Displaying publications 1 - 20 of 132 in total

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  1. Insurance and epidemics: SARS, West Nile virus and Nipah virus
    von Overbeck J
    J Insur Med, 2003;35(3-4):165-73.
    PMID: 14971089
    Severe acute respiratory syndrome (SARS) reminds us that sudden disease emergence is a permanent part of our world--and should be anticipated in our planning. Historically the emergence of new diseases has had little or no impact beyond a small, localized cluster of infections. However, given just the right conditions, a highly virulent pathogen can suddenly spread across time and space with massive consequences, as has occurred on several occasions in human history. In the wake of the SARS outbreak, we are now forced to confront the unpleasant fact that human activities are increasing the frequency and severity of these kinds of emergences. The idea of more frequent biological "invasions" with economic and societal impacts comparable to SARS, presents stakeholders in and the global economy with unprecedented new risks, challenges and even opportunities. As a major contributor to economic stability, the insurance industry must follow these trends very closely and develop scenarios to anticipate these events.
    Matched MeSH terms: Henipavirus Infections/epidemiology*; Henipavirus Infections/prevention & control
  2. Fulltext A single-dose ChAdOx1-vectored vaccine provides complete protection against Nipah Bangladesh and Malaysia in Syrian golden hamsters
    van Doremalen N, Lambe T, Sebastian S, Bushmaker T, Fischer R, Feldmann F, et al.
    PLoS Negl Trop Dis, 2019 06;13(6):e0007462.
    PMID: 31170144 DOI: 10.1371/journal.pntd.0007462
    Nipah virus (NiV) is a highly pathogenic re-emerging virus that causes outbreaks in South East Asia. Currently, no approved and licensed vaccine or antivirals exist. Here, we investigated the efficacy of ChAdOx1 NiVB, a simian adenovirus-based vaccine encoding NiV glycoprotein (G) Bangladesh, in Syrian hamsters. Prime-only as well as prime-boost vaccination resulted in uniform protection against a lethal challenge with NiV Bangladesh: all animals survived challenge and we were unable to find infectious virus either in oral swabs, lung or brain tissue. Furthermore, no pathological lung damage was observed. A single-dose of ChAdOx1 NiVB also prevented disease and lethality from heterologous challenge with NiV Malaysia. While we were unable to detect infectious virus in swabs or tissue of animals challenged with the heterologous strain, a very limited amount of viral RNA could be found in lung tissue by in situ hybridization. A single dose of ChAdOx1 NiVB also provided partial protection against Hendra virus and passive transfer of antibodies elicited by ChAdOx1 NiVB vaccination partially protected Syrian hamsters against NiV Bangladesh. From these data, we conclude that ChAdOx1 NiVB is a suitable candidate for further NiV vaccine pre-clinical development.
    Matched MeSH terms: Henipavirus Infections/immunology; Henipavirus Infections/prevention & control*
  3. Fulltext The Main Risk Factors of Nipah Disease and Its Risk Analysis in China
    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/epidemiology*; Henipavirus Infections/virology*
  4. Seroprevalence of Nipah Virus Infection in Peninsular Malaysia
    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/epidemiology*; Henipavirus Infections/virology*
  5. 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/prevention & control; Henipavirus Infections/virology*
  6. Fulltext Recombinant measles virus vaccine expressing the Nipah virus glycoprotein protects against lethal Nipah virus challenge
    Yoneda M, Georges-Courbot MC, Ikeda F, Ishii M, Nagata N, Jacquot F, et al.
    PLoS One, 2013;8(3):e58414.
    PMID: 23516477 DOI: 10.1371/journal.pone.0058414
    Nipah virus (NiV) is a member of the genus Henipavirus, which emerged in Malaysia in 1998. In pigs, infection resulted in a predominantly non-lethal respiratory disease; however, infection in humans resulted in over 100 deaths. Nipah virus has continued to re-emerge in Bangladesh and India, and person-to-person transmission appeared in the outbreak. Although a number of NiV vaccine studies have been reported, there are currently no vaccines or treatments licensed for human use. In this study, we have developed a recombinant measles virus (rMV) vaccine expressing NiV envelope glycoproteins (rMV-HL-G and rMV-Ed-G). Vaccinated hamsters were completely protected against NiV challenge, while the mortality of unvaccinated control hamsters was 90%. We trialed our vaccine in a non-human primate model, African green monkeys. Upon intraperitoneal infection with NiV, monkeys showed several clinical signs of disease including severe depression, reduced ability to move and decreased food ingestion and died at 7 days post infection (dpi). Intranasal and oral inoculation induced similar clinical illness in monkeys, evident around 9 dpi, and resulted in a moribund stage around 14 dpi. Two monkeys immunized subcutaneously with rMV-Ed-G showed no clinical illness prior to euthanasia after challenge with NiV. Viral RNA was not detected in any organ samples collected from vaccinated monkeys, and no pathological changes were found upon histopathological examination. From our findings, we propose that rMV-NiV-G is an appropriate NiV vaccine candidate for use in humans.
    Matched MeSH terms: Henipavirus Infections/mortality; Henipavirus Infections/prevention & control*
  7. Establishment of a Nipah virus rescue system
    Yoneda M, Guillaume V, Ikeda F, Sakuma Y, Sato H, Wild TF, et al.
    Proc Natl Acad Sci U S A, 2006 Oct 31;103(44):16508-13.
    PMID: 17053073
    Nipah virus (NiV), a paramyxovirus, was first discovered in Malaysia in 1998 in an outbreak of infection in pigs and humans and incurred a high fatality rate in humans. Fruit bats, living in vast areas extending from India to the western Pacific, were identified as the natural reservoir of the virus. However, the mechanisms that resulted in severe pathogenicity in humans (up to 70% mortality) and that enabled crossing the species barrier were not known. In this study, we established a system that enabled the rescue of replicating NiVs from a cloned DNA by cotransfection of a constructed full-length cDNA clone and supporting plasmids coding virus nucleoprotein, phosphoprotein, and polymerase with the infection of the recombinant vaccinia virus, MVAGKT7, expressing T7 RNA polymerase. The rescued NiV (rNiV), by using the newly developed reverse genetics system, showed properties in vitro that were similar to the parent virus and retained the severe pathogenicity in a previously established animal model by experimental infection. A recombinant NiV was also developed, expressing enhanced green fluorescent protein (rNiV-EGFP). Using the virus, permissibility of NiV was compared with the presence of a known cellular receptor, ephrin B2, in a number of cell lines of different origins. Interestingly, two cell lines expressing ephrin B2 were not susceptible for rNiV-EGFP, indicating that additional factors are clearly required for full NiV replication. The reverse genetics for NiV will provide a powerful tool for the analysis of the molecular mechanisms of pathogenicity and cross-species infection.
    Matched MeSH terms: Henipavirus Infections/genetics; Henipavirus Infections/metabolism; Henipavirus Infections/pathology*; Henipavirus Infections/virology*
  8. Fulltext A 'what-if' scenario: Nipah virus attacks pig trade chains in Thailand
    Wongnak P, Thanapongtharm W, Kusakunniran W, Karnjanapreechakorn S, Sutassananon K, Kalpravidh W, et al.
    BMC Vet Res, 2020 Aug 24;16(1):300.
    PMID: 32838786 DOI: 10.1186/s12917-020-02502-4
    BACKGROUND: Nipah virus (NiV) is a fatal zoonotic agent that was first identified amongst pig farmers in Malaysia in 1998, in an outbreak that resulted in 105 fatal human cases. That epidemic arose from a chain of infection, initiating from bats to pigs, and which then spilled over from pigs to humans. In Thailand, bat-pig-human communities can be observed across the country, particularly in the central plain. The present study therefore aimed to identify high-risk areas for potential NiV outbreaks and to model how the virus is likely to spread. Multi-criteria decision analysis (MCDA) and weighted linear combination (WLC) were employed to produce the NiV risk map. The map was then overlaid with the nationwide pig movement network to identify the index subdistricts in which NiV may emerge. Subsequently, susceptible-exposed-infectious-removed (SEIR) modeling was used to simulate NiV spread within each subdistrict, and network modeling was used to illustrate how the virus disperses across subdistricts.

    RESULTS: Based on the MCDA and pig movement data, 14 index subdistricts with a high-risk of NiV emergence were identified. We found in our infectious network modeling that the infected subdistricts clustered in, or close to the central plain, within a range of 171 km from the source subdistricts. However, the virus may travel as far as 528.5 km (R0 = 5).

    CONCLUSIONS: In conclusion, the risk of NiV dissemination through pig movement networks in Thailand is low but not negligible. The risk areas identified in our study can help the veterinary authority to allocate financial and human resources to where preventive strategies, such as pig farm regionalization, are required and to contain outbreaks in a timely fashion once they occur.

    Matched MeSH terms: Henipavirus Infections/epidemiology; Henipavirus Infections/transmission; Henipavirus Infections/veterinary*
  9. 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/complications; Henipavirus Infections/mortality; Henipavirus Infections/pathology*; Henipavirus Infections/virology
  10. 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/immunology; Henipavirus Infections/pathology*; Henipavirus Infections/virology
  11. Fulltext A golden hamster model for human acute Nipah virus infection
    Wong KT, Grosjean I, Brisson C, Blanquier B, Fevre-Montange M, Bernard A, et al.
    Am J Pathol, 2003 Nov;163(5):2127-37.
    PMID: 14578210 DOI: 10.1016/S0002-9440(10)63569-9
    A predominantly pig-to-human zoonotic infection caused by the novel Nipah virus emerged recently to cause severe morbidity and mortality in both animals and man. Human autopsy studies showed the pathogenesis to be related to systemic vasculitis that led to widespread thrombotic occlusion and microinfarction in most major organs especially in the central nervous system. There was also evidence of extravascular parenchymal infection, particularly near damaged vessels (Wong KT, Shieh WJ, Kumar S, Norain K, Abdullah W, Guarner J, Goldsmith CS, Chua KB, Lam SK, Tan CT, Goh KJ, Chong HT, Jusoh R, Rollin PE, Ksiazek TG, Zaki SR, Nipah Virus Pathology Working Group: Nipah virus infection: Pathology and pathogenesis of an emerging paramyxoviral zoonosis. Am J Pathol 2002, 161:2153-2167). We describe here a golden hamster (Mesocricetus auratus) model that appears to reproduce the pathology and pathogenesis of acute human Nipah infection. Hamsters infected by intranasal or intraperitoneal routes died within 9 to 29 days or 5 to 9 days, respectively. Pathological lesions were most severe and extensive in the hamster brain. Vasculitis, thrombosis, and more rarely, multinucleated endothelial syncytia, were found in blood vessels of multiple organs. Viral antigen and RNA were localized in both vascular and extravascular tissues including neurons, lung, kidney, and spleen, as demonstrated by immunohistochemistry and in situ hybridization, respectively. Paramyxoviral-type nucleocapsids were identified in neurons and in vessel walls. At the terminal stage of infection, virus and/or viral RNA could be recovered from most solid organs and urine, but not from serum. The golden hamster is proposed as a suitable model for further studies including pathogenesis studies, anti-viral drug testing, and vaccine development against acute Nipah infection.
    Matched MeSH terms: Henipavirus Infections/mortality; Henipavirus Infections/pathology*
  12. Fulltext Emerging epidemic viral encephalitides with a special focus on henipaviruses
    Wong KT
    Acta Neuropathol, 2010 Sep;120(3):317-25.
    PMID: 20652579 DOI: 10.1007/s00401-010-0720-z
    In the last few decades, there is an increasing emergence and re-emergence of viruses, such as West Nile virus, Enterovirus 71 and henipaviruses that cause epidemic viral encephalitis and other central nervous system (CNS) manifestations. The mortality and morbidity associated with these outbreaks are significant and frequently severe. While aspects of epidemiology, basic virology, etc., may be known, the pathology and pathogenesis are often less so, partly due to a lack of interest among pathologists or because many of these infections are considered "third world" diseases. In the study of epidemic viral encephalitis, the pathologist's role in unravelling the pathology and pathogenesis is critical. The novel henipavirus infection is a good example. The newly created genus Henipavirus within the family Paramyxoviridae consists of two viruses, viz., Hendra virus and Nipah virus. These two viruses emerged in Australia and Asia, respectively, to cause severe encephalitides in humans and animals. Studies show that the pathological features of the acute encephalitis caused by henipaviruses are similar and a unique dual pathogenetic mechanism of vasculitis-induced microinfarction and parenchymal cell infection in the CNS (mainly neurons) and other organs causes severe tissue damage. Both viruses can cause relapsing encephalitis months and years after the acute infection due to a true recurrent infection as evidenced by the presence of virus in infected cells. Future emerging viral encephalitides will no doubt continue to pose considerable challenges to the neuropathologist, and as the West Nile virus outbreak demonstrates, even economically advanced nations are not spared.
    Matched MeSH terms: Henipavirus Infections/epidemiology*; Henipavirus Infections/pathology*
  13. Henipaviruses: a new family of emerging Paramyxoviruses
    Wild TF
    Pathol. Biol., 2009 Mar;57(2):188-96.
    PMID: 18511217 DOI: 10.1016/j.patbio.2008.04.006
    Paramyxoviruses have been implicated in both animal and human infections. Some viruses, such as Morbilliviruses are responsible for large-scale epidemics. However, there are limited observations of these viruses crossing the host species barrier in nature. In 1994, in Australia a fatal infection in horses and humans was identified to be caused by a new Paramyxovirus, Hendra virus (HeV), and in 1998 in Malaysia, a closely related virus, Nipah virus (NiV) was responsible for fatal infections in pigs and humans. These two viruses were sufficiently different from previously described Paramyxoviruses to create a new genus, Henipaviruses. The natural reservoir of these viruses was the fruit bat (Pteropus), which is found in regions extending from the western Pacific to the eastern coast of Africa. Serological studies have established that as many as half the fruit bats in colonies throughout these regions may have antibodies against this family of viruses. The availability of diagnostic reagents for Nipah virus in humans have identified infections in several countries including, Bangladesh, India and Indonesia. In some of these epidemics, mortality in humans exceeds 75%. Deforestation is probably responsible for fruit bats leaving their ecological niches and approaching farms and villages. The infection of humans and animals may occur via contaminated foods or in certain cases by animals to man. At present, only within close families has human-to-human transmission been proposed. Henipavirus infections are probably more widespread than it is at presently known and so it is important to have an intense monitoring for these diseases, especially in countries where large-scale deforestation is happening.
    Matched MeSH terms: Henipavirus/isolation & purification*; Henipavirus/pathogenicity; Henipavirus Infections/epidemiology*; Henipavirus Infections/veterinary
  14. Recombinant nipah virus vaccines protect pigs against challenge
    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: Henipavirus Infections/veterinary*
  15. Fulltext A VLP-based vaccine provides complete protection against Nipah virus challenge following multiple-dose or single-dose vaccination schedules in a hamster model
    Walpita P, Cong Y, Jahrling PB, Rojas O, Postnikova E, Yu S, et al.
    NPJ Vaccines, 2017;2:21.
    PMID: 29263876 DOI: 10.1038/s41541-017-0023-7
    Nipah virus is a highly lethal zoonotic paramyxovirus that was first recognized in Malaysia during an outbreak in 1998. During this outbreak, Nipah virus infection caused a severe febrile neurological disease in humans who worked in close contact with infected pigs. The case fatality rate in humans was approximately 40%. Since 2001, NiV has re-emerged in Bangladesh and India where fruit bats (Pteropus spp.) have been identified as the principal reservoir of the virus. Transmission to humans is considered to be bat-to-human via food contaminated with bat saliva, or consumption of contaminated raw date palm sap, although human-to-human transmission of Nipah virus has also been documented. To date, there are no approved prophylactic options or treatment for NiV infection. In this study, we produced mammalian cell-derived native Nipah virus-like particles composed of Nipah virus G, F and M proteins for use as a novel Nipah virus vaccine. Previous studies demonstrated that the virus-like particles were structurally similar to authentic virus, functionally assembled and immunoreactive. In the studies reported here, purified Nipah virus-like particles were utilized either alone or with adjuvant to vaccinate golden Syrian hamsters with either three-dose or one-dose vaccination regimens followed by virus challenge. These studies found that Nipah virus-like particle immunization of hamsters induced significant neutralizing antibody titers and provided complete protection to all vaccinated animals following either single or three-dose vaccine schedules. These studies prove the feasibility of a virus-like particle-based vaccine for protection against Nipah virus infection.
    Matched MeSH terms: Henipavirus Infections
  16. Fulltext Molecular characterization of Nipah virus from Pteropus hypomelanus in Southern Thailand
    Wacharapluesadee S, Samseeneam P, Phermpool M, Kaewpom T, Rodpan A, Maneeorn P, et al.
    Virol J, 2016;13(1):53.
    PMID: 27016237 DOI: 10.1186/s12985-016-0510-x
    Nipah virus (NiV) first emerged in Malaysia in 1998, with two bat species (Pteropus hypomelanus and P. vampyrus) as the putative natural reservoirs. In 2002, NiV IgG antibodies were detected in these species from Thailand, but viral RNA could not be detected for strain characterization. Two strains of NiV (Malaysia and Bangladesh) have been found in P. lylei in central Thailand, although Bangladesh strain, the causative strain for the outbreak in Bangladesh since 2001, was dominant. To understand the diversity of NiV in Thailand, this study identified NiV strain, using molecular characterizations, from P. hypomelanus in southern Thailand.
    Matched MeSH terms: Henipavirus Infections
  17. A longitudinal study of the prevalence of Nipah virus in Pteropus lylei bats in Thailand: evidence for seasonal preference in disease transmission
    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/epidemiology; Henipavirus Infections/transmission; Henipavirus Infections/veterinary*; Henipavirus Infections/virology
  18. Nipah Virus Infection of Immature Dendritic Cells Increases Its Transendothelial Migration Across Human Brain Microvascular Endothelial Cells
    Tiong V, Shu MH, Wong WF, AbuBakar S, Chang LY
    Front Microbiol, 2018;9:2747.
    PMID: 30483242 DOI: 10.3389/fmicb.2018.02747
    Nipah virus (NiV) can infect multiple organs in humans with the central nervous system (CNS) being the most severely affected. Currently, it is not fully understood how NiV spreads throughout the body. NiV has been shown to infect certain leukocyte populations and we hypothesized that these infected cells could cross the blood-brain barrier (BBB), facilitating NiV entry into the CNS. Here, three leukocyte types, primary immature dendritic cells (iDC), primary monocytes (pMO), and monocytic cell line (THP-1), were evaluated for permissiveness to NiV. We found only iDC and THP-1 were permissive to NiV. Transendothelial migration of mock-infected and NiV-infected leukocytes was then evaluated using an in vitro BBB model established with human brain microvascular endothelial cells (HBMEC). There was approximately a threefold increase in migration of NiV-infected iDC across endothelial monolayer when compared to mock-infected iDC. In contrast, migration rates for pMO and THP-1 did not change upon NiV infection. Across TNF-α-treated endothelial monolayer, there was significant increase of almost twofold in migration of NiV-infected iDC and THP-1 over mock-infected cells. Immunofluorescence analysis showed the migrated NiV-infected leukocytes retained their ability to infect other cells. This study demonstrates for the first time that active NiV infection of iDC and THP-1 increased their transendothelial migration activity across HBMEC and activation of HBMEC by TNF-α further promoted migration. The findings suggest that NiV infection of leukocytes to disseminate the virus via the "Trojan horse" mechanism is a viable route of entry into the CNS.
    Matched MeSH terms: Henipavirus Infections
  19. Advances in diagnostics, vaccines and therapeutics for Nipah virus
    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: Henipavirus Infections/diagnosis*; Henipavirus Infections/epidemiology; Henipavirus Infections/prevention & control*; Henipavirus Infections/therapy
  20. Monoclonal antibody-based immunohistochemical diagnosis of Malaysian Nipah virus infection in pigs
    Tanimura N, Imada T, Kashiwazaki Y, Shahirudin S, Sharifah SH, Aziz AJ
    J Comp Pathol, 2004 Aug-Oct;131(2-3):199-206.
    PMID: 15276859
    Formalin-fixed, paraffin wax-embedded tissues of three Malaysian farm pigs naturally infected with Nipah virus were used to investigate the value of anti-Nipah virus mouse monoclonal antibodies (Mabs) and rabbit polyclonal antibody for immunohistochemical diagnosis. Mabs 11F6 and 12A5 gave intense immunolabelling in lung tissue that had been fixed in 10% neutral buffered formalin for about 4 years, whereas the reactivity of Mabs 13A5 and 18C4 and polyclonal antibody was reduced significantly by long-term formalin fixation. Immunohistochemical examination of Malaysian farm pig samples with Mab 11F6 confirmed the affinity of Nipah virus for respiratory epithelium, renal glomerular and tubular epithelium, meningeal arachnoidal cells, and systemic vascular endothelium and smooth muscle. In addition, Nipah virus antigens were identified in laryngeal epithelial cells, Schwann cells of peripheral nerve fascicles in the spleen, and endothelial cells in the atrioventricular valve. The study demonstrated the value of Mabs 11F6 and 12A5 for the immunohistochemical diagnosis of Nipah virus infection in pigs.
    Matched MeSH terms: Henipavirus Infections/diagnosis*; Henipavirus Infections/immunology; Henipavirus Infections/veterinary*
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