Aralkylamine N-acetyltransferase

Overview of antigenic variation in pathogens

Antigenic variation is a mechanism by which an infectious organism alters its surface proteins in order to evade a host immune response. This process is crucial for the survival of many pathogens, allowing them to persist in the host and cause chronic infections. Antigenic variation is a common strategy among viruses, bacteria, and protozoa.

Mechanisms

Antigenic variation can occur through several mechanisms, including:

Gene conversion

Gene conversion involves the replacement of one gene segment with another, leading to the expression of a different antigenic variant. This mechanism is well-studied in the African trypanosome, which uses gene conversion to switch its variant surface glycoprotein (VSG) coat.

Site-specific recombination

Site-specific recombination is a process where specific DNA sequences are rearranged, leading to changes in the expressed antigens. This mechanism is used by Borrelia burgdorferi, the causative agent of Lyme disease, to vary its outer surface proteins.

Hypermutation

Hypermutation involves rapid mutations in the genes encoding surface antigens. This is a common strategy in RNA viruses such as influenza and HIV, where the high mutation rate of the viral genome leads to frequent changes in the antigenic properties of the virus.

Epigenetic regulation

Epigenetic changes, such as DNA methylation and histone modification, can also lead to antigenic variation by altering the expression of surface antigen genes without changing the underlying DNA sequence. This mechanism is observed in Plasmodium falciparum, the parasite responsible for malaria.

Biological significance

Antigenic variation allows pathogens to:

• Evade the host's immune system by altering the antigens that are recognized by antibodies and T cells.
• Prolong infection and increase the chances of transmission to new hosts.
• Adapt to different host environments and immune pressures.

Examples in pathogens

Trypanosoma brucei

The African trypanosome, Trypanosoma brucei, is a protozoan parasite that causes African sleeping sickness. It uses antigenic variation to switch its VSG coat, allowing it to evade the host's immune response.

Plasmodium falciparum

Plasmodium falciparum, the most virulent species of malaria-causing parasites, uses antigenic variation to alter the expression of PfEMP1 proteins on the surface of infected red blood cells, helping it avoid immune detection.

Neisseria gonorrhoeae

Neisseria gonorrhoeae, the bacterium responsible for gonorrhea, undergoes antigenic variation of its pili and outer membrane proteins to escape immune surveillance.

Related pages

• Immune evasion
• Pathogen
• Vaccine development
• Molecular biology

Gallery

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  Mechanisms of VSG switching in Trypanosoma brucei.
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  Mutation effects on HIV gp120 binding.

Aralkylamine N-acetyltransferase

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  Structure of Aralkylamine N-acetyltransferase (PDB code 1KUX)
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  Synthesis of Melatonin from Serotonin through two enzymatic steps