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[Genetic variability of the human influenza virus during adaptation in mice]
Abstract:
After 12 passages of a mouse-nonpathogenic influenza A/USSR/90/77 virus in mouse lungs a pathogenic virus was obtained causing death of the animals at 4-7 days after intranasal inoculation. The genetic and structural analysis of the initial and pathogenic viruses performed by oligonucleotide mapping of individual virus genes demonstrated that in the course of adaptation to mice structural changes had occurred at least in 5 out of 8 genes of virus with the exception of the genes coding for matrix and nonstructural proteins. The greatest differences were found in the genes coding for surface glycoproteins: hemagglutinin and neuraminidase. The experimental results indicate an important functional role of surface glycoproteins of influenza virus, particularly hemagglutinin, in the process of adaptation and formation of the pathogenic properties of virus.
Insights
Adapting influenza A virus to mice increased its pathogenicity, causing animal deaths. Genetic analysis revealed significant changes in surface glycoproteins, hemagglutinin and neuraminidase, crucial for this adaptation and virulence.
Area of Science:
- Virology
- Molecular Biology
- Pathogenesis
Background:
- Influenza A virus is a significant human and animal pathogen.
- Understanding viral adaptation and virulence is crucial for public health.
- The genetic basis of influenza virus pathogenicity is complex and not fully understood.
Purpose of the Study:
- To investigate the genetic and structural changes in influenza virus during adaptation to a new host.
- To identify the viral components responsible for increased pathogenicity.
Main Methods:
- Passaging of influenza A virus in mouse lungs for 12 generations.
- Genetic and structural analysis using oligonucleotide mapping of individual virus genes.
- Intranasal inoculation of mice to assess pathogenicity.
Main Results:
- A mouse-nonpathogenic influenza A virus became pathogenic after 12 passages, causing mortality within 4-7 days.
- Structural changes were observed in at least 5 out of 8 viral genes, excluding matrix and nonstructural proteins.
- Significant genetic differences were identified in genes encoding hemagglutinin and neuraminidase.
Conclusions:
- Influenza virus surface glycoproteins, particularly hemagglutinin, play a critical role in host adaptation.
- Changes in surface glycoproteins are key to the development of pathogenic properties in influenza virus.
- This study highlights the importance of viral surface proteins in determining influenza virus virulence.