Relative resistance of MHC-B to Nef-mediated downregulation is conserved among primate lentiviruses and influences antiviral T cell responses in HIV-1-infected individuals.
Identifieur interne : 000D08 ( PubMed/Corpus ); précédent : 000D07; suivant : 000D09Relative resistance of MHC-B to Nef-mediated downregulation is conserved among primate lentiviruses and influences antiviral T cell responses in HIV-1-infected individuals.
Auteurs : Francis Mwimanzi ; Mako Toyoda ; Macdonald Mahiti ; Jaclyn K. Mann ; Jeffrey N. Martin ; David Bangsberg ; Mark A. Brockman ; Philip Goulder ; Frank Kirchhoff ; Zabrina L. Brumme ; Thumbi Ndung'U ; Takamasa UenoSource :
- Journal of virology [ 1098-5514 ] ; 2017.
Abstract
Patient-derived HIV-1 subtype B Nef clones downregulate HLA-A more efficiently than HLA-B. However, it remains unknown whether this property is common to Nef proteins across primate lentiviruses, and how antiviral immune responses may be affected. We examined 263 Nef clones from diverse primate lentiviruses including different pandemic HIV-1 group M subtypes for their ability to downregulate MHC-A and MHC-B from the cell surface. Though lentiviral Nef proteins differed markedly in their absolute MHC-A and MHC-B downregulation abilities, all lentiviral Nef lineages downregulated MHC-A on average 11-32% more efficiently than MHC-B. Nef genotype/phenotype analyses in a cohort of HIV-1 subtype C-infected patients (N=168), together with site-directed mutagenesis, revealed Nef position 9 as a subtype-specific determinant of differential HLA-A vs. HLA-B downregulation activity. Nef clones harboring non-consensus variants at codon 9 downregulated HLA-B (though not HLA-A) significantly better than those harboring consensus at this site, resulting in reduced recognition of infected target cells by HIV-1-specific CD8(+) effector cells in vitro Among persons expressing protective HLA class I alleles, carriage of Nef codon 9 variants was also associated with reduced ex vivo HIV-specific T-cell responses. Our results demonstrate that Nef's inferior ability to downregulate MHC-B compared to MHC-A is conserved across primate lentiviruses, and suggest that this property influences antiviral cellular immune responses.IMPORTANCE Primate lentiviruses encode the Nef protein that plays an essential role in establishing persistent infection in their respective host species. Nef interacts with the cytoplasmic region of MHC-A and MHC-B molecules and downregulates them from the infected cell surface to escape recognition by host cellular immunity. Using a panel of Nef alleles isolated from diverse primate lentiviruses including pandemic HIV-1 group M subtypes, we demonstrate that Nef proteins across all lentiviral lineages downregulate MHC-A approximately 20% more effectively than MHC-B. We further identify a naturally polymorphic site at Nef position 9 that contributes to MHC-B downregulation function in HIV-1 subtype C, and show that carriage of Nef variants with enhanced MHC-B downregulation ability is associated with reduced breadth and magnitude of MHC-B-restricted cellular immune responses in HIV-infected individuals. Our study underscores an evolutionally conserved interaction between lentiviruses and primate immune systems that may contribute to pathogenesis.
DOI: 10.1128/JVI.01409-17
PubMed: 29046444
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Mann</name><affiliation><nlm:affiliation>HIV Pathogenesis Programme, University of KwaZulu-Natal, Durban, South Africa.</nlm:affiliation></affiliation></author><author><name sortKey="Martin, Jeffrey N" sort="Martin, Jeffrey N" uniqKey="Martin J" first="Jeffrey N" last="Martin">Jeffrey N. Martin</name><affiliation><nlm:affiliation>Department of Epidemiology and Biostatistics, University of California, San Francisco, San Francisco, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Bangsberg, David" sort="Bangsberg, David" uniqKey="Bangsberg D" first="David" last="Bangsberg">David Bangsberg</name><affiliation><nlm:affiliation>School of Public Health, Oregon Health & Science University-Portland State University, Portland, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Brockman, Mark A" sort="Brockman, Mark A" uniqKey="Brockman M" first="Mark A" last="Brockman">Mark A. Brockman</name><affiliation><nlm:affiliation>Simon Fraser University, Burnaby, BC, Canada.</nlm:affiliation></affiliation></author><author><name sortKey="Goulder, Philip" sort="Goulder, Philip" uniqKey="Goulder P" first="Philip" last="Goulder">Philip Goulder</name><affiliation><nlm:affiliation>Department of Paediatrics, University of Oxford, Oxford, UK.</nlm:affiliation></affiliation></author><author><name sortKey="Kirchhoff, Frank" sort="Kirchhoff, Frank" uniqKey="Kirchhoff F" first="Frank" last="Kirchhoff">Frank Kirchhoff</name><affiliation><nlm:affiliation>Institute of Molecular Virology, Ulm University Medical Center, Ulm, Germany.</nlm:affiliation></affiliation></author><author><name sortKey="Brumme, Zabrina L" sort="Brumme, Zabrina L" uniqKey="Brumme Z" first="Zabrina L" last="Brumme">Zabrina L. Brumme</name><affiliation><nlm:affiliation>Simon Fraser University, Burnaby, BC, Canada.</nlm:affiliation></affiliation></author><author><name sortKey="Ndung U, Thumbi" sort="Ndung U, Thumbi" uniqKey="Ndung U T" first="Thumbi" last="Ndung'U">Thumbi Ndung'U</name><affiliation><nlm:affiliation>HIV Pathogenesis Programme, University of KwaZulu-Natal, Durban, South Africa.</nlm:affiliation></affiliation></author><author><name sortKey="Ueno, Takamasa" sort="Ueno, Takamasa" uniqKey="Ueno T" first="Takamasa" last="Ueno">Takamasa Ueno</name><affiliation><nlm:affiliation>Center for AIDS research, Kumamoto University, Kumamoto, Japan uenotaka@kumamoto-u.ac.jp.</nlm:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2017">2017</date><idno type="RBID">pubmed:29046444</idno><idno type="pmid">29046444</idno><idno type="doi">10.1128/JVI.01409-17</idno><idno type="wicri:Area/PubMed/Corpus">000D08</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000D08</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Relative resistance of MHC-B to Nef-mediated downregulation is conserved among primate lentiviruses and influences antiviral T cell responses in HIV-1-infected individuals.</title><author><name sortKey="Mwimanzi, Francis" sort="Mwimanzi, Francis" uniqKey="Mwimanzi F" first="Francis" last="Mwimanzi">Francis Mwimanzi</name><affiliation><nlm:affiliation>Center for AIDS research, Kumamoto University, Kumamoto, Japan.</nlm:affiliation></affiliation></author><author><name sortKey="Toyoda, Mako" sort="Toyoda, Mako" uniqKey="Toyoda M" first="Mako" last="Toyoda">Mako Toyoda</name><affiliation><nlm:affiliation>Center for AIDS research, Kumamoto University, Kumamoto, Japan.</nlm:affiliation></affiliation></author><author><name sortKey="Mahiti, Macdonald" sort="Mahiti, Macdonald" uniqKey="Mahiti M" first="Macdonald" last="Mahiti">Macdonald Mahiti</name><affiliation><nlm:affiliation>Center for AIDS research, Kumamoto University, Kumamoto, Japan.</nlm:affiliation></affiliation></author><author><name sortKey="Mann, Jaclyn K" sort="Mann, Jaclyn K" uniqKey="Mann J" first="Jaclyn K" last="Mann">Jaclyn K. Mann</name><affiliation><nlm:affiliation>HIV Pathogenesis Programme, University of KwaZulu-Natal, Durban, South Africa.</nlm:affiliation></affiliation></author><author><name sortKey="Martin, Jeffrey N" sort="Martin, Jeffrey N" uniqKey="Martin J" first="Jeffrey N" last="Martin">Jeffrey N. Martin</name><affiliation><nlm:affiliation>Department of Epidemiology and Biostatistics, University of California, San Francisco, San Francisco, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Bangsberg, David" sort="Bangsberg, David" uniqKey="Bangsberg D" first="David" last="Bangsberg">David Bangsberg</name><affiliation><nlm:affiliation>School of Public Health, Oregon Health & Science University-Portland State University, Portland, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Brockman, Mark A" sort="Brockman, Mark A" uniqKey="Brockman M" first="Mark A" last="Brockman">Mark A. Brockman</name><affiliation><nlm:affiliation>Simon Fraser University, Burnaby, BC, Canada.</nlm:affiliation></affiliation></author><author><name sortKey="Goulder, Philip" sort="Goulder, Philip" uniqKey="Goulder P" first="Philip" last="Goulder">Philip Goulder</name><affiliation><nlm:affiliation>Department of Paediatrics, University of Oxford, Oxford, UK.</nlm:affiliation></affiliation></author><author><name sortKey="Kirchhoff, Frank" sort="Kirchhoff, Frank" uniqKey="Kirchhoff F" first="Frank" last="Kirchhoff">Frank Kirchhoff</name><affiliation><nlm:affiliation>Institute of Molecular Virology, Ulm University Medical Center, Ulm, Germany.</nlm:affiliation></affiliation></author><author><name sortKey="Brumme, Zabrina L" sort="Brumme, Zabrina L" uniqKey="Brumme Z" first="Zabrina L" last="Brumme">Zabrina L. Brumme</name><affiliation><nlm:affiliation>Simon Fraser University, Burnaby, BC, Canada.</nlm:affiliation></affiliation></author><author><name sortKey="Ndung U, Thumbi" sort="Ndung U, Thumbi" uniqKey="Ndung U T" first="Thumbi" last="Ndung'U">Thumbi Ndung'U</name><affiliation><nlm:affiliation>HIV Pathogenesis Programme, University of KwaZulu-Natal, Durban, South Africa.</nlm:affiliation></affiliation></author><author><name sortKey="Ueno, Takamasa" sort="Ueno, Takamasa" uniqKey="Ueno T" first="Takamasa" last="Ueno">Takamasa Ueno</name><affiliation><nlm:affiliation>Center for AIDS research, Kumamoto University, Kumamoto, Japan uenotaka@kumamoto-u.ac.jp.</nlm:affiliation></affiliation></author></analytic><series><title level="j">Journal of virology</title><idno type="eISSN">1098-5514</idno><imprint><date when="2017" type="published">2017</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Patient-derived HIV-1 subtype B Nef clones downregulate HLA-A more efficiently than HLA-B. However, it remains unknown whether this property is common to Nef proteins across primate lentiviruses, and how antiviral immune responses may be affected. We examined 263 Nef clones from diverse primate lentiviruses including different pandemic HIV-1 group M subtypes for their ability to downregulate MHC-A and MHC-B from the cell surface. Though lentiviral Nef proteins differed markedly in their absolute MHC-A and MHC-B downregulation abilities, all lentiviral Nef lineages downregulated MHC-A on average 11-32% more efficiently than MHC-B. Nef genotype/phenotype analyses in a cohort of HIV-1 subtype C-infected patients (N=168), together with site-directed mutagenesis, revealed Nef position 9 as a subtype-specific determinant of differential HLA-A vs. HLA-B downregulation activity. Nef clones harboring non-consensus variants at codon 9 downregulated HLA-B (though not HLA-A) significantly better than those harboring consensus at this site, resulting in reduced recognition of infected target cells by HIV-1-specific CD8(+) effector cells in vitro Among persons expressing protective HLA class I alleles, carriage of Nef codon 9 variants was also associated with reduced ex vivo HIV-specific T-cell responses. Our results demonstrate that Nef's inferior ability to downregulate MHC-B compared to MHC-A is conserved across primate lentiviruses, and suggest that this property influences antiviral cellular immune responses.IMPORTANCE Primate lentiviruses encode the Nef protein that plays an essential role in establishing persistent infection in their respective host species. Nef interacts with the cytoplasmic region of MHC-A and MHC-B molecules and downregulates them from the infected cell surface to escape recognition by host cellular immunity. Using a panel of Nef alleles isolated from diverse primate lentiviruses including pandemic HIV-1 group M subtypes, we demonstrate that Nef proteins across all lentiviral lineages downregulate MHC-A approximately 20% more effectively than MHC-B. We further identify a naturally polymorphic site at Nef position 9 that contributes to MHC-B downregulation function in HIV-1 subtype C, and show that carriage of Nef variants with enhanced MHC-B downregulation ability is associated with reduced breadth and magnitude of MHC-B-restricted cellular immune responses in HIV-infected individuals. Our study underscores an evolutionally conserved interaction between lentiviruses and primate immune systems that may contribute to pathogenesis.</div></front></TEI><pubmed><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">29046444</PMID><DateCreated><Year>2017</Year><Month>10</Month><Day>19</Day></DateCreated><DateRevised><Year>2017</Year><Month>10</Month><Day>19</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1098-5514</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2017</Year><Month>Oct</Month><Day>18</Day></PubDate></JournalIssue><Title>Journal of virology</Title><ISOAbbreviation>J. Virol.</ISOAbbreviation></Journal><ArticleTitle>Relative resistance of MHC-B to Nef-mediated downregulation is conserved among primate lentiviruses and influences antiviral T cell responses in HIV-1-infected individuals.</ArticleTitle><ELocationID EIdType="pii" ValidYN="Y">JVI.01409-17</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1128/JVI.01409-17</ELocationID><Abstract><AbstractText>Patient-derived HIV-1 subtype B Nef clones downregulate HLA-A more efficiently than HLA-B. However, it remains unknown whether this property is common to Nef proteins across primate lentiviruses, and how antiviral immune responses may be affected. We examined 263 Nef clones from diverse primate lentiviruses including different pandemic HIV-1 group M subtypes for their ability to downregulate MHC-A and MHC-B from the cell surface. Though lentiviral Nef proteins differed markedly in their absolute MHC-A and MHC-B downregulation abilities, all lentiviral Nef lineages downregulated MHC-A on average 11-32% more efficiently than MHC-B. Nef genotype/phenotype analyses in a cohort of HIV-1 subtype C-infected patients (N=168), together with site-directed mutagenesis, revealed Nef position 9 as a subtype-specific determinant of differential HLA-A vs. HLA-B downregulation activity. Nef clones harboring non-consensus variants at codon 9 downregulated HLA-B (though not HLA-A) significantly better than those harboring consensus at this site, resulting in reduced recognition of infected target cells by HIV-1-specific CD8(+) effector cells in vitro Among persons expressing protective HLA class I alleles, carriage of Nef codon 9 variants was also associated with reduced ex vivo HIV-specific T-cell responses. Our results demonstrate that Nef's inferior ability to downregulate MHC-B compared to MHC-A is conserved across primate lentiviruses, and suggest that this property influences antiviral cellular immune responses.IMPORTANCE Primate lentiviruses encode the Nef protein that plays an essential role in establishing persistent infection in their respective host species. Nef interacts with the cytoplasmic region of MHC-A and MHC-B molecules and downregulates them from the infected cell surface to escape recognition by host cellular immunity. Using a panel of Nef alleles isolated from diverse primate lentiviruses including pandemic HIV-1 group M subtypes, we demonstrate that Nef proteins across all lentiviral lineages downregulate MHC-A approximately 20% more effectively than MHC-B. We further identify a naturally polymorphic site at Nef position 9 that contributes to MHC-B downregulation function in HIV-1 subtype C, and show that carriage of Nef variants with enhanced MHC-B downregulation ability is associated with reduced breadth and magnitude of MHC-B-restricted cellular immune responses in HIV-infected individuals. Our study underscores an evolutionally conserved interaction between lentiviruses and primate immune systems that may contribute to pathogenesis.</AbstractText><CopyrightInformation>Copyright © 2017 American Society for Microbiology.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Mwimanzi</LastName><ForeName>Francis</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>Center for AIDS research, Kumamoto University, Kumamoto, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Toyoda</LastName><ForeName>Mako</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Center for AIDS research, Kumamoto University, Kumamoto, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mahiti</LastName><ForeName>Macdonald</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Center for AIDS research, Kumamoto University, Kumamoto, Japan.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>International Research Center for Medical Sciences (IRCMS), Kumamoto University, Kumamoto, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mann</LastName><ForeName>Jaclyn K</ForeName><Initials>JK</Initials><AffiliationInfo><Affiliation>HIV Pathogenesis Programme, University of KwaZulu-Natal, Durban, South Africa.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Martin</LastName><ForeName>Jeffrey N</ForeName><Initials>JN</Initials><AffiliationInfo><Affiliation>Department of Epidemiology and Biostatistics, University of California, San Francisco, San Francisco, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bangsberg</LastName><ForeName>David</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>School of Public Health, Oregon Health & Science University-Portland State University, Portland, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Brockman</LastName><ForeName>Mark A</ForeName><Initials>MA</Initials><Identifier Source="ORCID">http://orcid.org/0000-0001-6432-1426</Identifier><AffiliationInfo><Affiliation>Simon Fraser University, Burnaby, BC, Canada.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>British Columbia Centre for Excellence in HIV/AIDS, Vancouver BC, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Goulder</LastName><ForeName>Philip</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Department of Paediatrics, University of Oxford, Oxford, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kirchhoff</LastName><ForeName>Frank</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>Institute of Molecular Virology, Ulm University Medical Center, Ulm, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Brumme</LastName><ForeName>Zabrina L</ForeName><Initials>ZL</Initials><AffiliationInfo><Affiliation>Simon Fraser University, Burnaby, BC, Canada.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>British Columbia Centre for Excellence in HIV/AIDS, Vancouver BC, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ndung'u</LastName><ForeName>Thumbi</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>HIV Pathogenesis Programme, University of KwaZulu-Natal, Durban, South Africa.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Africa Health Research Institute, Durban, South Africa.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Ragon Institute of Massachusetts General Hospital, Massachusetts Institute of Technology and Harvard University, Cambridge, MA, USA.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Max Planck Institute for Infection Biology, Berlin, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ueno</LastName><ForeName>Takamasa</ForeName><Initials>T</Initials><Identifier Source="ORCID">http://orcid.org/0000-0003-4852-4236</Identifier><AffiliationInfo><Affiliation>Center for AIDS research, Kumamoto University, Kumamoto, Japan uenotaka@kumamoto-u.ac.jp.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>International Research Center for Medical Sciences (IRCMS), Kumamoto University, Kumamoto, Japan.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2017</Year><Month>10</Month><Day>18</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J Virol</MedlineTA><NlmUniqueID>0113724</NlmUniqueID><ISSNLinking>0022-538X</ISSNLinking></MedlineJournalInfo></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2017</Year><Month>10</Month><Day>20</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2017</Year><Month>10</Month><Day>20</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2017</Year><Month>10</Month><Day>20</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>aheadofprint</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">29046444</ArticleId><ArticleId IdType="pii">JVI.01409-17</ArticleId><ArticleId IdType="doi">10.1128/JVI.01409-17</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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