Humoral and cellular immunity induced by influenza virus infection. (1) Influenza virus binds to the receptor on the host cell and entry the cell by receptor-mediated endocytosis. (2) The endosomal acidification permits fusion of the host and viral membranes by altering the conformation of hemagglutinin. (3) Upon the fusion, viral ribonucleoprotein complexes (RNP complex) are released into the cytoplasm and (4) transported to the nucleus, where the viral RNAs (vRNA) are transcribed into messenger RNAs (mRNA) and replicated by the viral RNA-dependent RNA polymerase complex into complementary RNA (cRNA). (5) mRNA are exported to the cytoplasm for translation of structural proteins. (6) Synthesis of envelope proteins take place on ribosomes of endoplasmic reticulum. (7) The newly synthesized viral RNPs are exported from the nucleus to the assembly site at the apical plasma membrane, where (8) new virus particles are budding and release out of host cells. Influenza virus infection triggers innate (not shown) and adaptive immune response where the effector cells and molecules are involved in restriction of viral spread, as follows: The cellular immune response (right) is initiated after recognition of viral antigens presented via MHCI and MHC II molecules by antigen presenting cells (APC), which then leads to activation, proliferation and differentiation of antigen-specific CD8+ T or CD4+ cells. These cells gain effector cell function and either they help directly (Th1 or Th2 cell) to produce antibodies or, CTL effector cells recognize antigen peptides presented by MHCI on APC and kill the virus infected cells by exocytosis of cytolytic granules. The humoral immune response (left) is mediated by specific antibodies (e.g IgG, IgA) produced by antibody secreting plasma cells (ASC) which are the final stage of B cell development. This process is aided by CD4+ T helper and T cell-derived cytokines essential for the activation and differentiation of both B-cell responses and CD8+ T cell responses.