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Antigenic variation. Read it and weep.

Antigenic variation refers to the mechanism by which an infectious organism such as a protozoan, bacterium or virus alters its surface proteins in order to evade a host immune response. Immune evasion is particularly important for organisms that target long-lived hosts, repeatedly infect a single host and are easily transmittable.

Antigenic variation not only enables immune evasion by the pathogen, but also allows the microbes to cause re-infection, as their antigens are no longer recognized by the host's immune system. When an organism is exposed to a particular antigen (i.e. a protein on the surface of a bacterium) an immune response is stimulated and antibodies are generated to target that specific antigen.

The immune system will then "remember" that particular antigen, and defenses aimed at that antigen become part of the immune system’s acquired immune response. If the same pathogen tries to re-infect the same host the antibodies will act rapidly to target the pathogen for destruction.

However, if the pathogen can alter its surface antigens, it can evade the host's acquired immune system. This will allow the pathogen to re-infect the host while the immune system generates new antibodies to target the newly identified antigen. Antigenic variation can occur by altering a variety of surface molecules including proteins and carbohydrates.

There are many molecular mechanisms behind antigenic variation, including gene conversion,[1] site-specific DNA inversions,[2] hypermutation,[3] as well as recombination of sequence cassettes.[1] In all cases, antigenic variation and phase variation, a type of antigenic variation, result in a heterogenic phenotype of a clonal population.[4] Individual cells either express the phase-variable protein(s) or express one of multiple antigenic forms of the protein. This form of regulation has been identified mainly, but not exclusively, for a wide variety of surface structures in pathogens and is implicated as a virulence strategy.[5]


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