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Immunity Against Respiratory Viruses
The elucidation of Immunity to microbes specifically viruses is delivered in this Sqadia video. Virus infection of respiratory epithelial cells is first detected by cytosolic and/or endosomal innate sensors in the infected epithelial cells. Recognition of the invading virus by these innate immune receptors leads to the production of pro-inflammatory cytokines such as interleukin and chemokines such as CC-chemokine ligand 2 (CCL2). Molecules derived from both innate and adaptive immune cells contribute to the regulation of excessive pulmonary inflammation during acute respiratory virus infection. T-helper 1 cells and type 1 cytotoxic T cells (TC1 cells) express the transcription factors T-bet and BLIMP1 (B lymphocyte-induced maturation protein 1) and produce high levels of the regulatory cytokine interleukin-10 (IL-10), in addition to effector cytokines and cytolytic molecules, during respiratory virus infection. Influenza virus infection induces the production of type I interferons (IFNs), which inhibit the recruitment of circulating neutrophils and macrophages to the lung following bacterial challenge.
HBV and HCV Immunity
Innate immunity against HBV and HCV includes the release of antiviral cytokines such as type 1 interferons (IFN-alpha and IFN-beta) and the activation of innate immune cells such as natural killer cells as well as the adaptive or acquired immune response specific to a given pathogen (CD4+ and CD8+ T cells). Previously produced Interferons provide interacellular defense and protect neighbouring unaffected cells. There are 3 lines of intracellular defense which performs the functions like degradation of viral mRNA, blockage of Viral proteins, apoptosis. Many viruses subvert particular parts of the immune system like synthesis of complement-regulatory molecules. Several viruses also produce molecules that interfere with chemokine responses, either by producing decoy chemokine receptors or chemokine homologs that interfere with natural ligand-induced signaling through chemokine receptors.
Immune Escape in HBV and HCV Infections
HBV (DNA Virus) Uses Three Strategies to Gently Sneak in the Immune System (Innate Immunity). Viruses may remain undetectable for long periods of time. Mainly because HBV are not cytolytic. It does not activate the interferon defense system. Antibodies against HBs Ag (antigen) are detected until rather later during the infection. The antibodies titre is an indication that the virus is cleared by immune system. HBV subverts the adaptive immune response by interfering with dendritic cell activation and maturation possibly myeloid DCs. This contributes to a high viral mutation rate and thus a change in its antigenicity, which allows it to evade adaptive immunity. Usually hepatocytes are in resting phase, therefore the damage caused by genotoxins is fixed before the damaged cells are replaced. p53 gene gaurds against any proliferation of any unchecked mutation. In the presence of genotoxins and proliferation burden the liver cells may get exposed to cancer causing mutations. Regulatory T-Cells play an important role in the pathogenesis of HBV and HCV infections. In most of the cases the induction of Treg cells is promoted by the pathogen. This mechanism seems to contribute to chronic liver infections caused by HBV and HCV. Studies that indicate the positive effects of Treg cells i.e. in restraining inflammation.
Immunological Response Against HIV
Innate immune cells are the first line of defence which HIV encounters upon entry to the body. SEVI (semen derived enhancer of virus infection) enhances in vitro HIV infection through formation of amyloid fibrils that capture and focus virus onto target cells. The CC chemokines (RANTES, MIP-1α and MIP-1β) may also block HIV access to the CCR5 co-receptors, able to attract the entire immunological repertoire of cells (T and B cells, DC and macrophage) to the mucosal site. Nk cells help in maturation of DCs in peripheral tissue. Type-I And Type-II Interferons up-regulate cell-surface MHC class I and induction of cell-mediated immunity. They also induce the expression of intrinsic defence factors, APOBEC, and tetherin.
A vaccine is a biological product containing an agent that improves the immunity to a particular disease. Vaccines are of 2 types:
- Live Attenuated Vaccines
- Inactivated Viral Vaccines
Live attenuated vaccines are naturally-occurring attenuated viruses or ones created by deletion of one or more genes can serve as vaccines. Example include Nef(-)strains that could offer protection against challenge with pathogenic SIV infection in Rhesus macaques. The initial results of inactivated viral vaccines were due to antigencity loss of envelope proteins, lower than usual doses of formalin. Cellular Vaccines provide a strong and specific T-cell immune (internal core protein) response in the absence of broadly neutralizing antibodies. Nucleic Acid Vaccines give DNA immunization by direct administration of viral genes, newly-formed antigen is then presented on the cell surface with host MHC class-I and class-II molecules. Following activation of vaccine, the pathogen-associated patterns contained in vaccine antigens attract dendritic cells, monocytes, and neutrophils that patrol throughout the body.