Displaying publications 41 - 60 of 62 in total

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  1. Fulltext [Study of pathogenicity of Nipah virus and its vaccine development]
    Yoneda M
    Uirusu, 2014;64(1):105-12.
    PMID: 25765986 DOI: 10.2222/jsv.64.105
    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. We established a system that enabled the rescue of replicating NiVs from a cloned DNA. Using the system, we analyzed the functions of accessory proteins in infected cells and the implications in in vivo pathogenicity. Further, we have developed a recombinant measles virus (rMV) vaccine expressing NiV envelope glycoproteins, which appeared to be an appropriate to NiV vaccine candidate for use in humans.
    Matched MeSH terms: Henipavirus Infections/virology*
  2. Current status of diagnostic methods for henipavirus
    Tamin A, Rota PA
    Dev Biol (Basel), 2013;135:139-45.
    PMID: 23689891 DOI: 10.1159/000189236
    Hendra virus (HeV) and Nipah virus (NiV) are the causative agents of emerging transboundary animal disease in pigs and horses. They also cause fatal disease in humans. NiV has a case fatality rate of 40 - 100%. In the initial NiV outbreak in Malaysia in 1999, about 1.1 million pigs had to be culled. The economic impact was estimated to be approximately US$450 million. Worldwide, HeV has caused more than 60 deaths in horses with 7 human cases and 4 deaths. Since the initial outbreak, HeV spillovers from Pteropus bats to horses and humans continue. This article presents a brief review on the currently available diagnostic methods for henipavirus infections, including advances achieved since the initial outbreak, and a gap analysis of areas needing improvement.
    Matched MeSH terms: Henipavirus Infections/virology
  3. Epidemiology of henipavirus disease in humans
    Luby SP, Gurley ES
    Curr. Top. Microbiol. Immunol., 2012;359:25-40.
    PMID: 22752412 DOI: 10.1007/82_2012_207
    All seven recognized human cases of Hendra virus (HeV) infection have occurred in Queensland, Australia. Recognized human infections have all resulted from a HeV infected horse that was unusually efficient in transmitting the virus and a person with a high exposure to infectious secretions. In the large outbreak in Malaysia where Nipah virus (NiV) was first identified, most human infections resulted from close contact with NiV infected pigs. Outbreak investigations in Bangladesh have identified drinking raw date palm sap as the most common pathway of NiV transmission from Pteropus bats to people, but person-to-person transmission of NiV has been repeatedly identified in Bangladesh and India. Although henipaviruses are not easily transmitted to people, these newly recognized, high mortality agents warrant continued scientific attention.
    Matched MeSH terms: Henipavirus Infections/virology
  4. Introduction: Nipah virus--discovery and origin
    Chua KB
    Curr. Top. Microbiol. Immunol., 2012;359:1-9.
    PMID: 22782307 DOI: 10.1007/82_2012_218
    Until the Nipah outbreak in Malaysia in 1999, knowledge of human infections with the henipaviruses was limited to the small number of cases associated with the emergence of Hendra virus in Australia in 1994. The Nipah outbreak in Malaysia alerted the global public health community to the severe pathogenic potential and widespread distribution of these unique paramyxoviruses. This chapter briefly describes the initial discovery of Nipah virus and the challenges encountered during the initial identification and characterisation of the aetiological agent responsible for the outbreak of febrile encephalitis. The initial attempts to isolate Nipah virus from the bat reservoir host are also described.
    Matched MeSH terms: Henipavirus Infections/virology
  5. Epidemiology. Breaking the chain in Bangladesh
    Stone R
    Science, 2011 Mar 4;331(6021):1128-31.
    PMID: 21385693 DOI: 10.1126/science.331.6021.1128
    Matched MeSH terms: Henipavirus Infections/virology*
  6. Organ- and endotheliotropism of Nipah virus infections in vivo and in vitro
    Maisner A, Neufeld J, Weingartl H
    Thromb. Haemost., 2009 Dec;102(6):1014-23.
    PMID: 19967130 DOI: 10.1160/TH09-05-0310
    Nipah virus (NiV) is a highly pathogenic paramyxovirus that was first isolated in 1999 during an outbreak in Malaysia. In contrast to other paramyxoviruses NiV infects many mammalian species. Because of its zoonotic potential, the high pathogenicity and the lack of therapeutic treatment, NiV was classified as a biosafety level 4 pathogen. In humans NiV causes a severe acute encephalitis whereas in some animal hosts respiratory symptoms are predominantly observed. Despite the differences in the clinical outcome, microvascular endothelial cell damage predominantly underlies the pathological changes in NiV infections in all susceptible host species. NiV generally induces a pronounced vasculitis which is primarily characterised by endothelial cell necrosis and inflammatory cell infiltration. For future developments of specific antiviral therapies or vaccines, a detailed understanding of the molecular basis of NiV pathogenesis is required. This article reviews the current knowledge about natural and experimental infections in different mammals, focusing on the main organ and cell tropism in vivo, and summarises some recent studies in cell culture on the role of ephrin-B2 and -B3 receptors in NiV infection of endothelial cells.
    Matched MeSH terms: Henipavirus Infections/virology
  7. Solubility, immunogenicity and physical properties of the nucleocapsid protein of Nipah virus produced in Escherichia coli
    Tan WS, Ong ST, Eshaghi M, Foo SS, Yusoff K
    J Med Virol, 2004 May;73(1):105-12.
    PMID: 15042656
    The nucleocapsid (N) protein of Nipah virus (NiV) can be produced in three Escherichia coli strains [TOP10, BL21(DE3) and SG935] under the control of trc promoter. However, most of the product existed in the form of insoluble inclusion bodies. There was no improvement in the solubility of the product when this protein was placed under the control of T7 promoter. However, the solubility of the N protein was significantly improved by lowering the growth temperature of E. coli BL21(DE3) cell cultures. Solubility analysis of N- and C-terminally deleted mutants revealed that the full-length N protein has the highest solubility. The soluble N protein could be purified efficiently by sucrose gradient centrifugation and nickel affinity chromatography. Electron microscopic analysis of the purified product revealed that the N protein assembled into herringbone-like particles of different lengths. The C-terminal end of the N protein contains the major antigenic region when probed with antisera from humans and pigs infected naturally.
    Matched MeSH terms: Henipavirus Infections/virology
  8. Fulltext Emergence and adaptive evolution of Nipah virus
    Li K, Yan S, Wang N, He W, Guan H, He C, et al.
    Transbound Emerg Dis, 2020 Jan;67(1):121-132.
    PMID: 31408582 DOI: 10.1111/tbed.13330
    Since its first emergence in 1998 in Malaysia, Nipah virus (NiV) has become a great threat to domestic animals and humans. Sporadic outbreaks associated with human-to-human transmission caused hundreds of human fatalities. Here, we collected all available NiV sequences and combined phylogenetics, molecular selection, structural biology and receptor analysis to study the emergence and adaptive evolution of NiV. NiV can be divided into two main lineages including the Bangladesh and Malaysia lineages. We formly confirmed a significant association with geography which is probably the result of long-term evolution of NiV in local bat population. The two NiV lineages differ in many amino acids; one change in the fusion protein might be involved in its activation via binding to the G protein. We also identified adaptive and positively selected sites in many viral proteins. In the receptor-binding G protein, we found that sites 384, 386 and especially 498 of G protein might modulate receptor-binding affinity and thus contribute to the host jump from bats to humans via the adaption to bind the human ephrin-B2 receptor. We also found that site 1645 in the connector domain of L was positive selected and involved in adaptive evolution; this site might add methyl groups to the cap structure present at the 5'-end of the RNA and thus modulate its activity. This study provides insight to assist the design of early detection methods for NiV to assess its epidemic potential in humans.
    Matched MeSH terms: Henipavirus Infections/virology*
  9. Fulltext Identifying Early Target Cells of Nipah Virus Infection in Syrian Hamsters
    Baseler L, Scott DP, Saturday G, Horne E, Rosenke R, Thomas T, et al.
    PLoS Negl Trop Dis, 2016 Nov;10(11):e0005120.
    PMID: 27812087 DOI: 10.1371/journal.pntd.0005120
    BACKGROUND: Nipah virus causes respiratory and neurologic disease with case fatality rates up to 100% in individual outbreaks. End stage lesions have been described in the respiratory and nervous systems, vasculature and often lymphoid organs in fatal human cases; however, the initial target organs of Nipah virus infection have not been identified. Here, we detected the initial target tissues and cells of Nipah virus and tracked virus dissemination during the early phase of infection in Syrian hamsters inoculated with a Nipah virus isolate from Malaysia (NiV-M) or Bangladesh (NiV-B).

    METHODOLOGY/PRINCIPAL FINDINGS: Syrian hamsters were euthanized between 4 and 48 hours post intranasal inoculation and tissues were collected and analyzed for the presence of viral RNA, viral antigen and infectious virus. Virus replication was first detected at 8 hours post inoculation (hpi). Nipah virus initially targeted type I pneumocytes, bronchiolar respiratory epithelium and alveolar macrophages in the lung and respiratory and olfactory epithelium lining the nasal turbinates. By 16 hpi, virus disseminated to epithelial cells lining the larynx and trachea. Although the pattern of viral dissemination was similar for both virus isolates, the rate of spread was slower for NiV-B. Infectious virus was not detected in the nervous system or blood and widespread vascular infection and lesions within lymphoid organs were not observed, even at 48 hpi.

    CONCLUSIONS/SIGNIFICANCE: Nipah virus initially targets the respiratory system. Virus replication in the brain and infection of blood vessels in non-respiratory tissues does not occur during the early phase of infection. However, virus replicates early in olfactory epithelium and may serve as the first step towards nervous system dissemination, suggesting that development of vaccines that block virus dissemination or treatments that can access the brain and spinal cord and directly inhibit virus replication may be necessary for preventing central nervous system pathology.

    Matched MeSH terms: Henipavirus Infections/virology*
  10. Fulltext Host gene expression profiles in ferrets infected with genetically distinct henipavirus strains
    Leon AJ, Borisevich V, Boroumand N, Seymour R, Nusbaum R, Escaffre O, et al.
    PLoS Negl Trop Dis, 2018 03;12(3):e0006343.
    PMID: 29538374 DOI: 10.1371/journal.pntd.0006343
    Henipavirus infection causes severe respiratory and neurological disease in humans that can be fatal. To characterize the pathogenic mechanisms of henipavirus infection in vivo, we performed experimental infections in ferrets followed by genome-wide gene expression analysis of lung and brain tissues. The Hendra, Nipah-Bangladesh, and Nipah-Malaysia strains caused severe respiratory and neurological disease with animals succumbing around 7 days post infection. Despite the presence of abundant viral shedding, animal-to-animal transmission did not occur. The host gene expression profiles of the lung tissue showed early activation of interferon responses and subsequent expression of inflammation-related genes that coincided with the clinical deterioration. Additionally, the lung tissue showed unchanged levels of lymphocyte markers and progressive downregulation of cell cycle genes and extracellular matrix components. Infection in the brain resulted in a limited breadth of the host responses, which is in accordance with the immunoprivileged status of this organ. Finally, we propose a model of the pathogenic mechanisms of henipavirus infection that integrates multiple components of the host responses.
    Matched MeSH terms: Henipavirus Infections/virology
  11. Fulltext Nipah shell disorder, modes of infection, and virulence
    Goh GK, Dunker AK, Foster JA, Uversky VN
    Microb Pathog, 2020 Apr;141:103976.
    PMID: 31940461 DOI: 10.1016/j.micpath.2020.103976
    The Nipah Virus (NiV) was first isolated during a 1998-9 outbreak in Malaysia. The outbreak initially infected farm pigs and then moved to humans from pigs with a case-fatality rate (CFR) of about 40%. After 2001, regular outbreaks occurred with higher CFRs (~71%, 2001-5, ~93%, 2008-12). The spread arose from drinking virus-laden palm date sap and human-to-human transmission. Intrinsic disorder analysis revealed strong correlation between the percentage of disorder in the N protein and CFR (Regression: r2 = 0.93, p 
    Matched MeSH terms: Henipavirus Infections/virology*
  12. Fulltext Emerging trends of Nipah virus: A review
    Sharma V, Kaushik S, Kumar R, Yadav JP, Kaushik S
    Rev Med Virol, 2019 Jan;29(1):e2010.
    PMID: 30251294 DOI: 10.1002/rmv.2010
    Since emergence of the Nipah virus (NiV) in 1998 from Malaysia, the NiV virus has reappeared on different occasions causing severe infections in human population associated with high rate of mortality. NiV has been placed along with Hendra virus in genus Henipavirus of family Paramyxoviridae. Fruit bats (Genus Pteropus) are known to be natural host and reservoir of NiV. During the outbreaks from Malaysia and Singapore, the roles of pigs as intermediate host were confirmed. The infection transmitted from bats to pigs and subsequently from pigs to humans. Severe encephalitis was reported in NiV infection often associated with neurological disorders. First NiV outbreak in India occurred in Siliguri district of West Bengal in 2001, where direct transmission of the NiV virus from bats-to-human and human-to-human was reported in contrast to the role of pigs in the Malaysian NiV outbreak. Regular NiV outbreaks have been reported from Bangladesh since 2001 to 2015. The latest outbreak of NiV has been recorded in May, 2018 from Kerala, India which resulted in the death of 17 individuals. Due to lack of vaccines and effective antivirals, Nipah encephalitis poses a great threat to public health. Routine surveillance studies in the infected areas can be useful in detecting early signs of infection and help in containment of these outbreaks.
    Matched MeSH terms: Henipavirus Infections/virology
  13. Fulltext Nipah virus dynamics in bats and implications for spillover to humans
    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: Henipavirus Infections/virology*
  14. Production of the matrix protein of Nipah virus in Escherichia coli: virus-like particles and possible application for diagnosis
    Subramanian SK, Tey BT, Hamid M, Tan WS
    J Virol Methods, 2009 Dec;162(1-2):179-83.
    PMID: 19666056 DOI: 10.1016/j.jviromet.2009.07.034
    The broad species tropism of Nipah virus (NiV) coupled with its high pathogenicity demand a rapid search for a new biomarker candidate for diagnosis. The matrix (M) protein was expressed in Escherichia coli and purified using a Ni-NTA affinity column chromatography and sucrose density gradient centrifugation. The recombinant M protein with the molecular mass (Mr) of about 43 kDa was detected by anti-NiV serum and anti-myc antibody. About 50% of the M protein was found to be soluble and localized in cytoplasm when the cells were grown at 30 degrees C. Electron microscopic analysis showed that the purified M protein assembled into spherical particles of different sizes with diameters ranging from 20 to 50 nm. The purified M protein showed significant reactivity with the swine sera collected during the NiV outbreak, demonstrating its potential as a diagnostic reagent.
    Matched MeSH terms: Henipavirus Infections/virology
  15. Fulltext Characterization of Nipah virus from naturally infected Pteropus vampyrus bats, Malaysia
    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: Henipavirus Infections/virology
  16. Fulltext Transmission routes for nipah virus from Malaysia and Bangladesh
    Clayton BA, Middleton D, Bergfeld J, Haining J, Arkinstall R, Wang L, et al.
    Emerg Infect Dis, 2012 Dec;18(12):1983-93.
    PMID: 23171621 DOI: 10.3201/eid1812.120875
    Human infections with Nipah virus in Malaysia and Bangladesh are associated with markedly different patterns of transmission and pathogenicity. To compare the 2 strains, we conducted an in vivo study in which 2 groups of ferrets were oronasally exposed to either the Malaysia or Bangladesh strain of Nipah virus. Viral shedding and tissue tropism were compared between the 2 groups. Over the course of infection, significantly higher levels of viral RNA were recovered from oral secretions of ferrets infected with the Bangladesh strain. Higher levels of oral shedding of the Bangladesh strain of Nipah virus might be a key factor in onward transmission in outbreaks among humans.
    Matched MeSH terms: Henipavirus Infections/virology
  17. Fulltext Characterization of Nipah virus from outbreaks in Bangladesh, 2008-2010
    Lo MK, Lowe L, Hummel KB, Sazzad HM, Gurley ES, Hossain MJ, et al.
    Emerg Infect Dis, 2012 Feb;18(2):248-55.
    PMID: 22304936 DOI: 10.3201/eid1802.111492
    Nipah virus (NiV) is a highly pathogenic paramyxovirus that causes fatal encephalitis in humans. The initial outbreak of NiV infection occurred in Malaysia and Singapore in 1998-1999; relatively small, sporadic outbreaks among humans have occurred in Bangladesh since 2001. We characterized the complete genomic sequences of identical NiV isolates from 2 patients in 2008 and partial genomic sequences of throat swab samples from 3 patients in 2010, all from Bangladesh. All sequences from patients in Bangladesh comprised a distinct genetic group. However, the detection of 3 genetically distinct sequences from patients in the districts of Faridpur and Gopalganj indicated multiple co-circulating lineages in a localized region over a short time (January-March 2010). Sequence comparisons between the open reading frames of all available NiV genes led us to propose a standardized protocol for genotyping NiV; this protcol provides a simple and accurate way to classify current and future NiV sequences.
    Matched MeSH terms: Henipavirus Infections/virology
  18. Clinical and pathological manifestations of human henipavirus infection
    Wong KT, Tan CT
    Curr. Top. Microbiol. Immunol., 2012;359:95-104.
    PMID: 22427144 DOI: 10.1007/82_2012_205
    The clinicopathological features of human Nipah virus and Hendra virus infections appear to be similar. The clinical manifestations may be mild, but if severe, includes acute encephalitic and pulmonary syndromes with a high mortality. The pathological features in human acute henipavirus infections comprise vasculopathy (vasculitis, endothelial multinucleated syncytia, thrombosis), microinfarcts and parenchymal cell infection in the central nervous system, lung, kidney and other major organs. Viral inclusions, antigens, nucleocapsids and RNA are readily demonstrated in blood vessel wall and numerous types of parenchymal cells. Relapsing henipavirus encephalitis is a rare complication reported in less than 10% of survivors of the acute infection and appears to be distinct from the acute encephalitic syndrome. Pathological evidence suggests viral recrudescence confined to the central nervous system as the cause.
    Matched MeSH terms: Henipavirus Infections/virology
  19. Human Hendra virus infection causes acute and relapsing encephalitis
    Wong KT, Robertson T, Ong BB, Chong JW, Yaiw KC, Wang LF, et al.
    Neuropathol. Appl. Neurobiol., 2009 Jun;35(3):296-305.
    PMID: 19473296 DOI: 10.1111/j.1365-2990.2008.00991.x
    To study the pathology of two cases of human Hendra virus infection, one with no clinical encephalitis and one with relapsing encephalitis.
    Matched MeSH terms: Henipavirus Infections/virology
  20. A review of Nipah and Hendra viruses with an historical aside
    Ksiazek TG, Rota PA, Rollin PE
    Virus Res, 2011 Dec;162(1-2):173-83.
    PMID: 21963678 DOI: 10.1016/j.virusres.2011.09.026
    The emergence of Hendra and Nipah viruses in the 1990s has been followed by the further emergence of these viruses in the tropical Old World. The history and current knowledge of the disease, the viruses and their epidemiology is reviewed in this article. A historical aside summarizes the role that Dr. Brian W.J. Mahy played at critical junctures in the early stories of these viruses.
    Matched MeSH terms: Henipavirus Infections/virology*
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