Questions about an immune response to viral infection. When exactly do we make a
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Questions about an immune response to viral infection. When exactly do we make antibodies? Does it occur right after an APC has connected to a CD4+ cell which sends "help" in the form of cytokines to CD8+ cells. CD8+ cells profiliferation process has increased and they fight off a viral infection by causing cell apoptosis. Does it mean that CD4+ cell also sends cytokines and attaches to a B cell which then starts producing plasma cells/ memory cells and antibodies? If that is true, then why do we need antibodies for a viral infection since viruses can't survive without a host cell and these antibodies are just floating around in the blood stream and can't target viruses?Thanks! Questions about an immune response to viral infection. When exactly do we make antibodies? Does it occur right after an APC has connected to a CD4+ cell which sends "help" in the form of cytokines to CD8+ cells. CD8+ cells profiliferation process has increased and they fight off a viral infection by causing cell apoptosis. Does it mean that CD4+ cell also sends cytokines and attaches to a B cell which then starts producing plasma cells/ memory cells and antibodies? If that is true, then why do we need antibodies for a viral infection since viruses can't survive without a host cell and these antibodies are just floating around in the blood stream and can't target viruses?
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Explanation / Answer
Virally infected cells produce and release small proteins called interferons, which play an important role in immune protection against viruses. Interferons prevent replication of viruses, by directly get involved with their capacity to replicate within an infected cell.
Virus can stimulate B lymphocytes to produce antibody (specific for viral antigens). Antibody neutralization is most effective when virus is present in large fluid spaces like as serum or on moist surfaces ( i,e gastrointestinal and respiratory tracts). Antibody can deactivate virus by blocking virus-host cell interactions and recognizing viral antigens on virus-infected cells which can lead to antibody-dependent cytotoxic cells or complement-mediated lysis. IgG antibodies are dependable for most antiviral activity in serum, while IgA is the most important antibody when viruses infect mucosal surfaces.
Activation of naive CD8+ T cells requires the interaction with antigen-presenting cells, mainly with matured dendritic cells. To generate lifelong memory T cells and to allow rhythmic stimulation of cytotoxic T cells, dendritic cells have to interact with both, activated CD4+ helper T cells and CD8+ T cells. During this process, the CD4+ helper T cells allow the dendritic cells to give a effective activating signal to the naive CD8+ T cells. Cytotoxic T cells have been exposed to become activated when targeted by other CD8 T cells . Once activated, the TC cells undergo clonal development with the help of the cytokine Interleukin, which is a growth and differentiation factor for T cells. This increases the number of cells specific for the target antigen that can move through the body in search of antigen-positive somatic cells. When exposed to infected somatic cells, TC cells release the cytotoxins perforin, granzymes, and granulysin. Through the action of perforin, granzymes enter the cytoplasm of the target cell and their serine protease function triggers the caspase cascade, which is a series of cysteine proteases that finally show the way of apoptosis (programmed cell death).
Helper T cells stimulate the B cell with the binding of CD4 on the T cell to CD4 on the B cell, by the interaction of TNF-TNF-receptor and the directed release of cytokines. The initial interaction occurs in the T-cell region of secondary lymphoid tissue, where both antigen-specific and helper T cells and antigen-specific B cells are trapped as a significance of binding antigen; interactions between T cells and B cells occur after migration into the B-cell follicle, and formation of a germinal center. Helper T cells induce a phase of vital B-cell proliferation, and direct the differentiation of the clonally increased progeny of the naive B cells into either antibody-secreting plasma cells or memory B cells.
Virus external covering( viral envelope), is almost identical to the host cell's membranes, making them complicated to target. We may never be able to totally beat viruses, but by connecting the power of vaccination, latest anti-virals and accepting the right behavior, we have a good chance of keeping one step ahead of viruses' most harmful effects.
Antibodies exist free floating through the bloodstream as a part of the humoral immune system. Antibodies exist in clonal lines that are specific to only one antigen, e.g., a virus hull protein. In binding to such antigens, they can cause agglutination and precipitation of antibody-antigen products prime in favor of phagocytosis (engulfing process) by macrophages, block viral receptors and stimulate other immune responses such as the complement pathway. Antibodies that recognize viruses can block these directly by their complete size.
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