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.

Innate and adaptive immune responses are invigorated when the influenza virus infects the cells of the respiratory tract. Innate immune system recognizes virus-infected cells through mechanisms that are not antigen-specific, the cytokines produced during this early phase of the host's defense do facilitate activation of subsequent antigen-specific adaptive immune mechanisms. The innate immune response develops very quickly and controls virus replication during the early stages of infection.  Transition from the innate to the adaptive immune response is the stimulation of Toll-like receptors (TLRs) in endosomes of antigen-presenting cells (primarily dendritic cells).  TLRs recognize and bind to structural components such as single-stranded viral RNA, which are shared by different pathogens, and are important triggers of the danger signal. Stimulation of immunological memory from prior exposure to viral antigens also stimulates specific pathways in the adaptive immune response. Stimulation of immunological memory accelerates the adaptive response, which is delayed during a primary exposure to the antigen. A major aspect of the adaptive immune response involves virus binding to immunoglobulin receptors on B lymphocytes, which subsequently differentiate to plasma cells that produce virus-specific antibodies.

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

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