Interferon Response:
1. Antiviral proteins: Upon viral infection, cells produce antiviral proteins known as interferons. Interferons bind to receptors on neighboring cells, triggering the expression of a range of antiviral proteins, including those that directly inhibit viral replication.
2. Protein kinase R (PKR): PKR is an enzyme activated by the presence of double-stranded RNA, which is a characteristic feature of influenza virus replication. PKR phosphorylates the translation initiation factor eIF2, leading to the inhibition of viral protein synthesis.
Pattern Recognition Receptors (PRRs):
1. Toll-like receptors (TLRs): TLRs located on the cell surface or within endosomes recognize viral components, such as viral RNA or hemagglutinin protein. TLR activation triggers immune responses, including the production of interferons and inflammatory mediators.
2. RIG-I-like receptors (RLRs): RLRs are cytoplasmic proteins that detect viral RNA in the cytoplasm. Upon recognition, RLRs stimulate the production of interferons and antiviral proteins.
APOBEC Proteins:
Apolipoprotein B mRNA editing enzyme, catalytic polypeptide-like (APOBEC) proteins are involved in RNA editing. Some APOBEC proteins can deaminate viral RNA, introducing mutations that disrupt viral replication and contribute to the generation of defective viral genomes.
Autophagy:
Autophagy is a cellular process that degrades and recycles cellular components. During viral infection, autophagy can target and degrade viral components, preventing viral replication and spread.
Inflammasome Activation:
Certain inflammasomes, such as the NLRP3 inflammasome, can be activated by influenza virus infection. Inflammasome activation promotes the release of pro-inflammatory cytokines, leading to the recruitment of immune cells and the initiation of inflammatory responses against the virus.
Antibody-Mediated Defense:
Antibodies produced by B cells can recognize and bind to specific viral proteins, such as the hemagglutinin and neuraminidase proteins of influenza A virus. Antibody binding can neutralize the virus, preventing its entry into cells or interfering with its replication.
These cellular defense mechanisms work together to protect cells from influenza A virus infection, contributing to the overall immune response against the virus.
