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  1. Wild TF
    Pathol. Biol., 2009 Mar;57(2):188-96.
    PMID: 18511217 DOI: 10.1016/j.patbio.2008.04.006
    Paramyxoviruses have been implicated in both animal and human infections. Some viruses, such as Morbilliviruses are responsible for large-scale epidemics. However, there are limited observations of these viruses crossing the host species barrier in nature. In 1994, in Australia a fatal infection in horses and humans was identified to be caused by a new Paramyxovirus, Hendra virus (HeV), and in 1998 in Malaysia, a closely related virus, Nipah virus (NiV) was responsible for fatal infections in pigs and humans. These two viruses were sufficiently different from previously described Paramyxoviruses to create a new genus, Henipaviruses. The natural reservoir of these viruses was the fruit bat (Pteropus), which is found in regions extending from the western Pacific to the eastern coast of Africa. Serological studies have established that as many as half the fruit bats in colonies throughout these regions may have antibodies against this family of viruses. The availability of diagnostic reagents for Nipah virus in humans have identified infections in several countries including, Bangladesh, India and Indonesia. In some of these epidemics, mortality in humans exceeds 75%. Deforestation is probably responsible for fruit bats leaving their ecological niches and approaching farms and villages. The infection of humans and animals may occur via contaminated foods or in certain cases by animals to man. At present, only within close families has human-to-human transmission been proposed. Henipavirus infections are probably more widespread than it is at presently known and so it is important to have an intense monitoring for these diseases, especially in countries where large-scale deforestation is happening.
    Matched MeSH terms: Henipavirus/pathogenicity
  2. Daszak P, Zambrana-Torrelio C, Bogich TL, Fernandez M, Epstein JH, Murray KA, et al.
    Proc Natl Acad Sci U S A, 2013 Feb 26;110 Suppl 1:3681-8.
    PMID: 22936052 DOI: 10.1073/pnas.1201243109
    Emerging infectious diseases (EIDs) pose a significant threat to human health, economic stability, and biodiversity. Despite this, the mechanisms underlying disease emergence are still not fully understood, and control measures rely heavily on mitigating the impact of EIDs after they have emerged. Here, we highlight the emergence of a zoonotic Henipavirus, Nipah virus, to demonstrate the interdisciplinary and macroecological approaches necessary to understand EID emergence. Previous work suggests that Nipah virus emerged due to the interaction of the wildlife reservoir (Pteropus spp. fruit bats) with intensively managed livestock. The emergence of this and other henipaviruses involves interactions among a suite of anthropogenic environmental changes, socioeconomic factors, and changes in demography that overlay and interact with the distribution of these pathogens in their wildlife reservoirs. Here, we demonstrate how ecological niche modeling may be used to investigate the potential role of a changing climate on the future risk for Henipavirus emergence. We show that the distribution of Henipavirus reservoirs, and therefore henipaviruses, will likely change under climate change scenarios, a fundamental precondition for disease emergence in humans. We assess the variation among climate models to estimate where Henipavirus host distribution is most likely to expand, contract, or remain stable, presenting new risks for human health. We conclude that there is substantial potential to use this modeling framework to explore the distribution of wildlife hosts under a changing climate. These approaches may directly inform current and future management and surveillance strategies aiming to improve pathogen detection and, ultimately, reduce emergence risk.
    Matched MeSH terms: Henipavirus/pathogenicity
  3. Mackenzie JS, Field HE
    PMID: 15119765
    Three newly recognized encephalitogenic zoonotic viruses spread from fruit bats of the genus Pteropus (order Chiroptera, suborder Megachiroptera) have been recognised over the past decade. These are: Hendra virus, formerly named equine morbillivirus, which was responsible for an outbreak of disease in horses and humans in Brisbane, Australia, in 1994; Australian bat lyssavirus, the cause of a severe acute encephalitis, in 1996; and Nipah virus, the cause of a major outbreak of encephalitis and pulmonary disease in domestic pigs and people in peninsula Malaysia in 1999. Hendra and Nipah viruses have been shown to be the first two members of a new genus, Henipavirus, in the family Paramyxoviridae, subfamily Paramyxovirinae, whereas Australian bat lyssavirus is closely related antigenically to classical rabies virus in the genus Lyssavirus, family Rhabdoviridae, although it can be distinguished on genetic grounds. Hendra and Nipah viruses have neurological and pneumonic tropisms. The first humans and equids with Hendra virus infections died from acute respiratory disease, whereas the second human patient died from an encephalitis. With Nipah virus, the predominant clinical syndrome in humans was encephalitic rather than respiratory, whereas in pigs, the infection was characterised by acute fever with respiratory involvement with or without neurological signs. Two human infections with Australian bat lyssavirus have been reported, the clinical signs of which were consistent with classical rabies infection and included a diffuse, non-suppurative encephalitis. Many important questions remain to be answered regarding modes of transmission, pathogenesis, and geographic range of these viruses.
    Matched MeSH terms: Henipavirus/pathogenicity*
  4. Khetawat D, Broder CC
    Virol J, 2010 Nov 12;7:312.
    PMID: 21073718 DOI: 10.1186/1743-422X-7-312
    BACKGROUND: Hendra virus (HeV) and Nipah virus (NiV) are newly emerged zoonotic paramyxoviruses discovered during outbreaks in Queensland, Australia in 1994 and peninsular Malaysia in 1998/9 respectively and classified within the new Henipavirus genus. Both viruses can infect a broad range of mammalian species causing severe and often-lethal disease in humans and animals, and repeated outbreaks continue to occur. Extensive laboratory studies on the host cell infection stage of HeV and NiV and the roles of their envelope glycoproteins have been hampered by their highly pathogenic nature and restriction to biosafety level-4 (BSL-4) containment. To circumvent this problem, we have developed a henipavirus envelope glycoprotein pseudotyped lentivirus assay system using either a luciferase gene or green fluorescent protein (GFP) gene encoding human immunodeficiency virus type-1 (HIV-1) genome in conjunction with the HeV and NiV fusion (F) and attachment (G) glycoproteins.

    RESULTS: Functional retrovirus particles pseudotyped with henipavirus F and G glycoproteins displayed proper target cell tropism and entry and infection was dependent on the presence of the HeV and NiV receptors ephrinB2 or B3 on target cells. The functional specificity of the assay was confirmed by the lack of reporter-gene signals when particles bearing either only the F or only G glycoprotein were prepared and assayed. Virus entry could be specifically blocked when infection was carried out in the presence of a fusion inhibiting C-terminal heptad (HR-2) peptide, a well-characterized, cross-reactive, neutralizing human mAb specific for the henipavirus G glycoprotein, and soluble ephrinB2 and B3 receptors. In addition, the utility of the assay was also demonstrated by an examination of the influence of the cytoplasmic tail of F in its fusion activity and incorporation into pseudotyped virus particles by generating and testing a panel of truncation mutants of NiV and HeV F.

    CONCLUSIONS: Together, these results demonstrate that a specific henipavirus entry assay has been developed using NiV or HeV F and G glycoprotein pseudotyped reporter-gene encoding retrovirus particles. This assay can be conducted safely under BSL-2 conditions and will be a useful tool for measuring henipavirus entry and studying F and G glycoprotein function in the context of virus entry, as well as in assaying and characterizing neutralizing antibodies and virus entry inhibitors.

    Matched MeSH terms: Henipavirus/pathogenicity*
  5. Mackenzie JS
    J Neurovirol, 2005 Oct;11(5):434-40.
    PMID: 16287684
    The last decade of the 20th Century saw the introduction of an unprecedented number of encephalitic viruses emerge or spread in the Southeast Asian and Western Pacific regions (Mackenzie et al, 2001; Solomon, 2003a). Most of these viruses are zoonotic, either being arthropod-borne viruses or bat-borne viruses. Thus Japanese encephalitis virus (JEV), a mosquito-borne flavivirus, has spread through the Indonesian archipelago to Papua New Guinea (PNG) and to the islands of the Torres Strait of northern Australia, to Pakistan, and to new areas in the Indian subcontinent; a strain of tick-borne encephalitis virus (TBEV) was described for the first time in Hokkaido, Japan; and a novel mosquito-borne alphavirus, Me Tri virus, was described from Vietnam. Three novel bat-borne viruses emerged in Australia and Malaysia; two, Hendra and Nipah viruses, represent the first examples of a new genus in the family Paramyxoviridae, the genus Henipaviruses, and the third, Australian bat lyssavirus (ABLV) is new lyssavirus closely related to classical rabies virus. These viruses will form the body of this brief review.
    Matched MeSH terms: Henipavirus/pathogenicity
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