Hendra and Nipah viruses: different and dangerous

Eaton, Bryan T.; Broder, Christopher C.; Middleton, Deborah; Wang, Lin‐Fa

doi:10.1038/nrmicro1323

Cited by 391 publications

(328 citation statements)

References 157 publications

(180 reference statements)

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“…Although these viruses typically cause benign infections in their natural reservoir hosts, cross-species transmission to humans can result in severe disease (2)(3)(4)(5)(6). Unfortunately, our understanding of host-specific attributes that determine whether disease develops following infection with zoonotic viruses is very limited.…”

mentioning

confidence: 99%

Distinctive TLR7 Signaling, Type I IFN Production, and Attenuated Innate and Adaptive Immune Responses to Yellow Fever Virus in a Primate Reservoir Host

Mandl

Akondy

Lawson

et al. 2011

The Journal of Immunology

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Why cross-species transmissions of zoonotic viral infections to humans are frequently associated with severe disease when viruses responsible for many zoonotic diseases appear to cause only benign infections in their reservoir hosts is unclear. Sooty mangabeys (SMs), a reservoir host for SIV, do not develop disease following SIV infection, unlike nonnatural HIV-infected human or SIV-infected rhesus macaque (RM) hosts. SIV infections of SMs are characterized by an absence of chronic immune activation, in association with significantly reduced IFN-α production by plasmacytoid dendritic cells (pDCs) following exposure to SIV or other defined TLR7 or TLR9 ligands. In this study, we demonstrate that SM pDCs produce significantly less IFN-α following ex vivo exposure to the live attenuated yellow fever virus 17D strain vaccine, a virus that we show is also recognized by TLR7, than do RM or human pDCs. Furthermore, in contrast to RMs, SMs mount limited activation of innate immune responses and adaptive T cell proliferative responses, along with only transient antiviral Ab responses, following infection with yellow fever vaccine 17D strain. However, SMs do raise significant and durable cellular and humoral immune responses comparable to those seen in RMs when infected with modified vaccinia Ankara, a virus whose immunogenicity does not require TLR7/9 recognition. Hence, differences in the pattern of TLR7 signaling and type I IFN production by pDCs between primate species play an important role in determining their ability to mount and maintain innate and adaptive immune responses to specific viruses, and they may also contribute to determining whether disease follows infection.

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confidence: 99%

Distinctive TLR7 Signaling, Type I IFN Production, and Attenuated Innate and Adaptive Immune Responses to Yellow Fever Virus in a Primate Reservoir Host

Mandl

Akondy

Lawson

et al. 2011

The Journal of Immunology

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“…Notably, henipaviruses have recently also been found outside of Australia and Asia, thus extending the number of endemic regions of one of the most pathogenic virus genera known in humans (3). The susceptibility of humans, the wide host range, and interspecies transmission, together with the absence of therapeutic agents, led to the classification of HeV and NiV as biosecurity level 4 (BSL4) pathogens (4).…”

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confidence: 99%

Characterization of the Interactions between the Nucleoprotein and the Phosphoprotein of Henipavirus

Habchi

Blangy

Mamelli

et al. 2011

Journal of Biological Chemistry

165

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The Henipavirus genome is encapsidated by the nucleoprotein (N) within a helical nucleocapsid that recruits the polymerase complex via the phosphoprotein (P). In a previous study, we reported that in henipaviruses, the N-terminal domain of the phosphoprotein and the C-terminal domain of the nucleoprotein (N TAIL ) are both intrinsically disordered. Here we show that Henipavirus N TAIL domains are also disordered in the context of full-length nucleoproteins. We also report the cloning, purification, and characterization of the C-terminal X domains (P XD ) of Henipavirus phosphoproteins. Using isothermal titration calorimetry, we show that N TAIL and P XD form a 1:1 stoichiometric complex that is stable under NaCl concentrations as high as 1 M and has a K D in the M range. Using far-UV circular dichroism and nuclear magnetic resonance, we show that P XD triggers an increase in the ␣-helical content of N TAIL . Using fluorescence spectroscopy, we show that P XD has no impact on the chemical environment of a Trp residue introduced at position 527 of the Henipavirus N TAIL domain, thus arguing for the lack of stable contacts between the C termini of N TAIL and P XD . Finally, we present a tentative structural model of the N TAIL -P XD interaction in which a short, order-prone region of N TAIL (␣-MoRE; amino acids 473-493) adopts an ␣-helical conformation and is embedded between helices ␣2 and ␣3 of P XD , leading to a relatively small interface dominated by hydrophobic contacts. The present results provide the first detailed experimental characterization of the N-P interaction in henipaviruses and designate the N TAIL -P XD interaction as a valuable target for rational antiviral approaches.

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“…In the period from 1994 to 1999, four new viruses in the family Paramyxoviridae were discovered, and all appeared to have bats as a reservoir host. Hendra virus emerged in Queensland, Australia, in 1994, killing one human and 14 horses (10), and was responsible for at least four other sporadic outbreaks involving horse and human cases between 1994 and 2006 (11). The closely related Nipah virus (NiV) emerged in 1998-1999 in Peninsular Malaysia, resulting in the death of Ͼ100 people and the culling of Ͼ1 million pigs (12).…”

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confidence: 99%

A previously unknown reovirus of bat origin is associated with an acute respiratory disease in humans

Chua

Crameri

Hyatt

et al. 2007

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

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208

259

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Respiratory infections constitute the most widespread human infectious disease, and a substantial proportion of them are caused by unknown etiological agents. Reoviruses (respiratory enteric orphan viruses) were first isolated from humans in the early 1950s and so named because they were not associated with any known disease. Here, we report a previously unknown reovirus (named ''Melaka virus'') isolated from a 39-year-old male patient in Melaka, Malaysia, who was suffering from high fever and acute respiratory disease at the time of virus isolation. Two of his family members developed similar symptoms Ϸ1 week later and had serological evidence of infection with the same virus. Epidemiological tracing revealed that the family was exposed to a bat in the house Ϸ1 week before the onset of the father's clinical symptoms. Genome sequence analysis indicated a close genetic relationship between Melaka virus and Pulau virus, a reovirus isolated in 1999 from fruit bats in Tioman Island, Malaysia. Screening of sera collected from human volunteers on the island revealed that 14 of 109 (13%) were positive for both Pulau and Melaka viruses. This is the first report of an orthoreovirus in association with acute human respiratory diseases. Melaka virus is serologically not related to the different types of mammalian reoviruses that were known to infect humans asymptomatically. These data indicate that batborne reoviruses can be transmitted to and cause clinical diseases in humans.respiratory infection ͉ zoonosis ͉ human-to-human transmission ͉ orthoreovirus ͉ Pulau virus

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Hendra and Nipah viruses: different and dangerous

Cited by 391 publications

References 157 publications

Distinctive TLR7 Signaling, Type I IFN Production, and Attenuated Innate and Adaptive Immune Responses to Yellow Fever Virus in a Primate Reservoir Host

Distinctive TLR7 Signaling, Type I IFN Production, and Attenuated Innate and Adaptive Immune Responses to Yellow Fever Virus in a Primate Reservoir Host

Characterization of the Interactions between the Nucleoprotein and the Phosphoprotein of Henipavirus

A previously unknown reovirus of bat origin is associated with an acute respiratory disease in humans

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