GrippeBresilV1, Main, Exploration, bibRecord, 000017

Human CCR5Δ32 (rs333) polymorphism has no influence on severity and mortality of influenza A(H1N1)pdm09 infection in Brazilian patients from the post pandemic period.

Identifieur interne : 000017 ( Main/Exploration ); précédent : 000016; suivant : 000018

Human CCR5Δ32 (rs333) polymorphism has no influence on severity and mortality of influenza A(H1N1)pdm09 infection in Brazilian patients from the post pandemic period.

Auteurs : Aline R. Matos [Brésil] ; Jéssica S C C. Martins [Brésil] ; Maria De Lourdes A. Oliveira [Brésil] ; Cristiana C. Garcia [Brésil] ; Marilda M. Siqueira [Brésil]

Source :

Infection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases [ 1567-7257 ] ; 2019.

RBID : pubmed:30389547

Descripteurs français

KwdFr :
- Adulte, Adulte d'âge moyen, Allèles, Brésil (épidémiologie), Délétion de séquence, Femelle, Fréquence d'allèle, Grippe humaine (génétique), Grippe humaine (mortalité), Grippe humaine (virologie), Grippe humaine (épidémiologie), Génotype, Humains, Indice de gravité médicale, Mortalité, Mâle, Polymorphisme génétique, Prédisposition génétique à une maladie, Récepteurs CCR5 (génétique), Sous-type H1N1 du virus de la grippe A, Surveillance de la santé publique.
MESH :
- génétique : Grippe humaine, Récepteurs CCR5.
- mortalité : Grippe humaine.
- virologie : Grippe humaine.
- épidémiologie : Brésil, Grippe humaine.
- Adulte, Adulte d'âge moyen, Allèles, Délétion de séquence, Femelle, Fréquence d'allèle, Génotype, Humains, Indice de gravité médicale, Mortalité, Mâle, Polymorphisme génétique, Prédisposition génétique à une maladie, Sous-type H1N1 du virus de la grippe A, Surveillance de la santé publique.
Wicri :
- geographic : Brésil.

English descriptors

KwdEn :
- Adult, Alleles, Brazil (epidemiology), Female, Gene Frequency, Genetic Predisposition to Disease, Genotype, Humans, Influenza A Virus, H1N1 Subtype, Influenza, Human (epidemiology), Influenza, Human (genetics), Influenza, Human (mortality), Influenza, Human (virology), Male, Middle Aged, Mortality, Polymorphism, Genetic, Public Health Surveillance, Receptors, CCR5 (genetics), Sequence Deletion, Severity of Illness Index.
MESH :
- chemical , genetics : Receptors, CCR5.
- geographic , epidemiology : Brazil.
- epidemiology : Influenza, Human.
- genetics : Influenza, Human.
- mortality : Influenza, Human.
- virology : Influenza, Human.
- Adult, Alleles, Female, Gene Frequency, Genetic Predisposition to Disease, Genotype, Humans, Influenza A Virus, H1N1 Subtype, Male, Middle Aged, Mortality, Polymorphism, Genetic, Public Health Surveillance, Sequence Deletion, Severity of Illness Index.

Abstract

BACKGROUND

Influenza is an acute and highly contagious viral respiratory infection that causes significant morbidity and mortality. The identification of host genetic factors associated with susceptibility and severity of influenza virus infection is of paramount importance. Previous studies evaluating the potential involvement of the CCR5Δ32 polymorphism (rs333), a 32 base pair deletion in CC motif chemokine receptor 5 (CCR5) gene, in severity and mortality of influenza A(H1N1)pdm09 infected individuals have been reported, but their results are quite conflicting.

OBJECTIVES

The aim of this study was the evaluation of the CCR5Δ32 frequency in individuals with mild, severe and fatal influenza A(H1N1)pdm09 infection and its putative association with clinical and epidemiologic data.

PATIENTS/METHODS

A total of 432 individuals were included in this study and classified according to their clinical status, into the following groups: influenza like illness (ILI) (n = 153); severe acute respiratory infection (SARI) (n = 173) and fatal (n = 106) cases. The samples were collected in the post pandemic period, from 2012 to 2018. Individuals were further stratified according to their clinical and epidemiological data. The CCR5Δ32 variant was genotyped by PCR amplification and a subset of samples was further submitted to Sanger sequencing.

RESULTS

The different clinical groups (ILI, SARI and fatal) presented similar distribution of wt/wt and wt/Δ32 genotypes and CCR5Δ32 allele frequencies. Genotype Δ32/Δ32 was not detected in our study. Additionally, no association between wt/wt and wt/Δ32 genotypes and dyspnea, a clinical factor for influenza complications was found. Similarly, no significant differences in the distribution of wt/wt and wt/Δ32 genotypes and CCR5Δ32 variant allele frequencies were observed in samples from the different Brazilian geographical regions.

CONCLUSIONS

The CCR5Δ32 variant does not influence the susceptibility to influenza A(H1N1)pdm09 severe disease or mortality in individuals from Brazil.

DOI: 10.1016/j.meegid.2018.10.024
PubMed: 30389547

Affiliations:

Links toward previous steps (curation, corpus...)

to stream Main, to step Corpus: 000030
to stream Main, to step Curation: 000030

Le document en format XML

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<term>Female</term>
<term>Gene Frequency</term>
<term>Genetic Predisposition to Disease</term>
<term>Genotype</term>
<term>Humans</term>
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<term>Alleles</term>
<term>Female</term>
<term>Gene Frequency</term>
<term>Genetic Predisposition to Disease</term>
<term>Genotype</term>
<term>Humans</term>
<term>Influenza A Virus, H1N1 Subtype</term>
<term>Male</term>
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<front><div type="abstract" xml:lang="en"><p><b>BACKGROUND</b>
</p>
<p>Influenza is an acute and highly contagious viral respiratory infection that causes significant morbidity and mortality. The identification of host genetic factors associated with susceptibility and severity of influenza virus infection is of paramount importance. Previous studies evaluating the potential involvement of the CCR5Δ32 polymorphism (rs333), a 32 base pair deletion in CC motif chemokine receptor 5 (CCR5) gene, in severity and mortality of influenza A(H1N1)pdm09 infected individuals have been reported, but their results are quite conflicting.</p>
</div>
<div type="abstract" xml:lang="en"><p><b>OBJECTIVES</b>
</p>
<p>The aim of this study was the evaluation of the CCR5Δ32 frequency in individuals with mild, severe and fatal influenza A(H1N1)pdm09 infection and its putative association with clinical and epidemiologic data.</p>
</div>
<div type="abstract" xml:lang="en"><p><b>PATIENTS/METHODS</b>
</p>
<p>A total of 432 individuals were included in this study and classified according to their clinical status, into the following groups: influenza like illness (ILI) (n = 153); severe acute respiratory infection (SARI) (n = 173) and fatal (n = 106) cases. The samples were collected in the post pandemic period, from 2012 to 2018. Individuals were further stratified according to their clinical and epidemiological data. The CCR5Δ32 variant was genotyped by PCR amplification and a subset of samples was further submitted to Sanger sequencing.</p>
</div>
<div type="abstract" xml:lang="en"><p><b>RESULTS</b>
</p>
<p>The different clinical groups (ILI, SARI and fatal) presented similar distribution of wt/wt and wt/Δ32 genotypes and CCR5Δ32 allele frequencies. Genotype Δ32/Δ32 was not detected in our study. Additionally, no association between wt/wt and wt/Δ32 genotypes and dyspnea, a clinical factor for influenza complications was found. Similarly, no significant differences in the distribution of wt/wt and wt/Δ32 genotypes and CCR5Δ32 variant allele frequencies were observed in samples from the different Brazilian geographical regions.</p>
</div>
<div type="abstract" xml:lang="en"><p><b>CONCLUSIONS</b>
</p>
<p>The CCR5Δ32 variant does not influence the susceptibility to influenza A(H1N1)pdm09 severe disease or mortality in individuals from Brazil.</p>
</div>
</front>
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<Title>Infection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases</Title>
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<ArticleTitle>Human CCR5Δ32 (rs333) polymorphism has no influence on severity and mortality of influenza A(H1N1)pdm09 infection in Brazilian patients from the post pandemic period.</ArticleTitle>
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<Abstract><AbstractText Label="BACKGROUND">Influenza is an acute and highly contagious viral respiratory infection that causes significant morbidity and mortality. The identification of host genetic factors associated with susceptibility and severity of influenza virus infection is of paramount importance. Previous studies evaluating the potential involvement of the CCR5Δ32 polymorphism (rs333), a 32 base pair deletion in CC motif chemokine receptor 5 (CCR5) gene, in severity and mortality of influenza A(H1N1)pdm09 infected individuals have been reported, but their results are quite conflicting.</AbstractText>
<AbstractText Label="OBJECTIVES">The aim of this study was the evaluation of the CCR5Δ32 frequency in individuals with mild, severe and fatal influenza A(H1N1)pdm09 infection and its putative association with clinical and epidemiologic data.</AbstractText>
<AbstractText Label="PATIENTS/METHODS">A total of 432 individuals were included in this study and classified according to their clinical status, into the following groups: influenza like illness (ILI) (n = 153); severe acute respiratory infection (SARI) (n = 173) and fatal (n = 106) cases. The samples were collected in the post pandemic period, from 2012 to 2018. Individuals were further stratified according to their clinical and epidemiological data. The CCR5Δ32 variant was genotyped by PCR amplification and a subset of samples was further submitted to Sanger sequencing.</AbstractText>
<AbstractText Label="RESULTS">The different clinical groups (ILI, SARI and fatal) presented similar distribution of wt/wt and wt/Δ32 genotypes and CCR5Δ32 allele frequencies. Genotype Δ32/Δ32 was not detected in our study. Additionally, no association between wt/wt and wt/Δ32 genotypes and dyspnea, a clinical factor for influenza complications was found. Similarly, no significant differences in the distribution of wt/wt and wt/Δ32 genotypes and CCR5Δ32 variant allele frequencies were observed in samples from the different Brazilian geographical regions.</AbstractText>
<AbstractText Label="CONCLUSIONS">The CCR5Δ32 variant does not influence the susceptibility to influenza A(H1N1)pdm09 severe disease or mortality in individuals from Brazil.</AbstractText>
<CopyrightInformation>Copyright © 2018 Elsevier B.V. All rights reserved.</CopyrightInformation>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Matos</LastName>
<ForeName>Aline R</ForeName>
<Initials>AR</Initials>
<AffiliationInfo><Affiliation>Laboratório de Vírus Respiratórios e do Sarampo, National Influenza Center (NIC)/World Health Organization (WHO), Instituto Oswaldo Cruz/Fiocruz, Rio de Janeiro, Brazil. Electronic address: aline.matos@ioc.fiocruz.br.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Martins</LastName>
<ForeName>Jéssica S C C</ForeName>
<Initials>JSCC</Initials>
<AffiliationInfo><Affiliation>Laboratório de Vírus Respiratórios e do Sarampo, National Influenza Center (NIC)/World Health Organization (WHO), Instituto Oswaldo Cruz/Fiocruz, Rio de Janeiro, Brazil.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Oliveira</LastName>
<ForeName>Maria de Lourdes A</ForeName>
<Initials>MLA</Initials>
<AffiliationInfo><Affiliation>Laboratório de Desenvolvimento Tecnológico em Virologia, Instituto Oswaldo Cruz/Fiocruz, Rio de Janeiro, Brazil.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Garcia</LastName>
<ForeName>Cristiana C</ForeName>
<Initials>CC</Initials>
<AffiliationInfo><Affiliation>Laboratório de Vírus Respiratórios e do Sarampo, National Influenza Center (NIC)/World Health Organization (WHO), Instituto Oswaldo Cruz/Fiocruz, Rio de Janeiro, Brazil.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Siqueira</LastName>
<ForeName>Marilda M</ForeName>
<Initials>MM</Initials>
<AffiliationInfo><Affiliation>Laboratório de Vírus Respiratórios e do Sarampo, National Influenza Center (NIC)/World Health Organization (WHO), Instituto Oswaldo Cruz/Fiocruz, Rio de Janeiro, Brazil.</Affiliation>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
<PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType>
<PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType>
</PublicationTypeList>
<ArticleDate DateType="Electronic"><Year>2018</Year>
<Month>10</Month>
<Day>31</Day>
</ArticleDate>
</Article>
<MedlineJournalInfo><Country>Netherlands</Country>
<MedlineTA>Infect Genet Evol</MedlineTA>
<NlmUniqueID>101084138</NlmUniqueID>
<ISSNLinking>1567-1348</ISSNLinking>
</MedlineJournalInfo>
<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D019713">Receptors, CCR5</NameOfSubstance>
</Chemical>
</ChemicalList>
<CitationSubset>IM</CitationSubset>
<MeshHeadingList><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000483" MajorTopicYN="N">Alleles</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D001938" MajorTopicYN="N" Type="Geographic">Brazil</DescriptorName>
<QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D005787" MajorTopicYN="N">Gene Frequency</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D020022" MajorTopicYN="Y">Genetic Predisposition to Disease</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D005838" MajorTopicYN="N">Genotype</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D053118" MajorTopicYN="Y">Influenza A Virus, H1N1 Subtype</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D007251" MajorTopicYN="N">Influenza, Human</DescriptorName>
<QualifierName UI="Q000453" MajorTopicYN="Y">epidemiology</QualifierName>
<QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName>
<QualifierName UI="Q000401" MajorTopicYN="N">mortality</QualifierName>
<QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName>
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<MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D009026" MajorTopicYN="N">Mortality</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D011110" MajorTopicYN="Y">Polymorphism, Genetic</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D062486" MajorTopicYN="N">Public Health Surveillance</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D019713" MajorTopicYN="N">Receptors, CCR5</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D017384" MajorTopicYN="Y">Sequence Deletion</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D012720" MajorTopicYN="N">Severity of Illness Index</DescriptorName>
</MeshHeading>
</MeshHeadingList>
<KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">A(H1N1)Pdm09</Keyword>
<Keyword MajorTopicYN="Y">CCR5delta32</Keyword>
<Keyword MajorTopicYN="Y">Host susceptibility</Keyword>
<Keyword MajorTopicYN="Y">Influenza</Keyword>
<Keyword MajorTopicYN="Y">Mortality</Keyword>
<Keyword MajorTopicYN="Y">Severity</Keyword>
</KeywordList>
</MedlineCitation>
<PubmedData><History><PubMedPubDate PubStatus="received"><Year>2018</Year>
<Month>07</Month>
<Day>23</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="revised"><Year>2018</Year>
<Month>10</Month>
<Day>12</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="accepted"><Year>2018</Year>
<Month>10</Month>
<Day>29</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="pubmed"><Year>2018</Year>
<Month>11</Month>
<Day>6</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="medline"><Year>2019</Year>
<Month>11</Month>
<Day>28</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="entrez"><Year>2018</Year>
<Month>11</Month>
<Day>4</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
</History>
<PublicationStatus>ppublish</PublicationStatus>
<ArticleIdList><ArticleId IdType="pubmed">30389547</ArticleId>
<ArticleId IdType="pii">S1567-1348(18)30538-0</ArticleId>
<ArticleId IdType="doi">10.1016/j.meegid.2018.10.024</ArticleId>
</ArticleIdList>
</PubmedData>
</pubmed>
<affiliations><list><country><li>Brésil</li>
</country>
<region><li>État de Rio de Janeiro</li>
</region>
<settlement><li>Rio de Janeiro</li>
</settlement>
</list>
<tree><country name="Brésil"><region name="État de Rio de Janeiro"><name sortKey="Matos, Aline R" sort="Matos, Aline R" uniqKey="Matos A" first="Aline R" last="Matos">Aline R. Matos</name>
</region>
<name sortKey="Garcia, Cristiana C" sort="Garcia, Cristiana C" uniqKey="Garcia C" first="Cristiana C" last="Garcia">Cristiana C. Garcia</name>
<name sortKey="Martins, Jessica S C C" sort="Martins, Jessica S C C" uniqKey="Martins J" first="Jéssica S C C" last="Martins">Jéssica S C C. Martins</name>
<name sortKey="Oliveira, Maria De Lourdes A" sort="Oliveira, Maria De Lourdes A" uniqKey="Oliveira M" first="Maria De Lourdes A" last="Oliveira">Maria De Lourdes A. Oliveira</name>
<name sortKey="Siqueira, Marilda M" sort="Siqueira, Marilda M" uniqKey="Siqueira M" first="Marilda M" last="Siqueira">Marilda M. Siqueira</name>
</country>
</tree>
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Human CCR5Δ32 (rs333) polymorphism has no influence on severity and mortality of influenza A(H1N1)pdm09 infection in Brazilian patients from the post pandemic period.

Human CCR5Δ32 (rs333) polymorphism has no influence on severity and mortality of influenza A(H1N1)pdm09 infection in Brazilian patients from the post pandemic period.

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