Tracking the Evolution in Phylogeny, Structure and Function of H5N1 Influenza Virus PA Gene

2014 ◽  
Vol 63 (5) ◽  
pp. 548-563 ◽  
Author(s):  
K. Wei ◽  
Y. Lin ◽  
Y. Li ◽  
Y. Chen
Keyword(s):  
Influenza Virus ◽  
Structure And Function ◽  
H5n1 Influenza Virus ◽  
H5n1 Influenza ◽  
And Function

Prophylactic effects of chitin microparticles on highly pathogenic H5N1 influenza virus

2007 ◽  
Vol 79 (6) ◽  
pp. 811-819 ◽  
Author(s):  
Takeshi Ichinohe ◽  
Noriyo Nagata ◽  
Peter Strong ◽  
Shin-ichi Tamura ◽  
Hidehiro Takahashi ◽  
...  
Keyword(s):  
Influenza Virus ◽  
H5n1 Influenza Virus ◽  
Highly Pathogenic ◽  
H5n1 Influenza ◽  
Pathogenic H5n1

scholarly journals H5N1 Influenza Virus Pathogenesis in Genetically Diverse Mice Is Mediated at the Level of Viral Load

mBio ◽  
2011 ◽  
Vol 2 (5) ◽  
Author(s):  
Adrianus C. M. Boon ◽  
David Finkelstein ◽  
Ming Zheng ◽  
Guochun Liao ◽  
John Allard ◽  
...  
Keyword(s):  
Influenza Virus ◽  
Viral Load ◽  
H5n1 Virus ◽  
Inbred Mouse ◽  
Severe Disease ◽  
Mouse Strains ◽  
H5n1 Influenza Virus ◽  
Resistant Mouse ◽  
H5n1 Influenza ◽  
Host Genetic

ABSTRACTThe genotype of the host is one of several factors involved in the pathogenesis of an infectious disease and may be a key parameter in the epidemiology of highly pathogenic H5N1 influenza virus infection in humans. Gene polymorphisms may affect the viral replication rate or alter the host’s immune response to the virus. In humans, it is unclear which aspect dictates the severity of H5N1 virus disease. To identify the mechanism underlying differential responses to H5N1 virus infection in a genetically diverse population, we assessed the host responses and lung viral loads in 21 inbred mouse strains upon intranasal inoculation with A/Hong Kong/213/03 (H5N1). Resistant mouse strains survived large inocula while susceptible strains succumbed to infection with 1,000- to 10,000-fold-lower doses. Quantitative analysis of the viral load after inoculation with an intermediate dose found significant associations with lethality as early as 2 days postinoculation, earlier than any other disease indicator. The increased viral titers in the highly susceptible strains mediated a hyperinflamed environment, indicated by the distinct expression profiles and increased production of inflammatory mediators on day 3. Supporting the hypothesis that viral load rather than an inappropriate response to the virus was the key severity-determining factor, we performed quantitative real-time PCR measuring the cytokine/viral RNA ratio. No significant differences between susceptible and resistant mouse strains were detected, confirming that it is the host genetic component controlling viral load, and therefore replication dynamics, that is primarily responsible for a host’s susceptibility to a given H5N1 virus.IMPORTANCEHighly pathogenic H5N1 influenza virus has circulated in Southeast Asia since 2003 but has been confirmed in relatively few individuals. It has been postulated that host genetic polymorphisms increase the susceptibility to infection and severe disease. The mechanisms and host proteins affected during severe disease are unknown. Inbred mouse strains vary considerably in their ability to resist H5N1 virus and were used to identify the primary mechanism determining disease severity. After inoculation with H5N1, resistant mouse strains had reduced amounts of virus in their lungs, which subsequently resulted in lower production of proinflammatory mediators and less pathology. We therefore conclude that the host genetic component controlling disease severity is primarily influencing viral replication. This is an important concept, as it emphasizes the need to limit virus replication through antiviral therapies and it shows that the hyperinflammatory environment is simply a reflection of more viral genetic material inducing a response.

Extended Parallel Process Model and H5N1 Influenza Virus

2008 ◽  
Vol 102 (2) ◽  
pp. 539-550 ◽  
Author(s):  
Wanda Siu
Keyword(s):  
Influenza Virus ◽  
Process Model ◽  
Parallel Process ◽  
H5n1 Influenza Virus ◽  
Extended Parallel Process Model ◽  
Persuasive Message ◽  
H5n1 Influenza ◽  
The Usa ◽  
Promotional Message ◽  
Significant Health

This study integrated the Extended Parallel Process Model and forewarning cues to assess the promotion of preventive measures against the H5N1 influenza virus, a significant health threat that affects Asia, Europe, and the USA. There are two types of forewarning, (1) telling the audience that they will hear messages intended to persuade them and (2) telling the audience the topic and stance of the impending persuasive message. Analysis of ratings by 265 undergraduates indicated that forewarnings of the topic and stance of a promotional message on the H5N1 virus facilitated elaboration of coping-related thoughts which enhance perceived self-efficacy and a stronger behavioral intention to combat H5N1. Conversely, the elaboration of danger-related thoughts evoked some fear but enhanced source perception.

scholarly journals Isolation of a genotypically unique H5N1 influenza virus from duck meat imported into Japan from China

Virology ◽  
2005 ◽  
Vol 339 (1) ◽  
pp. 101-109 ◽  
Author(s):  
Masaji Mase ◽  
Mariko Eto ◽  
Nobuhiko Tanimura ◽  
Kunitoshi Imai ◽  
Kenji Tsukamoto ◽  
...  
Keyword(s):  
Influenza Virus ◽  
H5n1 Influenza Virus ◽  
H5n1 Influenza

scholarly journals Immunogenicity of Avian H5N1 Influenza Virus Recombinant Vaccines in Cats

2010 ◽  
Vol 24 (S1) ◽  
Author(s):  
Elizabeth W Uhl ◽  
S. Mark Tompkins ◽  
Stephen B Harvey ◽  
Jon Gabbard ◽  
Frank Michel ◽  
...  
Keyword(s):  
Influenza Virus ◽  
Recombinant Vaccines ◽  
H5n1 Influenza Virus ◽  
H5n1 Influenza ◽  
Virus Recombinant ◽  
Avian H5n1 Influenza Virus

scholarly journals Cross-Reactive, Cell-Mediated Immunity and Protection of Chickens from Lethal H5N1 Influenza Virus Infection in Hong Kong Poultry Markets

2001 ◽  
Vol 75 (6) ◽  
pp. 2516-2525 ◽  
Author(s):  
Sang Heui Seo ◽  
Robert G. Webster
Keyword(s):  
T Cells ◽  
Influenza Virus ◽  
Hong Kong ◽  
Virus Infection ◽  
Cellular Immunity ◽  
Influenza Virus Infection ◽  
Influenza Viruses ◽  
H5n1 Influenza Virus ◽  
H9n2 Influenza Virus ◽  
H5n1 Influenza

ABSTRACT In 1997, avian H5N1 influenza virus transmitted from chickens to humans resulted in 18 confirmed infections. Despite harboring lethal H5N1 influenza viruses, most chickens in the Hong Kong poultry markets showed no disease signs. At this time, H9N2 influenza viruses were cocirculating in the markets. We investigated the role of H9N2 influenza viruses in protecting chickens from lethal H5N1 influenza virus infections. Sera from chickens infected with an H9N2 influenza virus did not cross-react with an H5N1 influenza virus in neutralization or hemagglutination inhibition assays. Most chickens primed with an H9N2 influenza virus 3 to 70 days earlier survived the lethal challenge of an H5N1 influenza virus, but infected birds shed H5N1 influenza virus in their feces. Adoptive transfer of T lymphocytes or CD8+ T cells from inbred chickens (B2/B2) infected with an H9N2 influenza virus to naive inbred chickens (B2/B2) protected them from lethal H5N1 influenza virus. In vitro cytotoxicity assays showed that T lymphocytes or CD8+ T cells from chickens infected with an H9N2 influenza virus recognized target cells infected with either an H5N1 or H9N2 influenza virus in a dose-dependent manner. Our findings indicate that cross-reactive cellular immunity induced by H9N2 influenza viruses protected chickens from lethal infection with H5N1 influenza viruses in the Hong Kong markets in 1997 but permitted virus shedding in the feces. Our findings are the first to suggest that cross-reactive cellular immunity can change the outcome of avian influenza virus infection in birds in live markets and create a situation for the perpetuation of H5N1 influenza viruses.

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