Heterogeneity in the Helicobacter pylori vacA and cagA genes: association with gastroduodenal disease in South Africa?

BACKGROUND Helicobacter pylori infection is universally associated with gastritis, but only sometimes with clinically significant disease. Candidate virulence markers seem to be useful in identifying the pathogenic infections in some populations. AIMS To investigate the association between putative...

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Published in:Gut 1999-10, Vol.45 (4), p.499-502
Main Authors: Kidd, M, Lastovica, A J, Atherton, J C, Louw, J A
Format: Article
Language:English
Subjects:
adenocarcinoma
Adenocarcinoma - microbiology
Antigens, Bacterial - genetics
Bacterial diseases
Bacterial diseases of the digestive system and abdomen
Bacterial Proteins - genetics
Biological and medical sciences
Biopsy
cagA
Deoxyribonucleic acid
DNA
Endoscopy
Gastric cancer
Gastritis - microbiology
Gastrointestinal Diseases - microbiology
Genes
Genotype
Genotype & phenotype
Helicobacter pylori
Helicobacter pylori - classification
Helicobacter pylori - genetics
Helicobacter pylori - pathogenicity
Human bacterial diseases
Humans
Infections
Infectious diseases
Medical sciences
Molecular weight
Pathology
Peptic Ulcer - microbiology
peptic ulceration
Polymerase Chain Reaction
Population
Proteins
South Africa
Species Specificity
Stomach Neoplasms - microbiology
Studies
Tropical medicine
vacuolating cytotoxin
Virulence
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Lastovica, A J
Atherton, J C
Louw, J A
description BACKGROUND Helicobacter pylori infection is universally associated with gastritis, but only sometimes with clinically significant disease. Candidate virulence markers seem to be useful in identifying the pathogenic infections in some populations. AIMS To investigate the association between putative virulence markers and disease in an African population. METHODS Fifty nineH pylori strains isolated from dyspeptic patients (11 with peptic ulceration, eight with gastric adenocarcinoma, and 28 with no pathology other than gastritis) were studied for differences in the genes vacA andcagA. RESULTS Forty seven (80%) of 59 strains had the vacA signal sequence genotype s1 (one s1a, 46 s1b) and 12 (20%) had subtype s2.vacA mid-region analysis revealed that 40 (68%) strains were vacA m1 and 19 (32%) were m2. All 14 strains from patients with peptic ulceration werevacA s1, in contrast to 23 (66%) of 35 strains from patients with gastritis alone (p
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Candidate virulence markers seem to be useful in identifying the pathogenic infections in some populations. AIMS To investigate the association between putative virulence markers and disease in an African population. METHODS Fifty nineH pylori strains isolated from dyspeptic patients (11 with peptic ulceration, eight with gastric adenocarcinoma, and 28 with no pathology other than gastritis) were studied for differences in the genes vacA andcagA. RESULTS Forty seven (80%) of 59 strains had the vacA signal sequence genotype s1 (one s1a, 46 s1b) and 12 (20%) had subtype s2.vacA mid-region analysis revealed that 40 (68%) strains were vacA m1 and 19 (32%) were m2. All 14 strains from patients with peptic ulceration werevacA s1, in contrast to 23 (66%) of 35 strains from patients with gastritis alone (p&lt;0.01).vacA s2 was found exclusively in patients with gastritis alone (p&lt;0.01). All strains isolated from patients with gastric adenocarcinoma were s1b/m1 (p&lt;0.005 versus gastritis alone).cagA was detectable in 56 (95%) of 59 isolates. Strains from patients with peptic ulceration (12/13 versus 19/30 with gastritis alone, p=0.05) had the shortest fragment length in the 3′ region of cagA, while 4/10 strains from patients with gastric cancer had the longest fragment length in this region (p&lt;0.02 versus gastritis alone). CONCLUSION In this study, thevacA s1 genotype, and fragment length of the 3′ region of cagA identified isolates associated with significant clinical disease. ThevacA s1bm1 genotype seems to be strongly associated with gastric cancer.</description><identifier>ISSN: 0017-5749</identifier><identifier>EISSN: 1468-3288</identifier><identifier>EISSN: 1458-3288</identifier><identifier>DOI: 10.1136/gut.45.4.499</identifier><identifier>PMID: 10486355</identifier><identifier>CODEN: GUTTAK</identifier><language>eng</language><publisher>London: BMJ Publishing Group Ltd and British Society of Gastroenterology</publisher><subject>adenocarcinoma ; Adenocarcinoma - microbiology ; Antigens, Bacterial - genetics ; Bacterial diseases ; Bacterial diseases of the digestive system and abdomen ; Bacterial Proteins - genetics ; Biological and medical sciences ; Biopsy ; cagA ; Deoxyribonucleic acid ; DNA ; Endoscopy ; Gastric cancer ; Gastritis - microbiology ; Gastrointestinal Diseases - microbiology ; Genes ; Genotype ; Genotype &amp; phenotype ; Helicobacter pylori ; Helicobacter pylori - classification ; Helicobacter pylori - genetics ; Helicobacter pylori - pathogenicity ; Human bacterial diseases ; Humans ; Infections ; Infectious diseases ; Medical sciences ; Molecular weight ; Pathology ; Peptic Ulcer - microbiology ; peptic ulceration ; Polymerase Chain Reaction ; Population ; Proteins ; South Africa ; Species Specificity ; Stomach Neoplasms - microbiology ; Studies ; Tropical medicine ; vacuolating cytotoxin ; Virulence</subject><ispartof>Gut, 1999-10, Vol.45 (4), p.499-502</ispartof><rights>British Society of Gastroenterology</rights><rights>1999 INIST-CNRS</rights><rights>Copyright: 1999 British Society of Gastroenterology</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-b507t-1c42e7a52e19de5cf418ec9237e261911a506cbb664a4611afdf1b403c75c8393</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1727692/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1727692/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&amp;idt=1952717$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10486355$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kidd, M</creatorcontrib><creatorcontrib>Lastovica, A J</creatorcontrib><creatorcontrib>Atherton, J C</creatorcontrib><creatorcontrib>Louw, J A</creatorcontrib><title>Heterogeneity in the Helicobacter pylori vacA and cagA genes: association with gastroduodenal disease in South Africa?</title><title>Gut</title><addtitle>Gut</addtitle><description>BACKGROUND Helicobacter pylori infection is universally associated with gastritis, but only sometimes with clinically significant disease. Candidate virulence markers seem to be useful in identifying the pathogenic infections in some populations. AIMS To investigate the association between putative virulence markers and disease in an African population. METHODS Fifty nineH pylori strains isolated from dyspeptic patients (11 with peptic ulceration, eight with gastric adenocarcinoma, and 28 with no pathology other than gastritis) were studied for differences in the genes vacA andcagA. RESULTS Forty seven (80%) of 59 strains had the vacA signal sequence genotype s1 (one s1a, 46 s1b) and 12 (20%) had subtype s2.vacA mid-region analysis revealed that 40 (68%) strains were vacA m1 and 19 (32%) were m2. All 14 strains from patients with peptic ulceration werevacA s1, in contrast to 23 (66%) of 35 strains from patients with gastritis alone (p&lt;0.01).vacA s2 was found exclusively in patients with gastritis alone (p&lt;0.01). All strains isolated from patients with gastric adenocarcinoma were s1b/m1 (p&lt;0.005 versus gastritis alone).cagA was detectable in 56 (95%) of 59 isolates. Strains from patients with peptic ulceration (12/13 versus 19/30 with gastritis alone, p=0.05) had the shortest fragment length in the 3′ region of cagA, while 4/10 strains from patients with gastric cancer had the longest fragment length in this region (p&lt;0.02 versus gastritis alone). CONCLUSION In this study, thevacA s1 genotype, and fragment length of the 3′ region of cagA identified isolates associated with significant clinical disease. ThevacA s1bm1 genotype seems to be strongly associated with gastric cancer.</description><subject>adenocarcinoma</subject><subject>Adenocarcinoma - microbiology</subject><subject>Antigens, Bacterial - genetics</subject><subject>Bacterial diseases</subject><subject>Bacterial diseases of the digestive system and abdomen</subject><subject>Bacterial Proteins - genetics</subject><subject>Biological and medical sciences</subject><subject>Biopsy</subject><subject>cagA</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>Endoscopy</subject><subject>Gastric cancer</subject><subject>Gastritis - microbiology</subject><subject>Gastrointestinal Diseases - microbiology</subject><subject>Genes</subject><subject>Genotype</subject><subject>Genotype &amp; phenotype</subject><subject>Helicobacter pylori</subject><subject>Helicobacter pylori - classification</subject><subject>Helicobacter pylori - genetics</subject><subject>Helicobacter pylori - pathogenicity</subject><subject>Human bacterial diseases</subject><subject>Humans</subject><subject>Infections</subject><subject>Infectious diseases</subject><subject>Medical sciences</subject><subject>Molecular weight</subject><subject>Pathology</subject><subject>Peptic Ulcer - microbiology</subject><subject>peptic ulceration</subject><subject>Polymerase Chain Reaction</subject><subject>Population</subject><subject>Proteins</subject><subject>South Africa</subject><subject>Species Specificity</subject><subject>Stomach Neoplasms - microbiology</subject><subject>Studies</subject><subject>Tropical medicine</subject><subject>vacuolating cytotoxin</subject><subject>Virulence</subject><issn>0017-5749</issn><issn>1468-3288</issn><issn>1458-3288</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1999</creationdate><recordtype>article</recordtype><recordid>eNp9kc2P0zAQxSMEYkvhxhlZAsGFFDvxR8wBVFXsFmkBCRY4Wo4zSd1N42I7hf73uGq1LBw4jaz385uneVn2mOAZISV_1Y1xRtmMzqiUd7IJobzKy6Kq7mYTjInImaDyLHsQwhpjXFWS3M_OCKYVLxmbZLslRPCugwFs3CM7oLgCtITeGldrkzS03ffOW7TTZo700CCjuzk6fAivkQ7BGaujdQP6aeMKdTpE75rRNTDoHjU2gA5w8P3ixqTPW2-Nfvswu9fqPsCj05xmX8_fXS2W-eWni_eL-WVeMyxiTgwtQGhWAJENMNNSUoGRRSmg4EQSohnmpq45p5ry9GybltQUl0YwU5WynGZvjr7bsd5AY2CIXvdq6-1G-71y2qq_lcGuVOd2iohC8LRomj0_GXj3Y4QQ1cYGA32vB3BjUALjUshKJPDpP-DajT7dICQvISXHHLNEvTxSxrsQPLQ3UQhWhzpVqlNRpqhKdSb8ye34t-Bjfwl4dgJ0MLpvvR6MDX84yQpBDuHyI2ZDhF83svbXiotSMPXx20J9rpZX8vzig_qe-BdHvt6s_5_wNwBuxcE</recordid><startdate>19991001</startdate><enddate>19991001</enddate><creator>Kidd, M</creator><creator>Lastovica, A J</creator><creator>Atherton, J C</creator><creator>Louw, J A</creator><general>BMJ Publishing Group Ltd and British Society of Gastroenterology</general><general>BMJ</general><general>BMJ Publishing Group LTD</general><scope>BSCLL</scope><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8AF</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>BTHHO</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>19991001</creationdate><title>Heterogeneity in the Helicobacter pylori vacA and cagA genes: association with gastroduodenal disease in South Africa?</title><author>Kidd, M ; Lastovica, A J ; Atherton, J C ; Louw, J A</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b507t-1c42e7a52e19de5cf418ec9237e261911a506cbb664a4611afdf1b403c75c8393</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1999</creationdate><topic>adenocarcinoma</topic><topic>Adenocarcinoma - microbiology</topic><topic>Antigens, Bacterial - genetics</topic><topic>Bacterial diseases</topic><topic>Bacterial diseases of the digestive system and abdomen</topic><topic>Bacterial Proteins - genetics</topic><topic>Biological and medical sciences</topic><topic>Biopsy</topic><topic>cagA</topic><topic>Deoxyribonucleic acid</topic><topic>DNA</topic><topic>Endoscopy</topic><topic>Gastric cancer</topic><topic>Gastritis - microbiology</topic><topic>Gastrointestinal Diseases - microbiology</topic><topic>Genes</topic><topic>Genotype</topic><topic>Genotype &amp; phenotype</topic><topic>Helicobacter pylori</topic><topic>Helicobacter pylori - classification</topic><topic>Helicobacter pylori - genetics</topic><topic>Helicobacter pylori - pathogenicity</topic><topic>Human bacterial diseases</topic><topic>Humans</topic><topic>Infections</topic><topic>Infectious diseases</topic><topic>Medical sciences</topic><topic>Molecular weight</topic><topic>Pathology</topic><topic>Peptic Ulcer - microbiology</topic><topic>peptic ulceration</topic><topic>Polymerase Chain Reaction</topic><topic>Population</topic><topic>Proteins</topic><topic>South Africa</topic><topic>Species Specificity</topic><topic>Stomach Neoplasms - microbiology</topic><topic>Studies</topic><topic>Tropical medicine</topic><topic>vacuolating cytotoxin</topic><topic>Virulence</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kidd, M</creatorcontrib><creatorcontrib>Lastovica, A J</creatorcontrib><creatorcontrib>Atherton, J C</creatorcontrib><creatorcontrib>Louw, J A</creatorcontrib><collection>Istex</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>ProQuest Health and Medical</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>STEM Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>AUTh Library subscriptions: ProQuest Central</collection><collection>ProQuest Natural Science Collection</collection><collection>BMJ Journals</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health &amp; Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health &amp; Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</collection><collection>ProQuest Science Journals</collection><collection>ProQuest Biological Science Journals</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Gut</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kidd, M</au><au>Lastovica, A J</au><au>Atherton, J C</au><au>Louw, J A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Heterogeneity in the Helicobacter pylori vacA and cagA genes: association with gastroduodenal disease in South Africa?</atitle><jtitle>Gut</jtitle><addtitle>Gut</addtitle><date>1999-10-01</date><risdate>1999</risdate><volume>45</volume><issue>4</issue><spage>499</spage><epage>502</epage><pages>499-502</pages><issn>0017-5749</issn><eissn>1468-3288</eissn><eissn>1458-3288</eissn><coden>GUTTAK</coden><abstract>BACKGROUND Helicobacter pylori infection is universally associated with gastritis, but only sometimes with clinically significant disease. Candidate virulence markers seem to be useful in identifying the pathogenic infections in some populations. AIMS To investigate the association between putative virulence markers and disease in an African population. METHODS Fifty nineH pylori strains isolated from dyspeptic patients (11 with peptic ulceration, eight with gastric adenocarcinoma, and 28 with no pathology other than gastritis) were studied for differences in the genes vacA andcagA. RESULTS Forty seven (80%) of 59 strains had the vacA signal sequence genotype s1 (one s1a, 46 s1b) and 12 (20%) had subtype s2.vacA mid-region analysis revealed that 40 (68%) strains were vacA m1 and 19 (32%) were m2. All 14 strains from patients with peptic ulceration werevacA s1, in contrast to 23 (66%) of 35 strains from patients with gastritis alone (p&lt;0.01).vacA s2 was found exclusively in patients with gastritis alone (p&lt;0.01). All strains isolated from patients with gastric adenocarcinoma were s1b/m1 (p&lt;0.005 versus gastritis alone).cagA was detectable in 56 (95%) of 59 isolates. Strains from patients with peptic ulceration (12/13 versus 19/30 with gastritis alone, p=0.05) had the shortest fragment length in the 3′ region of cagA, while 4/10 strains from patients with gastric cancer had the longest fragment length in this region (p&lt;0.02 versus gastritis alone). CONCLUSION In this study, thevacA s1 genotype, and fragment length of the 3′ region of cagA identified isolates associated with significant clinical disease. ThevacA s1bm1 genotype seems to be strongly associated with gastric cancer.</abstract><cop>London</cop><pub>BMJ Publishing Group Ltd and British Society of Gastroenterology</pub><pmid>10486355</pmid><doi>10.1136/gut.45.4.499</doi><tpages>4</tpages><oa>free_for_read</oa></addata></record>
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subjects adenocarcinoma
Adenocarcinoma - microbiology
Antigens, Bacterial - genetics
Bacterial diseases
Bacterial diseases of the digestive system and abdomen
Bacterial Proteins - genetics
Biological and medical sciences
Biopsy
cagA
Deoxyribonucleic acid
DNA
Endoscopy
Gastric cancer
Gastritis - microbiology
Gastrointestinal Diseases - microbiology
Genes
Genotype
Genotype & phenotype
Helicobacter pylori
Helicobacter pylori - classification
Helicobacter pylori - genetics
Helicobacter pylori - pathogenicity
Human bacterial diseases
Humans
Infections
Infectious diseases
Medical sciences
Molecular weight
Pathology
Peptic Ulcer - microbiology
peptic ulceration
Polymerase Chain Reaction
Population
Proteins
South Africa
Species Specificity
Stomach Neoplasms - microbiology
Studies
Tropical medicine
vacuolating cytotoxin
Virulence
title Heterogeneity in the Helicobacter pylori vacA and cagA genes: association with gastroduodenal disease in South Africa?
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