Host Genetics of Infection and Immunology

Initiation of the adaptive immune response happens through peptides derived from viral proteins, which are exhibited on antigen-presenting cells to the T lymphocytes. Helper T cells, through the production of cytokines, contribute to B cell proliferation and differentiation to plasma cells, and to the activation and proliferation of virus-specific cytotoxic T lymphocytes (CTLs). Due to the absence of RNA proofreading enzymes, the RNA-dependent RNA polymerase that copies the viral genome makes an error roughly every 10 thousand nucleotides, which is the approximate length of the influenza vRNA. Subsequently, the dominant part newly manufactured influenza viruses are mutants; this causes antigenic drift, which is a moderate change in the antigens on the viral surface after some time. The separation of the genome into eight separate portions of vRNA permits mixing or reassortment of vRNAs if more than one kind of influenza infection contaminates a s single cell. The subsequent quick change in viral hereditary qualities produces antigenic movements, which are sudden changes starting with one antigen then onto the next. These sudden extensive changes permit the infection to taint new host species and rapidly beat defensive insusceptibility.

  • Virulence and pathogenicity
  • Molecular virology and immunology
  • Molecular studies for vaccines and antivirals
  • Genetics of orthomyxovirus and other respiratory virus

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