Molecular biology of trypanosome antigenic variation.

Donelson, John E.; Rice-Ficht, A C

doi:10.1128/mmbr.49.2.107-125.1985

Cited by 74 publications

(20 citation statements)

References 106 publications

(187 reference statements)

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“…Ribosomal frameshitting and slipped-strand mispairing are involved in the differential expression and phase variation of the gonococcal P.II genes (Seifert and So, 1988). Trypanosoma brucei, Neisseria gonorrhoeae, and Borrelia hermsiivary their surface antigens by gene conversion between expressed and silent copies of the genes encoding for the surface protein (Donelson and Rice-Ficht, 1985;Hagbloom et ai. 1985;Meier etai, 1985).…”

Section: Discussionmentioning

confidence: 99%

Nucleotide substitutions and small‐scale insertion produce size and antigenic variation in group A streptococcal M1 protein

Harbaugh

Podbielski²,

Hügl³

et al. 1993

Molecular Microbiology

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The presence of M protein on the surface of group A streptococci (GAS) confers the ability of the cell to resist phagocytosis in the absence of type-specific antibodies. It undergoes antigenic variation with more than 80 different serotypes having been defined. We have sequenced the M protein gene (emm1.1) from strain CS190 and present evidence that individual nucleotide substitutions are responsible for sequence variation in the N-terminal non-repeat region of emm1.1 and these substitutions have altered antibody recognition of opsonic epitopes. The N-terminal non-repeat domains of two other closely related strains, 71-155 and 76-088, were found to have sequence identical to emm1.1 with the addition of a 21 bp insert. This study provides the first evidence that nucleotide substitutions and small insertions are responsible for size and antigenic variation in the N-terminal non-repeat domain of the M protein of GAS.

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Section: Discussionmentioning

confidence: 99%

Nucleotide substitutions and small‐scale insertion produce size and antigenic variation in group A streptococcal M1 protein

Harbaugh

Podbielski²,

Hügl³

et al. 1993

Molecular Microbiology

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“…This antigenic variation occurs spontaneously in culture, so that the immune response to the successive variants does not appear to trigger the induction of new variants but to serve a (negative) selective function. In consequence, although a strong immune response to VSG is elicited, it is rendered totally ineffective by the development of variant parasite clones (Borst & Cross 1982, Donelson & Rice-Ficht 1985. Variation of parasite-derived antigens expressed on the surface of infected red blood cells has also been demonstrated in infection with some species of Plasmodia.…”

Section: The Lures Of Cell Communication In the Mammalian Hostsmentioning

confidence: 99%

Molecular Basis of Host‐Parasite Relationship: Towards the Definition of Protective Antigens

Càpron

Dessaint

1989

Immunological Reviews

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In spite of some remarkable progress in our understanding of the immune response to parasites and in the molecular cloning of dozens of genes encoding for potentially protective proteins, no definitive step has yet been made towards operational vaccines against major human parasitic diseases. The reasons for our present failures are no longer attributable to the lack of appropriate tools but rather to our rather primitive knowledge of the basic mechanisms governing host-parasite relationship. Mainly on the basics of our personal observations, we have attempted to review and discuss some of the prominent factors in host-parasite interactions, such as molecular mimicry, phyletic convergence, molecular mechanisms of infectivity and lures of cell communication. In many respects, the development of efficient vaccines applicable to humans appears closely dependent on a better understanding of the basic biological mechanisms underlying the natural history of parasitic diseases. In this context, the development of new concepts regarding the definition of potentially protective antigens based on the study of non-surface molecules, cross-reactive stage antigens and antibody isotype selection might represent promising alternatives.

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“…Antigenic switching can occur either by replacement of the VSG gene in the active ES by another previously silent or basic copy VSG gene (Hoeijmakers et al, 1980;Bernards etal., 1981;De Lange and Borst, 1982;Pays etal., 1985), or by activation of another ES and inactivation of the formerly active one without detectable DNA rearrangements (Williams et al, 1979;Buck et al, 1984;Michels et al, 1984; . Gene replacement occurs by recombination or gene conversion (reviewed by Boothroyd, 1985;Donelson and Rice-Ficht, 1985;Borst, 1986;Borst and Greaves, 1987;Pays and Steinert, 1988).…”

Section: Introductionmentioning

confidence: 99%

The promoter for a variant surface glycoprotein gene expression site in Trypanosoma brucei.

et al. 1990

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The variant‐specific surface glycoprotein (VSG) gene 221 of Trypanosoma brucei is transcribed as part of a 60 kb expression site (ES). We have identified the promoter controlling this multigene transcription unit by the use of 221 chromosome‐enriched DNA libraries and VSG gene 221 expression site specific transcripts. The start of transcription was determined by hybridization and RNase protection analysis of nascent RNA. The 5′ ends of the major transcripts coming from the initiation region map at nucleotide sequences that do not strongly resemble rRNA transcriptional starts even though the transcripts are synthesized by an RNA polymerase highly resistant to alpha‐amanitin. The cloned VSG gene 221 ES transcription initiation region promotes high CAT gene expression, when reintroduced by electroporation into T. brucei. We show that the activity of this expression site is controlled at or near transcription initiation in bloodstream trypanosomes. The 221 ES is inactivated without any sequence alteration within 1.4 kb of the transcription start site. This excludes mechanisms of promoter inactivation involving DNA rearrangements in the vicinity of the transcription start site, e.g. promoter inversion or conversion.

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Molecular biology of trypanosome antigenic variation.

Cited by 74 publications

References 106 publications

Nucleotide substitutions and small‐scale insertion produce size and antigenic variation in group A streptococcal M1 protein

Nucleotide substitutions and small‐scale insertion produce size and antigenic variation in group A streptococcal M1 protein

Molecular Basis of Host‐Parasite Relationship: Towards the Definition of Protective Antigens

The promoter for a variant surface glycoprotein gene expression site in Trypanosoma brucei.

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