Adaptive mutations of neuraminidase stalk truncation and deglycosylation confer enhanced pathogenicity of influenza A viruses

Keyphrases

• Pathogenicity 100%
• Influenza Virus 100%
• Truncation 100%
• O-glycosylation 100%
• Neuraminidase 100%
• Adaptive mutation 100%
• Pandemic H1N1 Virus 40%
• Mutant Virus 20%
• Avian Influenza 20%
• Evolutionary Adaptation 20%
• Amino Acids 10%
• Virus 10%
• Virus Strains 10%
• Adaptation 10%
• Balb C Mice 10%
• Mouse Model 10%
• Pathologic 10%
• Systemic Infection 10%
• Reverse Genetics 10%
• Mouse-adapted 10%
• Mouse Lung 10%
• Respiratory Organs 10%
• N-linked 10%
• Molecular Alterations 10%
• Pathogenic Determinants 10%
• Pandemic (H1N1) 2009 10%
• Replication Property 10%
• H7N9 10%
• Ferret 10%
• Viral Pathogenicity 10%
• Wild Aquatic Birds 10%
• Lung Infection 10%
• Seasonal Influenza Viruses 10%
• Domestic Poultry 10%
• H7N9 Avian Influenza 10%
• Glycosite 10%

Immunology and Microbiology

• Pathogenicity 100%
• Influenzavirus A 100%
• Deglycosylation 100%
• Influenza A Virus (H1N1) 80%
• Virus Mutant 40%
• Avian Influenza Virus 40%
• Evolutionary Adaptation 40%
• Influenza A Virus (H7N9) 40%
• Virus Strain 20%
• Bagg Albino Mouse 20%
• Mouse Model 20%
• Influenza Virus 20%
• Water Bird 20%
• Virus Virulence 20%
• Mustela Putorius Furo 20%
• Vertebral Column 20%