martes, 27 de noviembre de 2012

Transmission Routes for Nipah Virus from Malaysia and Bangladesh - - Emerging Infectious Disease journal - CDC

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Transmission Routes for Nipah Virus from Malaysia and Bangladesh - - Emerging Infectious Disease journal - CDC


Transmission Routes for Nipah Virus from Malaysia and Bangladesh

Bronwyn A. Clayton, Deborah Middleton, Jemma Bergfeld, Jessica Haining, Rachel Arkinstall, Linfa Wang, and Glenn A. MarshComments to Author 
Author affiliations: Author affiliations: Commonwealth Scientific and Industrial Research Organisation Livestock Industries, Geelong, Victoria, Australia (B.A. Clayton, D. Middleton, J. Bergfeld, J. Haining, R. Arkinstall, L. Wang, G.A. Marsh); University of Melbourne, Parkville, Victoria, Australia (B.A. Clayton); Duke–National University of Singapore Graduate Medical School, Singapore (L. Wang)
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Human infections with Nipah virus in Malaysia and Bangladesh are associated with markedly different patterns of transmission and pathogenicity. To compare the 2 strains, we conducted an in vivo study in which 2 groups of ferrets were oronasally exposed to either the Malaysia or Bangladesh strain of Nipah virus. Viral shedding and tissue tropism were compared between the 2 groups. Over the course of infection, significantly higher levels of viral RNA were recovered from oral secretions of ferrets infected with the Bangladesh strain. Higher levels of oral shedding of the Bangladesh strain of Nipah virus might be a key factor in onward transmission in outbreaks among humans.
Nipah virus (NiV), a bat-borne paramyxovirus, has caused outbreaks of human disease with high mortality rates in Malaysia, Singapore, India, and Bangladesh. Two divergent NiV strains (NiV-Malaysia and NiV-Bangladesh) share 91.8% nt sequence identity (1).
NiV-Malaysia emerged in 1998 during an outbreak of infectious respiratory and neurologic disease in commercially farmed pigs, presumably after virus spillover from Malaysian flying foxes (2). Pigs were the source of infection for farm and abattoir workers, resulting in a widespread outbreak of severe febrile encephalitic disease among humans (35); >250 cases were reported in Malaysia and Singapore, and the case-fatality rate approached 40% (2,5,6). No cases of human-to-human transmission were reported during the outbreak (7,8). However, rare instances of human-to-human transmission have been suggested by asymptomatic seroconversion against NiV-Malaysia in a health care worker, which was recognized after the outbreak (9), and by a recently reported case of late-onset NiV encephalitis attributed to transmission from infected family members (10).
NiV-Bangladesh emerged in 2001 in Bangladesh (11,12), and subsequent outbreaks of disease have occurred almost annually (1220). Since 2001, >200 cases in humans have been identified in Bangladesh; the overall case-fatality rate is >70% (21). In contrast to the rare instances of human-to-human transmission of NiV-Malaysia, human-to-human transmission of NiV-Bangladesh is a major pathway for human infection (13).
The different transmission characteristics of NiV-Malaysia and NiV-Bangladesh might be attributable to differences in infectivity and pathogenicity of virus strains and in tissue tropism, reflected by higher incidence of respiratory disease in NiV-Bangladesh–infected patients (14,21). We assessed the role that tissue tropism and shedding characteristics of NiV-Malaysia and NiV-Bangladesh might play in clinical outcomes and increasing transmission risk. For this purpose, we used a mammalian infection model, the ferret, in which NiV causes fulminating systemic disease, with fever and neurologic and/or respiratory signs, similar to those in humans (15). Here we describe a ferret model for NiV-Bangladesh infection and our comparison of the characteristics of infections caused by NiV-Malaysia and NiV-Bangladesh in the ferret.

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