A Review of Hendra Virus and Nipah Virus Infections in Man and Other Animals

2014 ◽  
pp. 997-1012 ◽  
Author(s):  
Kim Halpin ◽  
Paul Rota
Keyword(s):  
Nipah Virus ◽  
Hendra Virus ◽  
Virus Infections

scholarly journals Reactivity of Anti-Nipah Virus Monoclonal Antibodies to Formalin-fixed, Paraffin-embedded Lung Tissues from Experimental Nipah and Hendra Virus Infections

2004 ◽  
Vol 66 (10) ◽  
pp. 1263-1266 ◽  
Author(s):  
Nobuhiko TANIMURA ◽  
Tadao IMADA ◽  
Yoshihito KASHIWAZAKI ◽  
Shahirudin SHAMUSUDIN ◽  
Sharifah SYED HASSAN ◽  
...  
Keyword(s):  
Monoclonal Antibodies ◽  
Nipah Virus ◽  
Hendra Virus ◽  
Virus Infections ◽  
Formalin Fixed Paraffin ◽  
Formalin Fixed Paraffin Embedded ◽  
Formalin Fixed

scholarly journals Henipavirus infection of the central nervous system

2019 ◽  
Vol 77 (2) ◽  
Author(s):  
Brian E Dawes ◽  
Alexander N Freiberg
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Nipah Virus ◽  
Hendra Virus ◽  
Cns Infection ◽  
Virus Infections ◽  
Cell Infection ◽  
Brain Infection ◽  
Causative Agents

ABSTRACT Nipah virus (NiV) and Hendra virus are highly pathogenic zoonotic viruses of the genus Henipavirus, family Paramyxoviridae. These viruses were first identified as the causative agents of severe respiratory and encephalitic disease in the 1990s across Australia and Southern Asia with mortality rates reaching up to 75%. While outbreaks of Nipah and Hendra virus infections remain rare and sporadic, there is concern that NiV has pandemic potential. Despite increased attention, little is understood about the neuropathogenesis of henipavirus infection. Neuropathogenesis appears to arise from dual mechanisms of vascular disease and direct parenchymal brain infection, but the relative contributions remain unknown while respiratory disease arises from vasculitis and respiratory epithelial cell infection. This review will address NiV basic clinical disease, pathology and pathogenesis with a particular focus on central nervous system (CNS) infection and address the necessity of a model of relapsed CNS infection. Additionally, the innate immune responses to NiV infection in vitro and in the CNS are reviewed as it is likely linked to any persistent CNS infection.

scholarly journals Chloroquine Administration Does Not Prevent Nipah Virus Infection and Disease in Ferrets

2009 ◽  
Vol 83 (22) ◽  
pp. 11979-11982 ◽  
Author(s):  
Jackie Pallister ◽  
Deborah Middleton ◽  
Gary Crameri ◽  
Manabu Yamada ◽  
Reuben Klein ◽  
...  
Keyword(s):  
Virus Infection ◽  
Nipah Virus ◽  
Disease Outbreaks ◽  
Mortality Rates ◽  
Hendra Virus ◽  
Malaria Therapy ◽  
Sporadic Disease

ABSTRACT Hendra virus and Nipah virus, two zoonotic paramyxoviruses in the genus Henipavirus, have recently emerged and continue to cause sporadic disease outbreaks in humans and animals. Mortality rates of up to 75% have been reported in humans, but there are presently no clinically licensed therapeutics for treating henipavirus-induced disease. A recent report indicated that chloroquine, used in malaria therapy for over 70 years, prevented infection with Nipah virus in vitro. Chloroquine was assessed using a ferret model of lethal Nipah virus infection and found to be ineffective against Nipah virus infection in vivo.

scholarly journals A strategy to suppress STAT1 signalling conserved in pathogenic poxviruses and paramyxoviruses

2021 ◽  
Author(s):  
Callum Talbot-Cooper ◽  
Teodors Pantelejevs ◽  
John P. Shannon ◽  
Christian R. Cherry ◽  
Marcus T. Au ◽  
...  
Keyword(s):  
Sequence Similarity ◽  
Nipah Virus ◽  
Sh2 Domain ◽  
Binding Motif ◽  
Virus Infections ◽  
Stat Proteins ◽  
Interferon Stimulated Genes ◽  
Independent Mode ◽  
Insight Into ◽  
Diverse Virus

The induction of interferon-stimulated genes by signal transducer and activator of transcription (STAT) proteins, is a critical host defence to fight virus infections. Here, a highly expressed poxvirus protein 018 is shown to inhibit IFN-induced signalling by binding the SH2 domain of STAT1 to prevent STAT1 association with an activated IFN receptor. Despite the presence of additional inhibitors of IFN-induced signalling, a poxvirus lacking 018 was attenuated in mice. The 2.0-angstrom crystal structure of the 018:STAT1 complex reveals a mechanism for a high-affinity, pTyr-independent mode of binding to an SH2 domain. Furthermore, the STAT1 binding motif of 018 shows sequence similarity to the STAT1-binding proteins from Nipah virus, which like 018, block the association of STAT1 with an IFN receptor. Taken together, these results provide detailed mechanistic insight into a potent mode of STAT1 antagonism, found to exist in genetically diverse virus families.

scholarly journals From The Cover: Ephrin-B2 ligand is a functional receptor for Hendra virus and Nipah virus

2005 ◽  
Vol 102 (30) ◽  
pp. 10652-10657 ◽  
Author(s):  
M. I. Bonaparte ◽  
A. S. Dimitrov ◽  
K. N. Bossart ◽  
G. Crameri ◽  
B. A. Mungall ◽  
...  
Keyword(s):  
Nipah Virus ◽  
Hendra Virus ◽  
Functional Receptor

scholarly journals Hendra and Nipah Virus Infection in Cultured Human Olfactory Epithelial Cells

mSphere ◽  
2017 ◽  
Vol 2 (3) ◽  
Author(s):  
Viktoriya Borisevich ◽  
Mehmet Hakan Ozdener ◽  
Bilal Malik ◽  
Barry Rockx
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Olfactory Epithelium ◽  
Neurological Disease ◽  
Nipah Virus ◽  
Hendra Virus ◽  
Olfactory Neurons ◽  
Zoonotic Pathogens ◽  
The Central Nervous System ◽  
A Site

ABSTRACT Henipaviruses are emerging zoonotic pathogens that can cause acute and severe respiratory and neurological disease in humans. The pathways by which henipaviruses enter the central nervous system (CNS) in humans are still unknown. The observation that human olfactory neurons are highly susceptible to infection with henipaviruses demonstrates that the olfactory epithelium can serve as a site of Henipavirus entry into the CNS. Henipaviruses are emerging zoonotic viruses and causative agents of encephalitis in humans. However, the mechanisms of entry into the central nervous system (CNS) in humans are not known. Here, we evaluated the possible role of olfactory epithelium in virus entry into the CNS. We characterized Hendra virus (HeV) and Nipah virus (NiV) infection of primary human olfactory epithelial cultures. We show that henipaviruses can infect mature olfactory sensory neurons. Henipaviruses replicated efficiently, resulting in cytopathic effect and limited induction of host responses. These results show that human olfactory epithelium is susceptible to infection with henipaviruses, suggesting that this could be a pathway for neuroinvasion in humans. IMPORTANCE Henipaviruses are emerging zoonotic pathogens that can cause acute and severe respiratory and neurological disease in humans. The pathways by which henipaviruses enter the central nervous system (CNS) in humans are still unknown. The observation that human olfactory neurons are highly susceptible to infection with henipaviruses demonstrates that the olfactory epithelium can serve as a site of Henipavirus entry into the CNS.

scholarly journals Microsphere Suspension Array Assays for Detection and Differentiation of Hendra and Nipah Viruses

2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
Adam J. Foord ◽  
John R. White ◽  
Axel Colling ◽  
Hans G. Heine
Keyword(s):  
Human Health ◽  
Virus Type ◽  
Nipah Virus ◽  
Hendra Virus ◽  
Diagnostic Specificity ◽  
Suspension Array ◽  
Specificity And Sensitivity ◽  
Nucleoprotein N ◽  
Encoding Genes ◽  
Single Reaction

Microsphere suspension array systems enable the simultaneous fluorescent identification of multiple separate nucleotide targets in a single reaction. We have utilized commercially available oligo-tagged microspheres (Luminex MagPlex-TAG) to construct and evaluate multiplexed assays for the detection and differentiation of Hendra virus (HeV) and Nipah virus (NiV). Both these agents are bat-borne zoonotic paramyxoviruses of increasing concern for veterinary and human health. Assays were developed targeting multiple sites within the nucleoprotein (N) and phosphoprotein (P) encoding genes. The relative specificities and sensitivities of the assays were determined using reference isolates of each virus type, samples from experimentally infected horses, and archival veterinary diagnostic submissions. Results were assessed in direct comparison with an established qPCR. The microsphere array assays achieved unequivocal differentiation of HeV and NiV and the sensitivity of HeV detection was comparable to qPCR, indicating high analytical and diagnostic specificity and sensitivity.

scholarly journals Inhibition of henipavirus infection by Nipah virus attachment glycoprotein occurs without cell-surface downregulation of ephrin-B2 or ephrin-B3

2007 ◽  
Vol 88 (2) ◽  
pp. 582-591 ◽  
Author(s):  
Bevan Sawatsky ◽  
Allen Grolla ◽  
Nina Kuzenko ◽  
Hana Weingartl ◽  
Markus Czub
Keyword(s):  
Cell Surface ◽  
Nipah Virus ◽  
Functional Expression ◽  
Hendra Virus ◽  
Pcr Analysis ◽  
Protein G ◽  
Attachment Protein ◽  
Genetic Characteristics ◽  
Virus Attachment ◽  
Fusion Inhibition

Nipah virus (NiV) and Hendra virus (HeV) are newly identified members of the family Paramyxoviridae and have been classified in the new genus Henipavirus based on unique genetic characteristics distinct from other paramyxoviruses. Transgenic cell lines were generated that expressed either the attachment protein (G) or the fusion protein (F) of NiV. Functional expression of NiV F and G was verified by complementation with the corresponding glycoprotein, which resulted in the development of syncytia. When exposed to NiV and HeV, expression of NiV G in Crandall feline kidney cells resulted in a qualitative inhibition of both cytopathic effect (CPE) and cell death by both viruses. RT-PCR analysis of surviving exposed cells showed a complete absence of viral positive-sense mRNA and genomic negative-sense viral RNA. Cells expressing NiV G were also unable to fuse with cells co-expressing NiV F and G in a fluorescent fusion inhibition assay. Cell-surface staining for the cellular receptors for NiV and HeV (ephrin-B2 and ephrin-B3) indicated that they were located on the surface of cells, regardless of NiV G expression or infection by NiV. These results indicated that viral interference can be established for henipaviruses and requires only the expression of the attachment protein, G. Furthermore, it was found that this interference probably occurs at the level of virus entry, as fusion was not observed in cells expressing NiV G. Finally, expression of NiV G by either transient transfection or NiV infection did not alter the cell-surface levels of the two known viral receptors.

scholarly journals Determination of the henipavirus phosphoprotein gene mRNA editing frequencies and detection of the C, V and W proteins of Nipah virus in virus-infected cells

2009 ◽  
Vol 90 (2) ◽  
pp. 398-404 ◽  
Author(s):  
Michael K. Lo ◽  
Brian H. Harcourt ◽  
Bruce A. Mungall ◽  
Azaibi Tamin ◽  
Mark E. Peeples ◽  
...  
Keyword(s):  
Nipah Virus ◽  
Hendra Virus ◽  
Mrna Editing ◽  
C Protein ◽  
Reading Frame ◽  
Frame Sequence ◽  
P Gene ◽  
Infected Cells ◽  
Phosphoprotein Gene

The henipaviruses, Nipah virus (NiV) and Hendra virus (HeV), are highly pathogenic zoonotic paramyxoviruses. Like many other paramyxoviruses, henipaviruses employ a process of co-transcriptional mRNA editing during transcription of the phosphoprotein (P) gene to generate additional mRNAs encoding the V and W proteins. The C protein is translated from the P mRNA, but in an alternate reading frame. Sequence analysis of multiple, cloned mRNAs showed that the mRNA editing frequencies of the P genes of the henipaviruses are higher than those reported for other paramyxoviruses. Antisera to synthetic peptides from the P, V, W and C proteins of NiV were generated to study their expression in infected cells. All proteins were detected in both infected cells and purified virions. In infected cells, the W protein was detected in the nucleus while P, V and C were found in the cytoplasm.

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