Displaying publications 1 - 20 of 62 in total

  1. Halpin K, Mungall BA
    Comp Immunol Microbiol Infect Dis, 2007 Sep;30(5-6):287-307.
    PMID: 17629946
    Following the discovery of two new paramyxoviruses in the 1990s, much effort has been placed on rapidly finding the reservoir hosts, characterising the genomes, identifying the viral receptors and formulating potential vaccines and therapeutic options for these viruses, Hendra and Nipah viruses caused zoonotic disease on a scale not seen before with other paramyxoviruses. Nipah virus particularly caused high morbidity and mortality in humans and high morbidity in pig populations in the first outbreak in Malaysia. Both viruses continue to pose a threat with sporadic outbreaks continuing into the 21st century. Experimental and surveillance studies identified that pteropus bats are the reservoir hosts. Research continues in an attempt to understand events that precipitated spillover of these viruses. Discovered on the cusp of the molecular technology revolution, much progress has been made in understanding these new viruses. This review endeavours to capture the depth and breadth of these recent advances.
    Matched MeSH terms: Henipavirus Infections/virology*
  2. Prasad AN, Agans KN, Sivasubramani SK, Geisbert JB, Borisevich V, Mire CE, et al.
    J Infect Dis, 2020 05 11;221(Suppl 4):S431-S435.
    PMID: 31665351 DOI: 10.1093/infdis/jiz469
    The high case-fatality rates and potential for use as a biological weapon make Nipah virus (NiV) a significant public health concern. Previous studies assessing the pathogenic potential of NiV delivered by the aerosol route in African green monkeys (AGMs) used the Malaysia strain (NiVM), which has caused lower instances of respiratory illness and person-to-person transmission during human outbreaks than the Bangladesh strain (NiVB). Accordingly, we developed a small particle aerosol model of NiVB infection in AGMs. Consistent with other mucosal AGM models of NiVB infection, we achieved uniform lethality and disease pathogenesis reflective of that observed in humans.
    Matched MeSH terms: Henipavirus Infections/virology*
  3. Epstein JH, Abdul Rahman S, Zambriski JA, Halpin K, Meehan G, Jamaluddin AA, et al.
    Emerg Infect Dis, 2006 Jul;12(7):1178-9.
    PMID: 16848051
    Matched MeSH terms: Henipavirus Infections/virology*
  4. Johnston SC, Briese T, Bell TM, Pratt WD, Shamblin JD, Esham HL, et al.
    PLoS One, 2015;10(2):e0117817.
    PMID: 25706617 DOI: 10.1371/journal.pone.0117817
    Henipaviruses are implicated in severe and frequently fatal pneumonia and encephalitis in humans. There are no approved vaccines or treatments available for human use, and testing of candidates requires the use of well-characterized animal models that mimic human disease. We performed a comprehensive and statistically-powered evaluation of the African green monkey model to define parameters critical to disease progression and the extent to which they correlate with human disease. African green monkeys were inoculated by the intratracheal route with 2.5 × 10(4) plaque forming units of the Malaysia strain of Nipah virus. Physiological data captured using telemetry implants and assessed in conjunction with clinical pathology were consistent with shock, and histopathology confirmed widespread tissue involvement associated with systemic vasculitis in animals that succumbed to acute disease. In addition, relapse encephalitis was identified in 100% of animals that survived beyond the acute disease phase. Our data suggest that disease progression in the African green monkey is comparable to the variable outcome of Nipah virus infection in humans.
    Matched MeSH terms: Henipavirus Infections/virology*
  5. Dups J, Middleton D, Long F, Arkinstall R, Marsh GA, Wang LF
    Virol J, 2014;11:102.
    PMID: 24890603 DOI: 10.1186/1743-422X-11-102
    Nipah virus and Hendra virus are closely related and following natural or experimental exposure induce similar clinical disease. In humans, encephalitis is the most serious outcome of infection and, hitherto, research into the pathogenesis of henipavirus encephalitis has been limited by the lack of a suitable model. Recently we reported a wild-type mouse model of Hendra virus (HeV) encephalitis that should facilitate detailed investigations of its neuropathogenesis, including mechanisms of disease recrudescence. In this study we investigated the possibility of developing a similar model of Nipah virus encephalitis.
    Matched MeSH terms: Henipavirus Infections/virology*
  6. Sohayati AR, Hassan L, Sharifah SH, Lazarus K, Zaini CM, Epstein JH, et al.
    Epidemiol Infect, 2011 Oct;139(10):1570-9.
    PMID: 21524339 DOI: 10.1017/S0950268811000550
    This study aimed to describe the transmission dynamics, the serological and virus excretion patterns of Nipah virus (NiV) in Pteropus vampyrus bats. Bats in captivity were sampled every 7-21 days over a 1-year period. The data revealed five NiV serological patterns categorized as high and low positives, waning, decreasing and increasing, and negative in these individuals. The findings strongly suggest that NiV circulates in wild bat populations and that antibody could be maintained for long periods. The study also found that pup and juvenile bats from seropositive dams tested seropositive, indicating that maternal antibodies against NiV are transmitted passively, and in this study population may last up to 14 months. NiV was isolated from the urine of one bat, and within a few weeks, two other seronegative bats seroconverted. Based on the temporal cluster of seroconversion, we strongly believe that the NiV isolated was recrudesced and then transmitted horizontally between bats during the study period.
    Matched MeSH terms: Henipavirus Infections/virology
  7. Luby SP, Gurley ES, Hossain MJ
    Clin Infect Dis, 2009 Dec 1;49(11):1743-8.
    PMID: 19886791 DOI: 10.1086/647951
    Nipah virus (NiV) is a paramyxovirus whose reservoir host is fruit bats of the genus Pteropus. Occasionally the virus is introduced into human populations and causes severe illness characterized by encephalitis or respiratory disease. The first outbreak of NiV was recognized in Malaysia, but 8 outbreaks have been reported from Bangladesh since 2001. The primary pathways of transmission from bats to people in Bangladesh are through contamination of raw date palm sap by bats with subsequent consumption by humans and through infection of domestic animals (cattle, pigs, and goats), presumably from consumption of food contaminated with bat saliva or urine with subsequent transmission to people. Approximately one-half of recognized Nipah case patients in Bangladesh developed their disease following person-to-person transmission of the virus. Efforts to prevent transmission should focus on decreasing bat access to date palm sap and reducing family members' and friends' exposure to infected patients' saliva.
    Matched MeSH terms: Henipavirus Infections/virology
  8. Lo MK, Rota PA
    J Clin Virol, 2008 Dec;43(4):396-400.
    PMID: 18835214 DOI: 10.1016/j.jcv.2008.08.007
    Nipah virus first emerged in Malaysia and Singapore between 1998 and 1999, causing severe febrile encephalitis in humans with a mortality rate of close to 40%. In addition, a significant portion of those recovering from acute infection had relapse encephalitis and long-term neurological defects. Since its initial outbreak, there have been numerous outbreaks in Bangladesh and India, in which the mortality rate rose to approximately 70%. These subsequent outbreaks were distinct from the initial outbreak, both in their epidemiology and in their clinical presentations. Recent developments in diagnostics may expedite disease diagnosis and outbreak containment, while progress in understanding the molecular biology of Nipah virus could lead to novel therapeutics and vaccines for this deadly pathogen.
    Matched MeSH terms: Henipavirus Infections/virology
  9. 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: Henipavirus Infections/virology
  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: Henipavirus Infections/virology*
  11. Olival KJ, Daszak P
    J Neurovirol, 2005 Oct;11(5):441-6.
    PMID: 16287685
    The authors review common themes in the ecology of emerging viruses that cause neurological disease. Three issues emerge. First, 49% of emerging viruses are characterized by encephalitis or serious neurological clinical symptoms. Second, all of these viruses are driven to emerge by ecological, environmental, or human demographic changes, some of which are poorly understood. Finally, the control of these viruses would be enhanced by collaborative multidisciplinary research into these drivers of emergence. The authors highlight this review with a case study of Nipah virus, which emerged in Malaysia due largely to shifts in livestock production and alterations to reservoir host habitat. Collaboration between virologists, ecologists, disease modelers and wildlife biologists has been instrumental in retracing the factors involved in this virus's emergence.
    Matched MeSH terms: Henipavirus Infections/virology*
  12. Wacharapluesadee S, Boongird K, Wanghongsa S, Ratanasetyuth N, Supavonwong P, Saengsen D, et al.
    Vector Borne Zoonotic Dis, 2010 Mar;10(2):183-90.
    PMID: 19402762 DOI: 10.1089/vbz.2008.0105
    After 12 serial Nipah virus outbreaks in humans since 1998, it has been noted that all except the initial event in Malaysia occurred during the first 5 months of the year. Increasingly higher morbidity and mortality have been observed in subsequent outbreaks in India and Bangladesh. This may have been related to different virus strains and transmission capability from bat to human without the need for an amplifying host and direct human-to-human transmission. A survey of virus strains in Pteropus lylei and seasonal preference for spillover of these viruses was completed in seven provinces of Central Thailand between May 2005 and June 2007. Nipah virus RNA sequences, which belonged to those of the Malaysian and Bangladesh strains, were detected in the urine of these bats, with the Bangladesh strain being dominant. Highest recovery of Nipah virus RNA was observed in May. Of two provincial sites where monthly surveys were done, the Bangladesh strain was almost exclusively detected during April to June. The Malaysian strain was found dispersed during December to June. Although direct contact during breeding (in December to April) was believed to be an important transmission factor, our results may not entirely support the role of breeding activities in spillage of virus. Greater virus shedding over extended periods in the case of the Malaysian strain and the highest peak of virus detection in May in the case of the Bangladesh strain when offspring started to separate may suggest that there may be responsible mechanisms other than direct contact during breeding in the same roost. Knowledge of seasonal preferences of Nipah virus shedding in P. lylei will help us to better understand the dynamics of Nipah virus transmission and have implications for disease management.
    Matched MeSH terms: Henipavirus Infections/virology
  13. Mbu'u CM, Mbacham WF, Gontao P, Sado Kamdem SL, Nlôga AMN, Groschup MH, et al.
    Vector Borne Zoonotic Dis, 2019 07;19(7):455-465.
    PMID: 30985268 DOI: 10.1089/vbz.2018.2365
    Nipah virus (NiV) and Hendra virus (HeV) are closely related members within the genus Henipavirus, family Paramyxoviridae, for which fruit bats serve as the reservoir. The initial emergence of NiV infections in pigs and humans in Malaysia, and HeV infections in horses and humans in Australia, posed severe impacts on human and animal health, and continues threatening lives of humans and livestock within Southeast Asia and Australia. Recently, henipavirus-specific antibodies have also been detected in fruit bats in a number of sub-Saharan African countries and in Brazil, thereby considerably increasing the known geographic distribution of henipaviruses. Africa is progressively being recognized as a new high prevalence zone for henipaviruses, as deduced from serological and molecular evidence of past infections in Madagascar, Ghana, Republic of Congo, Gulf of Guinea, Zambia, Tanzania, Cameroon, and Nigeria lately. Serological data suggest henipavirus spillover from bats to livestock and human populations in Africa without reported clinical disease in any of these species. All virus isolation attempts have been abortive, highlighting the need for further investigations. The genome of the Ghanaian bat henipavirus designated Ghana virus (GhV), which was detected in a pteropid Eidolon helvum bat, is the only African henipavirus that has been completely sequenced limiting our current knowledge on the genetic diversity and pathogenesis of African henipaviruses. In this review, we summarize the available data on the circulation of henipaviruses in Africa, discuss potential sources for virus spillover, and highlight existing research gaps.
    Matched MeSH terms: Henipavirus Infections/virology
  14. Mire CE, Satterfield BA, Geisbert JB, Agans KN, Borisevich V, Yan L, et al.
    Sci Rep, 2016 08 03;6:30916.
    PMID: 27484128 DOI: 10.1038/srep30916
    Nipah virus (NiV) is a paramyxovirus that causes severe disease in humans and animals. There are two distinct strains of NiV, Malaysia (NiVM) and Bangladesh (NiVB). Differences in transmission patterns and mortality rates suggest that NiVB may be more pathogenic than NiVM. To investigate pathogenic differences between strains, 4 African green monkeys (AGM) were exposed to NiVM and 4 AGMs were exposed to NiVB. While NiVB was uniformly lethal, only 50% of NiVM-infected animals succumbed to infection. Histopathology of lungs and spleens from NiVB-infected AGMs was significantly more severe than NiVM-infected animals. Importantly, a second study utilizing 11 AGMs showed that the therapeutic window for human monoclonal antibody m102.4, previously shown to rescue AGMs from NiVM infection, was much shorter in NiVB-infected AGMs. Together, these data show that NiVB is more pathogenic in AGMs under identical experimental conditions and suggests that postexposure treatments may need to be NiV strain specific for optimal efficacy.
    Matched MeSH terms: Henipavirus Infections/virology
  15. 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: Henipavirus Infections/virology*
  16. Lee JH, Hammoud DA, Cong Y, Huzella LM, Castro MA, Solomon J, et al.
    J Infect Dis, 2020 05 11;221(Suppl 4):S419-S430.
    PMID: 31687756 DOI: 10.1093/infdis/jiz502
    Nipah virus (NiV) is an emerging virus associated with outbreaks of acute respiratory disease and encephalitis. To develop a neurological model for NiV infection, we exposed 6 adult African green monkeys to a large-particle (approximately 12 μm) aerosol containing NiV (Malaysian isolate). Brain magnetic resonance images were obtained at baseline, every 3 days after exposure for 2 weeks, and then weekly until week 8 after exposure. Four of six animals showed abnormalities reminiscent of human disease in brain magnetic resonance images. Abnormalities ranged from cytotoxic edema to vasogenic edema. The majority of lesions were small infarcts, and a few showed inflammatory or encephalitic changes. Resolution or decreased size in some lesions resembled findings reported in patients with NiV infection. Histological lesions in the brain included multifocal areas of encephalomalacia, corresponding to known ischemic foci. In other regions of the brain there was evidence of vasculitis, with perivascular infiltrates of inflammatory cells and rare intravascular fibrin thrombi. This animal model will help us better understand the acute neurological features of NiV infection and develop therapeutic approaches for managing disease caused by NiV infection.
    Matched MeSH terms: Henipavirus Infections/virology*
  17. Prasad AN, Woolsey C, Geisbert JB, Agans KN, Borisevich V, Deer DJ, et al.
    J Infect Dis, 2020 05 11;221(Suppl 4):S436-S447.
    PMID: 32022850 DOI: 10.1093/infdis/jiz613
    BACKGROUND: The henipaviruses, Hendra virus (HeV) and Nipah virus (NiV), are capable of causing severe and often lethal respiratory and/or neurologic disease in animals and humans. Given the sporadic nature of henipavirus outbreaks, licensure of vaccines and therapeutics for human use will likely require demonstration of efficacy in animal models that faithfully reproduce the human condition. Currently, the African green monkey (AGM) best mimics human henipavirus-induced disease.

    METHODS: The pathogenic potential of HeV and both strains of NiV (Malaysia, Bangladesh) was assessed in cynomolgus monkeys and compared with henipavirus-infected historical control AGMs. Multiplex gene and protein expression assays were used to compare host responses.

    RESULTS: In contrast to AGMs, in which henipaviruses cause severe and usually lethal disease, HeV and NiVs caused only mild or asymptomatic infections in macaques. All henipaviruses replicated in macaques with similar kinetics as in AGMs. Infection in macaques was associated with activation and predicted recruitment of cytotoxic CD8+ T cells, Th1 cells, IgM+ B cells, and plasma cells. Conversely, fatal outcome in AGMs was associated with aberrant innate immune signaling, complement dysregulation, Th2 skewing, and increased secretion of MCP-1.

    CONCLUSION: The restriction factors identified in macaques can be harnessed for development of effective countermeasures against henipavirus disease.

    Matched MeSH terms: Henipavirus Infections/virology
  18. Yong MY, Lee SC, Ngui R, Lim YA, Phipps ME, Chang LY
    J Infect Dis, 2020 05 11;221(Suppl 4):S370-S374.
    PMID: 32392323 DOI: 10.1093/infdis/jiaa085
    Nipah virus (NiV) outbreak occurred in Malaysia in 1998. The natural host reservoir for NiV is Pteropus bats, which are commonly found throughout Malaysia. Humans become infected when NiV spills over from the reservoir species. In this study, NiV serosurveillance in Peninsular Malaysia, particularly among the indigenous population, was performed. The collected samples were tested for presence of NiV antibodies using a comparative indirect enzyme-linked immunosorbent assay based on the recombinant NiV nucleocapsid (rNiV-N) protein. We found that 10.73% of the participants recruited in this study had antibodies against rNiV-N, suggesting possible exposure to NiV.
    Matched MeSH terms: Henipavirus Infections/virology*
  19. 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*
  20. 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
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