RNA was detected in blood at day 6 post challenge in animals from Groups 2-4, the levels were orders of magnitude lower than animals from control Group 1.

    CONCLUSIONS: These data show protective efficacy against NiV in a relevant model of human infection. Further development of this technology has the potential to yield effective single injection vaccines for NiV infection.

    Matched MeSH terms: Nipah Virus/genetics
  10. Rahman MZ, Islam MM, Hossain ME, Rahman MM, Islam A, Siddika A, et al.
    Int J Infect Dis, 2021 Jan;102:144-151.
    PMID: 33129964 DOI: 10.1016/j.ijid.2020.10.041
    BACKGROUND: Nipah virus (NiV) infection, often fatal in humans, is primarily transmitted in Bangladesh through the consumption of date palm sap contaminated by Pteropus bats. Person-to-person transmission is also common and increases the concern of large outbreaks. This study aimed to characterize the molecular epidemiology, phylogenetic relationship, and the evolution of the nucleocapsid gene (N gene) of NiV.

    METHODS: We conducted molecular detection, genetic characterization, and Bayesian time-scale evolution analyses of NiV using pooled Pteropid bat roost urine samples from an outbreak area in 2012 and archived RNA samples from NiV case patients identified during 2012-2018 in Bangladesh.

    RESULTS: NiV-RNA was detected in 19% (38/456) of bat roost urine samples and among them; nine N gene sequences were recovered. We also retrieved sequences from 53% (21 out of 39) of archived RNA samples from patients. Phylogenetic analysis revealed that all Bangladeshi strains belonged to NiV-BD genotype and had an evolutionary rate of 4.64 × 10-4 substitutions/site/year. The analyses suggested that the strains of NiV-BD genotype diverged during 1995 and formed two sublineages.

    CONCLUSION: This analysis provides further evidence that the NiV strains of the Malaysian and Bangladesh genotypes diverged recently and continue to evolve. More extensive surveillance of NiV in bats and human will be helpful to explore strain diversity and virulence potential to infect humans through direct or person-to-person virus transmission.

    Matched MeSH terms: Nipah Virus/genetics*
  11. Rahman SA, Hassan SS, Olival KJ, Mohamed M, Chang LY, Hassan L, et al.
    Emerg Infect Dis, 2010 Dec;16(12):1990-3.
    PMID: 21122240 DOI: 10.3201/eid1612.091790
    We isolated and characterized Nipah virus (NiV) from Pteropus vampyrus bats, the putative reservoir for the 1998 outbreak in Malaysia, and provide evidence of viral recrudescence. This isolate is monophyletic with previous NiVs in combined analysis, and the nucleocapsid gene phylogeny species.
    Matched MeSH terms: Nipah Virus/genetics
  12. 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: Nipah Virus/genetics*
  13. Halpin K, Hyatt AD, Fogarty R, Middleton D, Bingham J, Epstein JH, et al.
    Am J Trop Med Hyg, 2011 Nov;85(5):946-51.
    PMID: 22049055 DOI: 10.4269/ajtmh.2011.10-0567
    Bats of the genus Pteropus have been identified as the reservoir hosts for the henipaviruses Hendra virus (HeV) and Nipah virus (NiV). The aim of these studies was to assess likely mechanisms for henipaviruses transmission from bats. In a series of experiments, Pteropus bats from Malaysia and Australia were inoculated with NiV and HeV, respectively, by natural routes of infection. Despite an intensive sampling strategy, no NiV was recovered from the Malaysian bats and HeV was reisolated from only one Australian bat; no disease was seen. These experiments suggest that opportunities for henipavirus transmission may be limited; therefore, the probability of a spillover event is low. For spillover to occur, a range of conditions and events must coincide. An alternate assessment framework is required if we are to fully understand how this reservoir host maintains and transmits not only these but all viruses with which it has been associated.
    Matched MeSH terms: Nipah Virus/genetics
  14. 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: Nipah Virus/genetics
  15. 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: Nipah Virus/genetics*
  16. Pong LY, Rabu A, Ibrahim N
    Mol Genet Genomics, 2020 Nov;295(6):1501-1516.
    PMID: 32767127 DOI: 10.1007/s00438-020-01716-3
    Encapsidation by nucleocapsid (N) protein is crucial for viral RNA to serve as a functional template for virus replication. However, the potential region that is vital for RNA encapsidation of Nipah virus (NiV) is still unknown. Thus, this study was aimed to identify these regions using a NiV minireplicon system. A series of broad range internal deletion mutations was generated in the 5' non-translated region (NTR) of the N gene mRNA region of NiV leader promoter via site-directed overlapping PCR-mediated mutagenesis. The mutation effects on synthesis and encapsidation of antigenome RNA, transcription, and RNA binding affinity of N protein were evaluated. The deletions of nucleotides 73-108, 79-108, and 85-108 from NiV leader promoter inhibited the encapsidation of antigenome RNA, while the deletion of nucleotides 103-108 suppressed the synthesis and encapsidation of antigenome RNA, implying that these regions are required for genome replication. Surprisingly, none of the mutations had detrimental effect on viral transcription. Using isothermal titration calorimetry, the binding of NiV N protein to genome or antigenome RNA transcript lacking of nucleotides 73-108 was found to be suppressed. Additionally, in silico analysis on secondary structure of genome RNA further supported the plausible cause of inefficient encapsidation of antigenome RNA by the loss of encapsidation signal in genome template. In conclusion, this study suggests that the nucleotides 73-90 within 5' NTR of the N gene mRNA region in NiV leader promoter contain cis-acting RNA element that is important for efficient encapsidation of antigenome RNA.
    Matched MeSH terms: Nipah Virus/genetics*
  17. Griffin BD, Leung A, Chan M, Warner BM, Ranadheera C, Tierney K, et al.
    Sci Rep, 2019 08 01;9(1):11171.
    PMID: 31371748 DOI: 10.1038/s41598-019-47549-y
    Nipah virus (NiV) has emerged as a highly lethal zoonotic paramyxovirus that is capable of causing a febrile encephalitis and/or respiratory disease in humans for which no vaccines or licensed treatments are currently available. There are two genetically and geographically distinct lineages of NiV: NiV-Malaysia (NiV-M), the strain that caused the initial outbreak in Malaysia, and NiV-Bangladesh (NiV-B), the strain that has been implicated in subsequent outbreaks in India and Bangladesh. NiV-B appears to be both more lethal and have a greater propensity for person-to-person transmission than NiV-M. Here we describe the generation and characterization of stable RNA polymerase II-driven infectious cDNA clones of NiV-M and NiV-B. In vitro, reverse genetics-derived NiV-M and NiV-B were indistinguishable from a wildtype isolate of NiV-M, and both viruses were pathogenic in the Syrian hamster model of NiV infection. We also describe recombinant NiV-M and NiV-B with enhanced green fluorescent protein (EGFP) inserted between the G and L genes that enable rapid and sensitive detection of NiV infection in vitro. This panel of molecular clones will enable studies to investigate the virologic determinants of henipavirus pathogenesis, including the pathogenic differences between NiV-M and NiV-B, and the high-throughput screening of candidate therapeutics.
    Matched MeSH terms: Nipah Virus/genetics*
  18. Yu J, Lv X, Yang Z, Gao S, Li C, Cai Y, et al.
    Viruses, 2018 10 19;10(10).
    PMID: 30347642 DOI: 10.3390/v10100572
    Nipah disease is a highly fatal zoonosis which is caused by the Nipah virus. The Nipah virus is a BSL-4 virus with fruit bats being its natural host. It is mainly prevalent in Southeast Asia. The virus was first discovered in 1997 in Negeri Sembilan, Malaysia. Currently, it is mainly harmful to pigs and humans with a high mortality rate. This study describes the route of transmission of the Nipah virus in different countries and analyzes the possibility of the primary disease being in China and the method of its transmission to China. The risk factors are analyzed for different susceptible populations to Nipah disease. The aim is to improve people's risk awareness and prevention and control of the disease and reduce its risk of occurring and spreading in China.
    Matched MeSH terms: Nipah Virus/genetics
  19. Dietzel E, Kolesnikova L, Sawatsky B, Heiner A, Weis M, Kobinger GP, et al.
    J Virol, 2016 Mar;90(5):2514-22.
    PMID: 26676785 DOI: 10.1128/JVI.02920-15
    Nipah virus (NiV) causes fatal encephalitic infections in humans. To characterize the role of the matrix (M) protein in the viral life cycle, we generated a reverse genetics system based on NiV strain Malaysia. Using an enhanced green fluorescent protein (eGFP)-expressing M protein-deleted NiV, we observed a slightly increased cell-cell fusion, slow replication kinetics, and significantly reduced peak titers compared to the parental virus. While increased amounts of viral proteins were found in the supernatant of cells infected with M-deleted NiV, the infectivity-to-particle ratio was more than 100-fold reduced, and the particles were less thermostable and of more irregular morphology. Taken together, our data demonstrate that the M protein is not absolutely required for the production of cell-free NiV but is necessary for proper assembly and release of stable infectious NiV particles.
    Matched MeSH terms: Nipah Virus/genetics
  20. 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: Nipah Virus/genetics
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