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Antigenic variation

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Antigenic variation is the process by which an infectious organism alters its surface proteins in order to evade a host immune response. Antigenic variation not only enables immune evasion but also allows pathogens to cause reinfection as they are not recognised 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 (immunological memory) and if the host is exposed to that same antigen again, those antibodies will act rapidly to destroy the pathogen. However, if the antigen is changed, the host's immune system will not recognise it and the pathogen can cause infection again whilst the immune system generates new antibodies to target the new antigen. Antigenic variation enables viruses to cross the species barrier (e.g. H5N1 virus "jumping" from birds to then infect humans). Finally, it also allows pathogens to establish persistent infections in their host.

This change in antigenic profile may occur as the pathogen passes through a host population (also called "antigenic diversity") or may take place in the originally infected host. The strategy is particularly important for organisms that target long-lived hosts, repeatedly infect a single host, and are easily transmitted. Pathogens that express these characteristics and undergo antigenic variation have a selective advantage over their more genetically stable counterparts.

Antigenic variation occurs in bacteria, viruses and protozoa.

Antigenic 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. The Neisseria species mentioned variate their pili (protein polymers made up of subunits called pilin which play a critical role in bacterial adhesion, they are antigens which stimulate a vigorous host immune response) and the Streptococci variate their M-protein.

Antigenic variation in viruses is best demonstrated by HIV (Human Immunodeficiency Virus); Influenza virus and Hepatitis C virus. It is believed that SIV (Simian Immunodeficiency Virus) jumped species from chimpanzees to humans, to give HIV, due to antigenic variation. This antigenic variation enabled the virus to evade the human immune system and establish a chronic infection. Arguably however, perhaps the master of viral antigenic variation is the influenza virus. This highly adaptable virus possesses two glycoproteins, haemagglutinin and neuraminidase, which regularly and rapidly mutate to give antigenically distinct variants. Due to this regular antigenic variation, lifelong immunity to the influenza virus is impossible.

Antigenic variation in protozoa is best demonstrated by species of the genus Plasmodium (responsible for causing malaria) and the trypanosomes (Trypanosoma cruzi which causes Chagas Disease and T. brucei gambiense and T. brucei rhodesiense which both cause African Sleeping Sickness). Plasmodium species carry out antigenic polymorphism and the trypanosomes variate one surface protein called the variant surface glycoprotein (VSG). The number of VSGs that a trypanosome can produce (referred to as the repertoire of VSGs) can vary from 100 to 1000.

Antigenic variation can occur through three broadly defined genetic processes: gene mutation, recombination, and switching. In all cases, antigenic variation results in pathogens that are immunologically distinct from the parental strains. This enables pathogens to evade the host immune system, cause reinfection and persist in a host resulting in chronic infection.

References

  • Barbour AG, Dai Q, Restrepo BI, Stoenner HG, Frank SA., Pathogen escape from host immunity by a genome program for antigenic variation, Proc Natl Acad Sci U S A. 2006 Nov 13;
  • Barbour AG, Restrepo BI., Antigenic variation in vector-borne pathogens.Emerg Infect Dis. 2000 Sep-Oct;6(5):449-57. Review.
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