Isolation and Molecular Identification of Nipah Virus from Pigs

AbuBakar, Sazaly; Chang, Li; Ali, Asad; Sharifah, S. H.; Yusoff, Khatijah; Zamrod, Zulkeflie

doi:10.3201/eid1012.040452

Cited by 113 publications

(75 citation statements)

References 13 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Subsequent studies have shown that NiV is widespread throughout Asia and may even produce annual epidemics in countries such as Bangladesh (6,10). The viruses involved in the outbreaks incurred mortality rates in humans varying from 40% to 70% and can be distinguished by nucleic acid sequencing (29,30). To analyze the different parameters involved in the disease induced by the henipaviruses, we developed an animal model in hamsters (22).…”

Section: Discussionmentioning

confidence: 99%

Establishment of a Nipah virus rescue system

Yoneda

Guillaume²,

Ikeda³

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

View full text Add to dashboard Cite

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.henipavirus ͉ infectious clone ͉ recombinant virus ͉ reverse genetics

show abstract

Section: Discussionmentioning

confidence: 99%

Establishment of a Nipah virus rescue system

Yoneda

Guillaume²,

Ikeda³

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

View full text Add to dashboard Cite

show abstract

“…In agreement with the distinct clinical representation, host-specific differences in lung pathology have been demonstrated histologically in fixed lung tissue samples from NiV-infected pigs and fatal human cases (Chua et al, 2000;Hooper et al, 2001;Maisner et al, 2009;Middleton et al, 2002;Tanimura et al, 2004;Weingartl et al, 2005;Wong et al, 2002). As porcine and human NiV isolates did not differ in their sequence (AbuBakar et al, 2004), species-specific host factors rather than genetic variabilities must be responsible for the differences in NiV replication in the respiratory tract of pigs and humans. On a molecular level, these host factors are not well understood, not least because direct comparative studies on NiV replication in airway epithelia of the two species have not been performed so far.…”

Section: Introductionmentioning

confidence: 99%

Species-specific and individual differences in Nipah virus replication in porcine and human airway epithelial cells

Sauerhering

Zickler

Elvert

et al. 2016

Journal of General Virology

View full text Add to dashboard Cite

Highly pathogenic Nipah virus (NiV) causes symptomatic infections in pigs and humans. The severity of respiratory symptoms is much more pronounced in pigs than in humans, suggesting species-specific differences of NiV replication in porcine and human airways. Here, we present a comparative study on productive NiV replication in primary airway epithelial cell cultures of the two species. We reveal that NiV growth substantially differs in primary cells between pigs and humans, with a more rapid spread of infection in human airway epithelia. Increased replication, correlated with higher endogenous expression levels of the main NiV entry receptor ephrin-B2, not only significantly differed between airway cells of the two species but also varied between cells from different human donors. To our knowledge, our study provides the first experimental evidence of species-specific and individual differences in NiV receptor expression and replication kinetics in primary airway epithelial cells. It remains to be determined whether and how these differences contribute to the viral host range and pathogenicity.

show abstract

“…The virus was isolated in 1999 from the cerebrospinal fluid of a human fatality. Although Pteropus bats are considered to be a reservoir of the virus (7), human infections in Malaysia were considered to be due to transmission of the virus from pigs (1). In the field, the infection in pigs may go unnoticed or cause respiratory disease and, rarely, encephalitis (porcine respiratory and encephalitis syndrome) (26).…”

mentioning

confidence: 99%