Immunologic Defences Against Extracellular Organisms

Immunity
Immunity Part 1
Immunity Part 2
Origin of Antibody Diversity
Germ Line Theory
Somatic Recombination Theory
Somatic Hypermutation Theory
Immune Response
Lymphocete
Humoral Immunity
Clonal Selection Model
Cell Mediated Immunity
Primary and Secondary Immune Response
Ontogeny of the Immune Response
Immune Tolerance
Immunologic Response to Infectious Disease
Immunologic Defences at the Mucous Membranes
Immunologic Defences against Extracellular Microorganisms
Immunologic Defences against Intracellular Organisms
Immunologic Defences against Extracellular Organisms
Immunologic Defences against Intracellular Viruses

Immunologic Defences Against Extracellular Organisms

	Immunologic Defences Against Extracellular Organisms The immunologic defence against viral infection has many similarities with those against bacteria and fungi. In the lytic cycle, viruses may spread from the primary infection site to other tissues. This is frequently dependent upon the development of a high titre of extracellular, virus in circulation. Viral infection leads to the production of specific antibody of either IgO, IgM, or IgA class. Secretory IgA plays little role in the defence against primary viral infection. However, lymphocytes and, plasma cells of the tonsils, the adenoids, and the mucosal lamina propria may persistently elaborate high levels of specific secretory IgA. Interaction of a specific antibody with the virion leads to viral neutralization.
Such neutralization may occur in two ways: 1. The antibody may bind to certain specific sites on the viral surface and change the structural conformation of the viral coat, so as to prevent adsorption, penetration, or uncoating, or 2. Binding of the antibody to non-specific viral determinants may fix large amount of complement on the viral surface, so that adsorption in prevented. The later mechanism requires fixation of only the first two complement components, C1 and C4. It is independent of either virolysis, opsonization, of mediator release, all of which require fixation of more terminal components. Viral neutralization is not enough to destroy or eliminate the infectious agent. Antibody and complement may dissociate from the virus or be digested by serum or intracellular proteases, thus restoring viral infectivity. The destruction and clearance of neutralized virus therefore requires additional mechanisms. Specific immune lymphocytes appear in the lymphoid tissues and in the circulation within the first week of primary infection with many viruses.
This often precedes detectable antibody production. Immune lymphocytes can transfer immunity to uninfected animals. In vitro, these cells, in the presence of viral antigens, are stimulated to undergo blastogenesis, and elaborate lymphokines, include dinginterferon. These lymphocytes help in the lysis of infected cells. The principal effect of the interaction of virus with either immune lymphocytes or antibody and complement is to induce phagocytosis. This is achieved through agglutination and opsonization of the virus and localization and activation of phagocytes. Although neutrophils may play some role in viral clearance- from blood, macrophages are the dominant antiviral phagocytes. There is a direct relationship between the virulence of many viruses and their ability to replicate with in macrophages of the host. Host susceptibility to some viruses is under genetic control.
The presence - of such a gene correlates directly with the capacity of the macrophage to support the replication of the specific virus. However, the inhibition mechanism of viral replication by macrophages from a resistant host is not clear. Neonatal macrophages fail to inhibit viral replication. The antiviral capacity of the macrophage is related to maturation. There are evidences which suggest that T-cells are stimulated by various ubiquitous nonviral antigens to elaborate soluble factors that induce macrophage maturation. Whether one of these maturation factors is interferon is a subject of current controversy.

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