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Constructing Mutants in Serotype 1 Streptococcus pneumoniae strain 519/43
Published on: September 11, 2020
Antigenic variation in pneumocystis
1Department of Molecular Genetics, Biochemistry and Microbiology, University of Cincinnati, Cincinnati, Ohio 45267-0524, USA. stringjr@ucmail.uc.edu
Abstract:
Pneumocystis is a genus containing many species of non-culturable fungi, each of which infects a different mammalian host. Pneumonia caused by Pneumocystis is a problem in immunodeficient humans, but not in normal humans. Nevertheless, it appears that Pneumocystis organisms cannot survive and proliferate outside of their mammalian hosts, suggesting that Pneumocystis parasitizes immunocompetent mammals. Residence in immunocompetent hosts may rely on camouflage perpetrated by antigenic variation. In P. carinii, which is found in rats, there exist three families of genes that appear to be designed to create antigenic variation. One gene family, which encodes the major surface glycoprotein (MSG), contains nearly 100 members. Expression of the MSG family is controlled by restricting transcription to the one gene that is linked to a unique expression site. Changes in the sequence of the MSG gene linked to the expression site occur and appear to be caused by recombination with MSG genes not at the expression site. Preliminary evidence suggests that gene conversion is the predominant recombination mechanism.
Insights
Pneumocystis fungi evade host immunity through antigenic variation. In Pneumocystis carinii, the major surface glycoprotein gene family undergoes recombination, likely via gene conversion, to alter surface proteins and evade detection.
Area of Science:
- Mycology
- Immunology
- Molecular Biology
Background:
- Pneumocystis fungi are host-specific and non-culturable.
- Pneumocystis pneumonia (PCP) affects immunocompromised individuals.
- Fungal survival in immunocompetent hosts may involve immune evasion strategies.
Purpose of the Study:
- To investigate the mechanisms of immune evasion in Pneumocystis.
- To explore the role of antigenic variation in Pneumocystis carinii.
Main Methods:
- Analysis of gene families encoding the major surface glycoprotein (MSG) in P. carinii.
- Investigation of gene expression control and recombination mechanisms.
Main Results:
- P. carinii possesses nearly 100 MSG genes for antigenic variation.
- MSG gene expression is regulated by a unique transcription-linked expression site.
- Recombination between MSG genes, potentially through gene conversion, alters expressed surface proteins.
Conclusions:
- Antigenic variation via MSG gene recombination is a key survival strategy for Pneumocystis in immunocompetent hosts.
- Gene conversion is the likely mechanism driving sequence changes in the expressed MSG gene.
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