Displaying publications 1 - 20 of 42 in total

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  1. Chakraborty S, Deb B, Barbhuiya PA, Uddin A
    Virus Res, 2019 04 02;263:129-138.
    PMID: 30664908 DOI: 10.1016/j.virusres.2019.01.011
    Codon usage bias (CUB) is the unequal usage of synonymous codons of an amino acid in which some codons are used more often than others and is widely used in understanding molecular biology, genetics, and functional regulation of gene expression. Nipah virus (NiV) is an emerging zoonotic paramyxovirus that causes fatal disease in both humans and animals. NiV was first identified during an outbreak of a disease in Malaysia in 1998 and then occurred periodically since 2001 in India, Bangladesh, and the Philippines. We used bioinformatics tools to analyze the codon usage patterns in a genome-wide manner among 11 genomes of NiV as no work was reported yet. The compositional properties revealed that the overall GC and AT contents were 41.96 and 58.04%, respectively i.e. Nipah virus genes were AT-rich. Correlation analysis between overall nucleotide composition and its 3rd codon position suggested that both mutation pressure and natural selection might influence the CUB across Nipah genomes. Neutrality plot revealed natural selection might have played a major role while mutation pressure had a minor role in shaping the codon usage bias in NiV genomes.
    Matched MeSH terms: Nipah Virus/genetics*
  2. 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
  3. Ong ST, Yusoff K, Kho CL, Abdullah JO, Tan WS
    J Gen Virol, 2009 Feb;90(Pt 2):392-397.
    PMID: 19141448 DOI: 10.1099/vir.0.005710-0
    The nucleocapsid protein of Nipah virus produced in Escherichia coli assembled into herringbone-like particles. The amino- and carboxy-termini of the N protein were shortened progressively to define the minimum contiguous sequence involved in capsid assembly. The first 29 aa residues of the N protein are dispensable for capsid formation. The 128 carboxy-terminal residues do not play a role in the assembly of the herringbone-like particles. A region with amino acid residues 30-32 plays a crucial role in the formation of the capsid particle. Deletion of any of the four conserved hydrophobic regions in the N protein impaired capsid formation. Replacement of the central conserved regions with the respective sequences from the Newcastle disease virus restored capsid formation.
    Matched MeSH terms: Nipah Virus/genetics*
  4. 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*
  5. 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*
  6. 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*
  7. 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*
  8. 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
  9. 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*
  10. AbuBakar S, Chang LY, Ali AR, Sharifah SH, Yusoff K, Zamrod Z
    Emerg Infect Dis, 2004 Dec;10(12):2228-30.
    PMID: 15663869
    Nipah viruses from pigs from a Malaysian 1998 outbreak were isolated and sequenced. At least two different Nipah virus strains, including a previously unreported strain, were identified. The findings highlight the possibility that the Malaysia outbreaks had two origins of Nipah virus infections.
    Matched MeSH terms: Nipah Virus/genetics*
  11. 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
  12. 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
  13. Lo MK, Nichol ST, Spiropoulou CF
    Antiviral Res, 2014 Jun;106:53-60.
    PMID: 24680955 DOI: 10.1016/j.antiviral.2014.03.011
    Nipah virus (NiV) outbreaks have occurred in Malaysia, India, and Bangladesh, and the virus continues to cause annual outbreaks of fatal human encephalitis in Bangladesh due to spillover from its bat host reservoir. Due to its high pathogenicity, its potential use for bio/agro-terrorism, and to the current lack of approved therapeutics, NiV is designated as an overlap select agent requiring biosafety level-4 containment. Although the development of therapeutic monoclonal antibodies and soluble protein subunit vaccines have shown great promise, the paucity of effective antiviral drugs against NiV merits further exploration of compound libraries using rapid quantitative antiviral assays. As a proof-of-concept study, we evaluated the use of fluorescent and luminescent reporter NiVs for antiviral screening. We constructed and rescued NiVs expressing either Renilla luciferase or green fluorescent protein, and characterized their reporter signal kinetics in different cell types as well as in the presence of several inhibitors. The 50% effective concentrations (EC50s) derived for inhibitors against both reporter viruses are within range of EC50s derived from virus yield-based dose-response assays against wild-type NiV (within 1Log10), thus demonstrating that both reporter NiVs can serve as robust antiviral screening tools. Utilizing these live NiV-based reporter assays requires modest instrumentation, and circumvents the time and labor-intensive steps associated with cytopathic effect or viral antigen-based assays. These reporter NiVs will not only facilitate antiviral screening, but also the study of host cell components that influence the virus life cycle.
    Matched MeSH terms: Nipah Virus/genetics
  14. 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
  15. 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: Nipah Virus/genetics
  16. 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
  17. 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*
  18. Eshaghi M, Tan WS, Mohidin TB, Yusoff K
    Virus Res, 2004 Nov;106(1):71-6.
    PMID: 15522449
    A method for serological diagnosis of Nipah virus (NiV) is described. DNA encoding truncated G protein of NiV was cloned into the pFastBac HT vector, and the fusion protein to His-tag was expressed in insect cells by recombinant baculovirus. The resulting His-G recombinant fusion protein was purified by affinity chromatography and used as the coating antigen for serological testing by indirect enzyme-linked immunosorbant assay (ELISA). When tested against a panel of swine serum samples, the recombinant G protein-based ELISA successfully discriminated all 40 samples previously determined to be serum neutralizing test (SNT) positive from 11 SNT negatives samples. The data show that the recombinant G protein exhibits the antigenic epitopes and conformation necessary for specific antigen-antibody recognition. The main advantage of the recombinant G protein-based NiV ELISA compared to an ELISA using whole virus antigen is the use of a single antigenic protein instead of inactivated whole virus which is required to be prepared under high risk and cost. This test is suitable for routine diagnosis of NiV and also for epidemiological surveys as it allows highly reliable testing of a large number of sera rapidly.
    Matched MeSH terms: Nipah Virus/genetics*
  19. 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*
  20. 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: Nipah Virus/genetics*
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