Expression of the Pneumocystis carinii major surface glycoprotein epitope is correlated with linkage of the cognate gene to the upstream conserved sequence locus

Schaffzin, Joshua K.; Stringer, James R.

doi:10.1099/mic.0.26542-0

Cited by 12 publications

(6 citation statements)

References 49 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, the following lines of evidence support it. (1) Many different MSG genes can occupy the expression site (Keely, Cushion, and Stringer 2003;Schaffzin and Stringer 2004;Stringer 2003Stringer , 2005Stringer and Keely 2001;Stringer 1996, 1997;Wada et al 1995). In the first population of P. carinii studied at the UCS locus, there were at least 27 different MSG genes at the expression site (Keely, Cushion, and Stringer 2003).…”

mentioning

confidence: 99%

Antigenic Variation in Pneumocystis¹

Stringer

2007

J Eukaryotic Microbiology

Self Cite

View full text Add to dashboard Cite

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.

show abstract

mentioning

confidence: 99%

Antigenic Variation in Pneumocystis¹

Stringer

2007

J Eukaryotic Microbiology

Self Cite

View full text Add to dashboard Cite

show abstract

“…50 A genomic promoter region for the MSG is called the upstream conserved sequence (UCS) and is adjacent to the expressed MSG isoform gene. [51][52][53][54][55] UCS encodes a peptide that carries the MSG to the endoplasmic reticulum for glycosylation, UCS cleavage, and surface expression. It is presumed, based on the genetic structure and observations in other species, that subtelomeric recombination accounts for antigenic switching; the stimulus for this event is unknown.…”

Section: History and Backgroundmentioning

confidence: 99%

Pneumocystis jiroveci

Fishman

2020

Semin Respir Crit Care Med

View full text Add to dashboard Cite

Pneumocystis jiroveci remains an important fungal pathogen in a broad range of immunocompromised hosts. The natural reservoir of infection remains unknown. Pneumocystis jiroveci Pneumonia (PJP) develops via airborne transmission or reactivation of inadequately treated infection. Nosocomial clusters of infection have been described among immunocompromised hosts. Subclinical infection or colonization may occur. Pneumocystis pneumonia occurs most often within 6 months of organ transplantation and with intensified or prolonged immunosuppression, notably with corticosteroids. Infection is also common during neutropenia and low-lymphocyte counts, with hypogammaglobulinemia, and following cytomegalovirus (CMV) infection. The clinical presentation generally includes fever, dyspnea with hypoxemia, and nonproductive cough. Chest radiographic patterns are best visualized by computed tomography (CT) scan with diffuse interstitial processes. Laboratory examination reveals hypoxemia, elevated serum lactic dehydrogenase levels, and elevated serum (1→3) β-D-glucan assays. Specific diagnosis is achieved using respiratory specimens with direct immunofluorescent staining; invasive procedures may be required and are important to avoid unnecessary therapies. Quantitative nucleic acid amplification is a useful adjunct to diagnosis but may be overly sensitive. Trimethoprim-sulfamethoxazole (TMP-SMX) remains the drug of choice for therapy; drug allergy should be documented before resorting to alternative therapies. Adjunctive corticosteroids may be useful early in the clinical course; aggressive reductions in immunosuppression may provoke immune reconstitution syndromes. Pneumocystis pneumonia (PJP) prophylaxis is recommended and effective for immunocompromised individuals in the most commonly affected risk groups.

show abstract

“…This locus is termed ‘the expression site’ (Wada et al ., ; Sunkin & Stringer, ; Wada & Nakamura, ). Consequently, a single Msg protein is expressed on the fungal surface at a time (Angus et al ., ; Schaffzin & Stringer, ). The msg gene in the ES appears to be replaced periodically by another msg gene by means of homologous DNA recombination through a yet unknown mechanism.…”

Section: Gene Conversion–induced Antigenic Variation In Eukaryotesmentioning

confidence: 99%

Microbial antigenic variation mediated by homologous DNA recombination

2012

View full text Add to dashboard Cite

Pathogenic microorganisms employ numerous molecular strategies in order to delay or circumvent recognition by the immune system of their host. One of the most widely used strategies of immune evasion is antigenic variation, in which immunogenic molecules expressed on the surface of a microorganism are continuously modified. As a consequence, the host is forced to constantly adapt its humoral immune response against this pathogen. An antigenic change thus provides the microorganism with an opportunity to persist and/or replicate within the host (population) for an extended period of time or to effectively infect a previously infected host. In most cases, antigenic variation is caused by genetic processes that lead to modification of the amino acid sequence of a particular antigen or to alterations in the expression of biosynthesis genes that induce changes in expression of a variant antigen. Here, we will review antigenic variation systems that rely on homologous DNA recombination and which are found in a wide range of cellular, human pathogens, including bacteria (such as Neisseria spp., Borrelia spp., Treponema pallidum and Mycoplasma spp.), fungi (like Pneumocystis carinii) and parasites (such as the African trypanosome Trypanosoma brucei). Specifically, the various DNA recombination-based antigenic variation systems will be discussed with a focus on the employed mechanisms of recombination, the DNA substrates, and the enzymatic machinery involved.

show abstract

Expression of the Pneumocystis carinii major surface glycoprotein epitope is correlated with linkage of the cognate gene to the upstream conserved sequence locus

Cited by 12 publications

References 49 publications

Antigenic Variation in Pneumocystis¹

Antigenic Variation in Pneumocystis¹

Pneumocystis jiroveci

Microbial antigenic variation mediated by homologous DNA recombination

Contact Info

Product

Resources

About

Expression of the Pneumocystis carinii major surface glycoprotein epitope is correlated with linkage of the cognate gene to the upstream conserved sequence locus

Cited by 12 publications

References 49 publications

Antigenic Variation in Pneumocystis1

Antigenic Variation in Pneumocystis1

Pneumocystis jiroveci

Microbial antigenic variation mediated by homologous DNA recombination

Contact Info

Product

Resources

About

Antigenic Variation in Pneumocystis¹

Antigenic Variation in Pneumocystis¹