Studies on Immunity to Asiatic Cholera: I. Introduction

Burrows, William; Mather, Adaline N.; Elliott, Marian E.; Wagner, Stephen S.

doi:10.1093/infdis/79.2.159

Cited by 12 publications

(5 citation statements)

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“…The O1 Inaba El Tor reference strain (ET 259), which does not produce cholera toxin although it carries at least part of the ctxA gene, is not closely related to the O1/O139 cluster of pandemic strains or to the toxigenic O37 clone (ET 5). According to T. Shimada (38a), the reference strain is the NIH 35-a-3 isolate listed by Burrows et al (7) as one of the strains used for vaccine preparation by the U.S. Army in the early 1940s. It was received from the Central Research Institute in Kasauli, India, in 1942, without indication of collection date or source of isolation.…”

Section: Species Limits Strains Of Ets 276 To 279 In the Deep Lineagesmentioning

confidence: 99%

Genetic Diversity and Population Structure of Vibrio cholerae

et al. 1999

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Multilocus enzyme electrophoresis (MLEE) of 397 Vibrio cholerae isolates, including 143 serogroup reference strains and 244 strains from Mexico and Guatemala, identified 279 electrophoretic types (ETs) distributed in two major divisions (I and II). Linkage disequilibrium was demonstrated in both divisions and in subdivision Ic of division I but not in subdivision Ia, which includes 76% of the ETs. Despite this evidence of relatively frequent recombination, clonal lineages may persist for periods of time measured in at least decades. In addition to the pandemic clones of serogroups O1 and O139, which form a tight cluster of four ETs in subdivision Ia, MLEE analysis identified numerous apparent clonal lineages of non-O1 strains with intercontinental distributions. A clone of serogroup O37 that demonstrated epidemic potential in the 1960s is closely related to the pandemic O1/O139 clones, but the nontoxigenic O1 Inaba El Tor reference strain is not. A strain of serogroup O22, which has been identified as the most likely donor of exogenous rfb region DNA to the O1 progenitor of the O139 clone, is distantly related to the O1/O139 clones. The close evolutionary relationships of the O1, O139, and O37 epidemic clones indicates that new cholera clones are likely to arise by the modification of a lineage that is already epidemic or is closely related to such a clone.

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Section: Species Limits Strains Of Ets 276 To 279 In the Deep Lineagesmentioning

confidence: 99%

Genetic Diversity and Population Structure of Vibrio cholerae

et al. 1999

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“…The somatic antigen is extractable from cholera vibrios by conventional procedures used for isolation of endotoxic LPS from other gram-negative species (12). Organisms belonging to serogroup 0:1 are characterized by the presence of group-specific antigen A and are subdivided into serotypes Ogawa and Inaba; each of these serotypes is characterized by a type-specific antigen (antigens B and C, respectively) (7,8,13,18,28). Standard sera prepared in national laboratories have been used as references for the preparation of grouping and typing antisera in various smaller laboratories (governmental, commercial, and university).…”

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confidence: 99%

Monoclonal antibodies to outer membrane antigens of Vibrio cholerae

Sciortino¹,

Zhou²,

Finkelstein³

1985

Infect Immun

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Hybridoma-derived monoclonal antibodies were prepared against outer membrane antigens of four strains of Vibrio cholerae that were cultivated under iron-limited conditions, and these antibodies were partially characterized. We established a library of 66 hybridomas which produced monoclonal antibodies defining 16 different V. chokrae antigens. Two antigens (molecular weights, 18,000 and 112,000) were heat modifiable, whereas the reacting epitope of a third antigen (40,000-dalton-18,000-dalton doublet) was completely destroyed when it was heated at 100°C. The 112,000-dalton heat-modifiable protein was an iron-regulated outer membrane protein. This protein bound 59Fe in vitro when it was combined with the V. chokrae siderophoreiron complex 59Fe-vibriobactin; it was also found in in vivo grown V. cholerae, as were three other antigens. A total of 26 hybridomas produced antibody to V. cholerae lipopolysaccharide. Of these, 12 were cross-reactive with lipopolysaccharides of other gram-negative bacteria, including 2 which recognized lipid A. Several of these anti-lipopolysaccharide monoclonal antibodies appeared to be lipopolysaccharide region specific. Some membrane antigens were strain specific, whereas others were common to both 0 group 1 and non-O group 1 vibrios.

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“…It exists as two biotypes, classical and El Tor, which can be differentiated on the basis of a number of biochemical and genetic tests. Both can exist as three serotypes, Inaba, Ogawa and Hikojima, that have been distinguished on the basis of three antigens, A, B and C associated with the O‐antigen of the lipopolysaccharide (LPS) and defined using cross‐absorbed antisera [1–3]. These antigens are absent in rough mutants lacking the O‐antigen [4–6].…”

Section: Introductionmentioning

confidence: 99%

Lipopolysaccharide O-antigen expression and the effect of its absence on virulence in rfb mutants of Vibrio cholerae O1

Iredell

Stroeher

Ward

et al. 2006

FEMS Immunology &Amp; Medical Microbiology

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Using defined rfb mutants, defective in the biosynthesis of the O‐antigen of the lipopolysaccharide (LPS), and monoclonal antibodies (MAbs) to the A, B and C LPS antigens, we have examined the distribution of the antigens and the effects of their loss. By immunogold electron microscopy, it has been possible to determine the relative amounts of the A, B and C antigens on Inaba and Ogawa cells, confirming previous studies based upon bacterial agglutination and hemagglutination inhibitions. These antigens are absent from rfb::Tn mutants selected as resistant to phages which have been shown to use the O‐antigen as their receptor. These mutants were severely attenuated as measured by both LD50 and their ability to compete with the wild‐type parents when analyzed in the infant mouse cholera model. These mutants were unchanged in the export of cholera toxin or other secreted proteins but revealed an altered outer membrane protein profile. The competition defect suggested an effect on TCP (toxin‐coregulated pilus). An analysis of the rfb::Tn mutants revealed that they were unable to assemble TCP on their surface, but the major subunit, TcpA, could be found as an intracellular pool. These mutants could be complemented back to wild‐type using the cloned rfb region, implying that functional TCP assembly is dependent upon an intact LPS.

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Studies on Immunity to Asiatic Cholera: I. Introduction

Cited by 12 publications

References 0 publications

Genetic Diversity and Population Structure of Vibrio cholerae

Genetic Diversity and Population Structure of Vibrio cholerae

Monoclonal antibodies to outer membrane antigens of Vibrio cholerae

Lipopolysaccharide O-antigen expression and the effect of its absence on virulence in rfb mutants of Vibrio cholerae O1

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