12/29/2022 0 Comments Antigenic shift![]() ![]() brucei has multiple potential expression sites. In addition to homologous recombination, transcriptional regulation is also important in antigen switching, since T. brucei BRCA2 gene with RAD51 (however, this is not the only possible mechanism, as BRCA2 variants still display some VSG switching). This process is partially dependent on homologous recombination of DNA, which is mediated in part by the interaction of the T. Each new gene is switched in turn into a VSG expression site (ES). Only one VSG is expressed at any given time. These VSG genes become activated by gene conversion in a hierarchical order: telomeric VSGs are activated first, followed by array VSGs, and finally pseudogene VSGs. #Antigenic shift codeHowever, the parasite's genome has over 1,000 genes that code for different variants of the VSG protein, located on the subtelomeric portion of large chromosomes, or on intermediate chromosomes. The host eventually identifies the VSG as a foreign antigen and mounts an attack against the microbe. In the early stages of invasion, the VSG coat is sufficient to protect the parasite from immune detection. To protect itself, the parasite decorates itself with a dense, homogeneous coat (~10^7 molecules) of the variant surface glycoprotein (VSG). Replicates extracellularly in the bloodstream of infected mammals and is subjected to numerous host defense mechanisms including the complement system, and the innate and adaptive immune systems. Trypanosoma brucei, the organism that causes sleeping sickness, ![]() Trypanosoma brucei and Plasmodium falciparum are some of the best studied examples. In protozoa Īntigenic variation is employed by a number of different protozoan parasites. Segments of the silent cassettes recombine with the vlsE gene, generating variants of the surface lipoprotein antigen. The bacterium carries a plasmid that contains fifteen silent vls cassettes and one functional copy of vlsE. In the bacterium Borrelia burgdorferi, the cause of Lyme disease, the surface lipoprotein VlsE can undergo recombination which results in antigenic diversity. The Neisseria species vary their pili (protein polymers made up of subunits called pilin which play a critical role in bacterial adhesion, and stimulate a vigorous host immune response) and the Streptococci vary their M-protein. Īntigenic variation in bacteria is best demonstrated by species of the genus Neisseria (most notably, Neisseria meningitidis and Neisseria gonorrhoeae, the gonococcus) species of the genus Streptococcus and the Mycoplasma. Many of the proteins known to show antigenic or phase variation are related to virulence. The result is that even a clonal population of pathogens expresses a heterogeneous phenotype. ![]() Antigenic variation can result from gene conversion, site-specific DNA inversions, hypermutation, or recombination of sequence cassettes. Antigenic variation can occur by altering a variety of surface molecules including proteins and carbohydrates. If the pathogen's dominant antigen can be altered, the pathogen can then evade the host's acquired immune system. Immunity to re-infection is based on recognition of the antigens carried by the pathogen, which are "remembered" by the acquired immune response. Antigenic variation not only enables the pathogen to avoid the immune response in its current host, but also allows re-infection of previously infected hosts. Not to be confused with Antigenic drift or Antigenic shift.Īntigenic variation or antigenic alteration refers to the mechanism by which an infectious agent such as a protozoan, bacterium or virus alters the proteins or carbohydrates on its surface and thus avoids a host immune response, making it one of the mechanisms of antigenic escape. ![]()
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