Nipah Virus Encephalitis Reemergence, Bangladesh

Hsu, Vincent; Hossain, M. Jahangir; Parashar, Umesh D.; Ali, Mohammed Monsur; Ksiazek, Thomas G.; Kuzmin, Ivan V.; Niezgoda, Michael; Rupprecht, Charles E.; Bresee, Joseph S.; Breiman, Robert F.

doi:10.3201/eid1012.040701

Cited by 481 publications

(439 citation statements)

References 15 publications

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“…In the Naogaon (Bangladesh) investigation, 2 of 19 P. giganteus specimens had antibody against NiV. None of 31 other animals from various species had Nipah antibodies [39].…”

Section: Historical Backgroundmentioning

confidence: 99%

“…Investigation of different Nipah outbreaks in Bangladesh have identified different routes of transmission including climbing trees (probably contaminated with infected date palm sap), contact with sick persons, and contact with sick animals [39,[44][45][46]68]. Another way of NiV getting transmitted from P. giganteus to humans recorded in Bangladesh is food-borne.…”

Section: The Transmission Route Of Nipah Virusmentioning

confidence: 99%

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Nipah virus infection: current scenario

et al. 2013

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“…In the Naogaon (Bangladesh) investigation, 2 of 19 P. giganteus specimens had antibody against NiV. None of 31 other animals from various species had Nipah antibodies [39].…”

Section: Historical Backgroundmentioning

confidence: 99%

Section: The Transmission Route Of Nipah Virusmentioning

confidence: 99%

Nipah virus infection: current scenario

et al. 2013

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“…NiV was first identified in Malaysia in 1998 during an outbreak of neurological and respiratory disease in swine, which resulted in severe febrile encephalitis in humans who had contact with infected pigs (Chua et al, 2000). NiV has been associated with subsequent outbreaks of fatal, febrile encephalitis in Bangladesh and India between (Hsu et al, 2004Luby et al, 2006). Molecular characterization of NiV revealed that it was related closely to Hendra virus, another zoonotic paramyxovirus, which had emerged in Australia in 1994 (Chua et al, 2000;Harcourt et al, 2000Harcourt et al, , 2001.…”

Section: Introductionmentioning

confidence: 99%

The C, V and W proteins of Nipah virus inhibit minigenome replication

Sleeman

Bankamp

Hummel

et al. 2008

Journal of General Virology

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Nipah virus (NiV) is a recently emergent, highly pathogenic, zoonotic paramyxovirus of the genus Henipavirus. Like the phosphoprotein (P) gene of other paramyxoviruses, the P gene of NiV is predicted to encode three additional proteins, C, V and W. When the C, V and W proteins of NiV were tested for their ability to inhibit expression of the chloramphenicol acetyltransferase (CAT) reporter gene in plasmid-based, minigenome replication assays, each protein inhibited CAT expression in a dose-dependent manner. The C, V and W proteins of NiV also inhibited expression of CAT from a measles virus (MV) minigenome, but not from a human parainfluenzavirus 3 (hPIV3) minigenome. Interestingly, the C and V proteins of MV, which have previously been shown to inhibit MV minigenome replication, also inhibited NiV minigenome replication; however, they were not able to inhibit hPIV3 minigenome replication. In contrast, the C protein of hPIV3 inhibited minigenome replication of hPIV3, NiV and MV. Although there is very limited amino acid sequence similarity between the C, V and W proteins within the paramyxoviruses, the heterotypic inhibition of replication suggests that these proteins may share functional properties. INTRODUCTIONNipah virus (NiV) is a recently emergent, highly pathogenic, zoonotic paramyxovirus. NiV was first identified in Malaysia in 1998 during an outbreak of neurological and respiratory disease in swine, which resulted in severe febrile encephalitis in humans who had contact with infected pigs (Chua et al., 2000). NiV has been associated with subsequent outbreaks of fatal, febrile encephalitis in Bangladesh and India between (Hsu et al., 2004Luby et al., 2006). Molecular characterization of NiV revealed that it was related closely to Hendra virus, another zoonotic paramyxovirus, which had emerged in Australia in 1994 (Chua et al., 2000;Harcourt et al., 2000Harcourt et al., , 2001. These two viruses constitute the recently recognized genus Henipavirus (Mayo, 2002).The genome of NiV is 18 246 nt in length and contains six transcription units encoding six viral structural proteins (39-N-P-M-F-G-L-59) and three predicted non-structural proteins, C, V and W . As in other paramyxoviruses, the C protein of NiV is expressed from an alternative open reading frame (ORF) within the phosphoprotein (P) gene, whereas the V and W proteins are expressed by RNA editing (Lamb & Kolakofsky, 2001). At a unique, highly conserved RNA-editing site in the P gene, the polymerase protein (L) inserts a single, nontemplated G residue that results in a frame shift and the expression of the V protein. Insertion of two nontemplated G residues results in expression of the W protein . Whilst the C proteins of NiV and of other paramyxoviruses are unique and share no sequence similarity with the P protein (Lamb & Kolakofsky, 2001), the V and W proteins share an amino-terminal 407 aa domain with P and each possesses a unique carboxyl-terminal domain consisting of 52 aa for V and 47 aa for W . The sequences of the P proteins of paramyxoviruses a...

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“…HeV is restricted to Australia and of the seven outbreaks to date all have involved infection of horses from unidentified sources, with subsequent direct transmission to humans on three occasions (8,9,20). NiV outbreaks have occurred in Malaysia, Singapore, India and Bangladesh following various chains of transmission including intermediate host species (3), human-to-human transmission (2,13), possible bat-to-human transmission (10) and vehicle-borne transmission (16).…”

Section: Introductionmentioning

confidence: 99%

Henipavirus susceptibility to environmental variables

et al. 2008

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The routes of henipavirus transmission between hosts are poorly understood. The purpose of this study was to measure the persistence of henipaviruses under various environmental conditions and thereby gain an insight into likely mechanisms of transmission. Henipaviruses survived for more than four days at 22°C in pH-neutral fruit bat urine but were sensitive to higher temperatures and pH changes. On mango flesh, survival time varied depending on temperature and fruit pH, ranging from two hours to more than two days. Desiccation of viruses substantially reduced survival time to less than two hours. The sensitivity of henipaviruses to pH, temperature and desiccation indicates a need for close contact between hosts for transmission to occur, although under ideal conditions henipaviruses can persist for extended periods facilitating vehicle-borne transmission.

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Nipah Virus Encephalitis Reemergence, Bangladesh

Abstract: Two Nipah virus encephalitis outbreaks in Bangladesh may be associated with person-to-person transmission.

Cited by 481 publications

References 15 publications

Nipah virus infection: current scenario

Nipah virus infection: current scenario

The C, V and W proteins of Nipah virus inhibit minigenome replication

Henipavirus susceptibility to environmental variables

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