scholarly journals Mx1 Gene Protects Mice Against the Highly Lethal Human H5N1 Influenza Virus

Cell Cycle ◽  
2007 ◽  
Vol 6 (19) ◽  
pp. 2417-2421 ◽  
Author(s):  
Rachelle Salomon ◽  
Peter Staeheli ◽  
Georg Kochs ◽  
Hui-Ling Yen ◽  
John Franks ◽  
...  
Keyword(s):  
Influenza Virus ◽  
H5n1 Influenza Virus ◽  
H5n1 Influenza ◽  
Mx1 Gene ◽  
Human H5n1

scholarly journals Indications that Live Poultry Markets Are a Major Source of Human H5N1 Influenza Virus Infection in China

2011 ◽  
Vol 85 (24) ◽  
pp. 13432-13438 ◽  
Author(s):  
X.-F. Wan ◽  
L. Dong ◽  
Y. Lan ◽  
L.-P. Long ◽  
C. Xu ◽  
...  
Keyword(s):  
Influenza Virus ◽  
Virus Infection ◽  
Influenza Virus Infection ◽  
H5n1 Influenza Virus ◽  
H5n1 Influenza ◽  
Live Poultry ◽  
Human H5n1 ◽  
Live Poultry Markets

Evolution and adaptation of hemagglutinin gene of human H5N1 influenza virus

Virus Genes ◽  
2012 ◽  
Vol 44 (3) ◽  
pp. 450-458 ◽  
Author(s):  
Kaifa Wei ◽  
Yanfeng Chen ◽  
Juan Chen ◽  
Lingjuan Wu ◽  
Daoxin Xie
Keyword(s):  
Influenza Virus ◽  
H5n1 Influenza Virus ◽  
H5n1 Influenza ◽  
Hemagglutinin Gene ◽  
Human H5n1

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.

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