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At least 19 recordsLinked to original sources

PubMed2005

Production and characterization of monoclonal antibodies against binary ethylenimine inactivated Nipah virus.

Nipah virus, a zoonotic paramyxovirus which emerged recently was chemically inactivated using binary ethylenimine (BEI). The inactivated virus was concentrated and purified by sucrose gradient centrifugation. The gradient fractions were examined by electron microscopy and Western immunoblot, and gradient fraction containing mainly Nipah matrix (M) and nucleocapsid (N) proteins was used for immunizing BALB/c mice to generate hybridomas. Screening of the resultant hybridoma clones identified five strongly positive clones producing IgG monoclonal antibodies (mAbs) reactive to the Nipah virus antigen. The protein specificity of these mAbs was determined by Western immunoblot using Nipah virus and recombinant Nipah virus proteins expressed in mammalian cells. Four mAbs reacted with Nipah N protein and one reacted with Nipah M protein. None of the mAbs neutralized Nipah virus infectivity in vitro. However, all mAbs recognized Nipah virus in ELISA and immunofluorescence assay. F45G2 mAb was most suitable for immunohistochemistry on long term formalin-fixed Nipah virus infected swine tissues. Three of the anti-nucleocapsid mAbs (F45G2, F45G3 and F45G6) showed cross-reactivity with closely related Hendra virus N protein in both immunofluorescence and Western Immunoblot assays. Two of the mAbs were specific for the Nipah virus only, F45G4 (anti-N) and F45G5 (anti-M), and could be used in the primary identification of Nipah virus. The use of these immunoreagents to develop new diagnostic assays is discussed.

Animals↗

PubMed2005

Invasion of the central nervous system in a porcine host by nipah virus.

Nipah virus, a newly emerged zoonotic paramyxovirus, infects a number of species. Human infections were linked to direct contact with pigs, specifically with their body fluids. Clinical signs in human cases indicated primarily involvement of the central nervous system, while in pigs the respiratory system was considered the primary virus target, with only rare involvement of the central nervous system. Eleven 5-week-old piglets were infected intranasally, orally, and ocularly with 2.5 x 10(5) PFU of Nipah virus per animal and euthanized between 3 and 8 days postinoculation. Nipah virus caused neurological signs in two out of eleven inoculated pigs. The rest of the pigs remained clinically healthy. Virus was detected in the respiratory system (turbinates, nasopharynx, trachea, bronchus, and lung in titers up to 10(5.3) PFU/g) and in the lymphoreticular system (endothelial cells of blood and lymphatic vessels, submandibular and bronchiolar lymph nodes, tonsil, and spleen with titers up to 10(6) PFU/g). Virus presence was confirmed in the nervous system of both sick and apparently healthy animals (cranial nerves, trigeminal ganglion, brain, and cerebrospinal fluid, with titers up to 10(7.7) PFU/g of tissue). Nipah virus distribution was confirmed by immunohistochemistry. The study presents novel findings indicating that Nipah virus invaded the central nervous system of the porcine host via cranial nerves as well as by crossing the blood-brain barrier after initial virus replication in the upper respiratory tract.

Animals↗

PubMed2004

Host evasion by emerging paramyxoviruses: Hendra virus and Nipah virus v proteins inhibit interferon signaling.

Interferon (IFN) can activate Signal Transducer and Activator of Transcription (STAT) proteins to establish a cellular antiviral response and inhibit virus replication. Many viruses have evolved strategies to inhibit this antiviral mechanism, but paramyxoviruses are unique in their abilities to directly target the IFN-responsive STAT proteins. Hendra virus and Nipah virus (Henipaviruses) are recently emerged paramyxoviruses that are the causative agents of fatal disease outbreaks in Australia and peninsular Malaysia. Similar to other paramyxoviruses, Henipaviruses inhibit IFN signal transduction through a virus-encoded protein called V. Recent studies have shown that Henipavirus V proteins target STAT proteins by inducing the formation of cytoplasmically localized high molecular weight STAT-containing complexes. This sequestration of STAT1 and STAT2 prevents STAT activation and blocks antiviral IFN signaling. As the V proteins are important factors for host evasion, they represent logical targets for therapeutics directed against Henipavirus epidemics.

Antigens, Viral↗

PubMed2002

Functional properties of the fusion and attachment glycoproteins of Nipah virus.

Nipah virus (NV) and Hendra virus (HV) are recently emergent, related viruses that can cause severe disease in humans and animals. The goal of this study was to investigate the immunogenic and functional properties of the fusion (F) and attachment (G) glycoproteins of NV. Vaccination of mice with recombinant vaccinia viruses (rVVs) expressing either the F (rVV/NV-F) or G (rVV/NV-G) proteins of NV induced neutralizing antibody responses to NV, with higher titers produced after vaccination with rVV/NV-G. When the homologous pairs of F and G proteins from either HV or NV were coexpressed in a transient expression system, fusion was detected in less than 12 h. An equivalent amount of fusion was observed when the heterologous pairs of F and G proteins from HV and NV were coexpressed. Membrane fusion was inhibited by antiserum from mice vaccinated with rVV/NV-G and rVV/NV-F. Therefore, as with other paramyxoviruses, the membrane glycoproteins of NV are the targets of neutralizing antibodies and membrane fusion mediated by NV requires the presence of both the F and the G proteins. Data from these biological assays support the taxonomic grouping of both HV and NV in the new genus, Henipavirus, within the family Paramyxoviridae.

Animals↗

PubMed2005

Ephrin-B2 ligand is a functional receptor for Hendra virus and Nipah virus.

Hendra virus (HeV) and Nipah virus (NiV) belong to the genus Henipavirus of the family Paramyxoviridae and are unique in that they exhibit a broad species tropism and cause fatal disease in both animals and humans. They infect cells through a pH-independent membrane fusion process mediated by their fusion and attachment glycoproteins. Previously, we demonstrated identical cell fusion tropisms for HeV and NiV and the protease-sensitive nature of their unknown cell receptor and identified a human cell line (HeLa-USU) that was nonpermissive for fusion and virus infection. Here, a microarray analysis was performed on the HeLa-USU cells, permissive HeLa-CCL2 cells, and two other permissive human cell lines. From this analysis, we identified a list of genes encoding known and predicted plasma membrane surface-expressed proteins that were highly expressed in all permissive cells and absent from the HeLa-USU cells and rank-ordered them based on their relative levels. Available expression vectors containing the first 10 genes were obtained and individually transfected into HeLa-USU cells. One clone, encoding human ephrin-B2 (EFNB2), was found capable of rendering HeLa-USU cells permissive for HeV- and NiV-mediated cell fusion as well as infection by live virus. A soluble recombinant EFNB2 could potently block fusion and infection and bind soluble recombinant HeV and NiV attachment glycoproteins with high affinity. Together, these data indicate that EFNB2 serves as a functional receptor for both HeV and NiV. The highly conserved nature of EFNB2 in humans and animals is consistent with the broad tropism exhibited by these emerging zoonotic viruses.

Ephrin-B2↗

PubMed2001

Ultrastructure of Hendra virus and Nipah virus within cultured cells and host animals.

The ultrastructure of Hendra and Nipah viruses is described in cultured cells, pigs, horses and humans. Differences in ultrastructure between the viruses are evident within infected cell cultures and lungs from infected amplifier hosts. These differences are important in viral identification and differentiation and understanding the pathogenesis of disease.

Animals↗

PubMed2003

Insurance and epidemics: SARS, West Nile virus and Nipah virus.

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.

China↗

PubMed2001

The presence of Nipah virus in respiratory secretions and urine of patients during an outbreak of Nipah virus encephalitis in Malaysia.

OBJECTIVES: To study the excretion of Nipah virus in the upper respiratory secretions and urine of infected patients in relation to other clinical features. METHODS: Isolation of Nipah virus from the respiratory secretions and urine was made in Vero cells and identified by indirect immunofluorescence assay using anti-Hendra specific hyperimmune mouse ascitic fluid and FITC-conjugated goat anti-mouse IgG. RESULTS: During the peak outbreak of Nipah virus encephalitis in Malaysia, Nipah virus was isolated from the upper respiratory secretions and urine in eight of 20 patients who were virologically and/or serologically confirmed to be infected with the virus. From these eight patients, Nipah virus was isolated from six throat swab specimens, three urine specimens and only one nasal swab specimen. The positive virus isolation rate was related to the collection of these specimens during the early phase of the illness (P = 0.068). The presence of serum anti-Nipah specific IgM appeared to reduce the chance of isolating the virus (P = 0.049). There was no significant difference in the isolation rate with respect to the age, gender, ethnic group and clinical features associated with grave prognosis and mortality outcome of the patients. CONCLUSION: This study shows that it is possible to be infected from secretions of infected patients, but epidemiological survey on close contacts so far did not suggest that human-to-human transmission is common.

Adolescent↗

PubMed2000

Nipah virus: a recently emergent deadly paramyxovirus.

A paramyxovirus virus termed Nipah virus has been identified as the etiologic agent of an outbreak of severe encephalitis in people with close contact exposure to pigs in Malaysia and Singapore. The outbreak was first noted in late September 1998 and by mid-June 1999, more than 265 encephalitis cases, including 105 deaths, had been reported in Malaysia, and 11 cases of encephalitis or respiratory illness with one death had been reported in Singapore. Electron microscopic, serologic, and genetic studies indicate that this virus belongs to the family Paramyxoviridae and is most closely related to the recently discovered Hendra virus. We suggest that these two viruses are representative of a new genus within the family Paramyxoviridae. Like Hendra virus, Nipah virus is unusual among the paramyxoviruses in its ability to infect and cause potentially fatal disease in a number of host species, including humans.

Animals↗

PubMed2005

[Nipah virus infections].

Nipah virus (NiV) is a zoonotic paramyxovirus that was first recognized in 1999 as the causative agent of outbreaks of human encephalitis in Malaysia and Singapore, in association with severe respiratory and neurological disease in pigs. Since then, outbreaks of NiV encephalitis have also occurred in Bangladesh during 2001-2004, but without an association to infected swine or other animals. Although NiV infections typically result in acute encephalitis with high mortality, other clinical manifestations, including asymptomatic infection, relapsed encephalitis, and pulmonary disease, have been observed. The article will summarize the virology, epidemiology, clinical features, treatment, and control and prevention of NiV infections in humans.

Animals↗

PubMed2004

[Nipah virus infection].

Nipah virus (NiV), emerged in Peninsular Malaysia, caused an outbreak of severe febrile encephalitis in humans and respiratory diseases in pigs between 1998 and 1999. By May of 1999, the death of 105 humans and the culling of about 1.1 million pigs were reported. Fruitbats of Pteropid species were identified as the natural reservoir hosts. The epidemiological studies suggested that NiV was introduced into pig farms by fruitbats, and was than transmitted to humans (mainly pig farmers) and other animals such as dogs, cats and horses. In 2004, NiV reappeared in Bangladesh with greater lethality. In contrast to the Malaysia case, epidemiologic characteristics of this outbreak suggested the possibility of fruitbats-to-person, or person-to-person transmission. In this article, the epidemiological comparison between two outbreaks in Malaysia and Bangladesh, and the new-trends of virological studies of NiV will be discussed.

Animals↗

PubMed2005

Endocytosis of the Nipah virus glycoproteins.

Nipah virus (NiV), a highly pathogenic member of the family Paramyxoviridae, encodes the surface glycoproteins F and G. Since internalization of the NiV envelope proteins from the cell surface might be of functional importance for viral pathogenesis either by regulating cytopathogenicity or by modulating recognition of infected cells by the immune system, we analyzed the endocytosis of the NiV F and G proteins. Interestingly, we found both glycoproteins to be internalized in infected and transfected cells. As endocytosis is normally mediated by tyrosine- or dileucine-dependent signals in the cytoplasmic tails of transmembrane proteins, all potential internalization signals in the NiV glycoproteins were mutated. Whereas the G protein appeared to be constitutively internalized with the bulk flow during membrane turnover, uptake of the F protein was found to be signal mediated. F endocytosis clearly depended on a membrane-proximal YXXPhi motif and was found to be of functional importance for the biological activity of the protein.

Amino Acid Motifs↗

PubMed2006

[Generation of recombinant vaccinia virus expressing attachment glycoprotein of Nipah virus].

The mammalian condon optimized G gene was synthesized by over-lapping PCR and used to generate recombinant vaccinia virus, rWR-NiV-G. The expression of Nipah virus G protein in rWR-NiV-G infected HeLa cells was confirmed by western-blot with NiV G protein specific mouse antiserum generated by DNA immunization.The recombinant G protein showed sensitive and specific antigenic reaction to rabbit serum anti-Nipah virus in indirect florescence. Syncytium formation was induced in BHK cells by rWR-NiV-G infection following NiV F protein expressing plasmid pCAGG-NiV-F transfection. Immunization with rWR-NiV-G elicited G protein specific antibody responses in mice. The prokaryotic expressing G protein fragment showed sensitive and specific antigenic reaction to NiV G protein specific antibody from rWR-NiV-G immunized mice serum in indirect ELISA. Furthermore, the G protein specific antibodies could neutralize the infectivity of the recombinant Vesicular Stomatitis Virus pseudotype VSVAG * F/G, in which the VSV envelope protein G gene was replaced with the green fluorescent protein gene (VSVAG * G, Whitt MA) and complemented with Nipah virus F and G glycoprotein expressed in transient (VSVAG * F/G).The results here demonstrated the G protein expressed by rWR-NiV-G keeps native immunogenicity and biological activity. The recombinant virus could be promising vaccine strategy for the prevention of Nipah virus.

Animals↗

PubMed2001

Serological examination for evidence of infection with Hendra and Nipah viruses in Queensland piggeries.

OBJECTIVE: To examine piggeries in Queensland for evidence of infection with Hendra virus and Nipah virus. DESIGN: A serological survey was designed to provide 99% confidence of detecting at least one infected pig herd in Queensland, assuming that for each virus, at least 5% of herds would have been exposed to virus and that at least 40% of the finisher pigs in these herds would have detectable antibodies to virus. PROCEDURE: A two stage sampling regimen was used. All samples were tested with serum neutralisation tests developed and performed at the Australian Animal Health Laboratory. RESULTS: There was no evidence of antibody to either virus in the 500 samples collected from 100 herds. CONCLUSION: The results of the survey support a case that commercial pigs in Queensland are free of both Hendra virus and Nipah virus infections.

Animals↗

PubMed2004

Isolation and molecular identification of Nipah virus from pigs.

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.

Animals↗

PubMed2003

Late clinical and magnetic resonance imaging follow up of Nipah virus infection.

The Nipah virus is a newly identified paramyxovirus responsible for an outbreak of fatal encephalitis in Malaysia and Singapore. This paper reports the follow up clinical and magnetic resonance imaging findings in 22 affected subjects. Of 13 patients with encephalitis, one died, one was lost to follow up, and seven recovered. Among the four remaining patients, one had residual sixth nerve palsy, another suffered from severe clinical depression, and a third patient had evidence of retinal artery occlusion. One patient with delayed onset Horner syndrome had a single lesion in the cervical spinal cord. The brain magnetic resonance findings were stable or improved in nine patients over 18 months of follow up. Among a second group of nine asymptomatic seropositive abattoir workers, magnetic resonance examination in seven subjects revealed discrete small lesions in the brain; similar to those detected in encephalitis patients. These findings suggest that in addition to encephalitis, the newly discovered Nipah virus affects the spinal cord and the retina. Late clinical and radiological findings can occur in Nipah virus infections as with other paramyxoviruses.

Abducens Nerve Diseases↗

PubMed2006

Quantitative estimation of Nipah virus replication kinetics in vitro.

BACKGROUND: 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. RESULTS: The qRT-PCR had a dynamic range of at least seven orders of magnitude and can detect Nipah virus from as low as one PFU/microL. Following initiation of infection, it was estimated that Nipah virus RNA doubles at every approximately 40 minutes and attained peak intracellular virus RNA level of approximately 8.4 log PFU/microL at about 32 hours post-infection (PI). Significant extracellular Nipah virus RNA release occurred only after 8 hours PI and the level peaked at approximately 7.9 log PFU/microL at 64 hours PI. The estimated rate of Nipah virus RNA released into the cell culture medium was approximately 0.07 log PFU/muL per hour and less than 10% of the released Nipah virus RNA was infectious. CONCLUSION: The SYBR Green I-based qRT-PCR assay enabled quantitative assessment of Nipah virus RNA synthesis in Vero cells. A low rate of Nipah virus extracellular RNA release and low infectious virus yield together with extensive syncytial formation during the infection support a cell-to-cell spread mechanism for Nipah virus infection.

Animals↗

PubMed2006

Hendra and Nipah viruses: different and dangerous.

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.

Animals↗