HCV Viremia Drives an Increment of CD86 Expression by Myeloid Dendritic Cells

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dc.contributorSistema FMUSP-HC: Faculdade de Medicina da Universidade de São Paulo (FMUSP) e Hospital das Clínicas da FMUSP
dc.contributor.authorMALTA, F. M.
dc.contributor.authorBRUNO, F. R.
dc.contributor.authorCARVALHO, K. I.
dc.contributor.authorNASTRI, A. C. S. S.
dc.contributor.authorKALIL, J.
dc.contributor.authorCARRILHO, F. J.
dc.contributor.authorKALLAS, E. G.
dc.contributor.authorPINHO, J. R. R.
dc.date.accessioned2014-04-25T21:50:18Z
dc.date.available2014-04-25T21:50:18Z
dc.date.issued2013
dc.description.abstractThe host immune response, including innate and adaptive immunity, plays a critical role in determining the outcome of viral infection. Nevertheless, little is known about the exact reasons for the failure of the host immune system in controlling hepatitis C virus (HCV) infection. Impairment of dendritic cells (DCs) function is probably one of the mechanisms responsible for immune evasion of HCV. In this study, the frequency and phenotype of DCs subsets were analyzed in three groups: HCV-infected individuals who developed viral persistence (1), HCV-infected individuals who spontaneously cleared the virus (2) and HCV-seronegative uninfected subjects (3). The results showed that the frequency of DCs subsets was not statistically significant between groups. Plasmacytoid DCs circulating exhibited an immature phenotype characterized by low expression of CD86. On the other hand, CD86 expression in myeloid DCs was significantly higher in chronic infected individuals compared to healthy controls (P=0.037). A positive correlation was observed between CD86(+) myeloid DC (mDC) and HCV viral load (r=0.4121, P=0.0263). These results suggest that HCV did not have an inhibitory effect on mDC maturation and the HCV viremia drives the increase of CD86 expression in mDC. The regulation of DCs maturation and migration lies at the level of intracellular signaling. HCV can activate or block intracellular signaling pathways and alter DC function. In conclusion, the present study suggests that imbalance of DC maturation by the virus represents a mechanism of evasion of the immune system despite the fact that HCV viremia appears to exert a stimulatory effect on cell-surface immune phenotype. J Med. Virol. 85:1919-1924, 2013. (c) 2013 Wiley Periodicals, Inc.
dc.description.indexMEDLINE
dc.description.sponsorshipFundacao de Amparo a Pesquisa do Estado de Sao Paulo (FAPESP) [09/53270-0, 09/53306-4]
dc.description.sponsorshipFundacao Faculdade de Medicina (FFM)
dc.description.sponsorshipHC-FMUSP
dc.description.sponsorshipAlves de Queiroz Family Fund
dc.description.sponsorshipTropical Medicine Institute of Sao Paulo
dc.identifier.citationJOURNAL OF MEDICAL VIROLOGY, v.85, n.11, p.1919-1924, 2013
dc.identifier.doi10.1002/jmv.23692
dc.identifier.eissn1096-9071
dc.identifier.issn0146-6615
dc.identifier.urihttps://observatorio.fm.usp.br/handle/OPI/5078
dc.language.isoeng
dc.publisherWILEY-BLACKWELL
dc.relation.ispartofJournal of Medical Virology
dc.rightsrestrictedAccess
dc.rights.holderCopyright WILEY-BLACKWELL
dc.subjectinnate immunity
dc.subjectdendritic cell
dc.subjectchronic infection
dc.subjectCD86
dc.subject.otherhepatitis-c virus
dc.subject.othergenetic-variation
dc.subject.otherfunctional-capacity
dc.subject.otherimmune-responses
dc.subject.otherinfection
dc.subject.otherinnate
dc.subject.otheril28b
dc.subject.otherassociation
dc.subject.othermaturation
dc.subject.otherclearance
dc.subject.wosVirology
dc.titleHCV Viremia Drives an Increment of CD86 Expression by Myeloid Dendritic Cells
dc.typearticle
dc.type.categoryoriginal article
dc.type.versionpublishedVersion
dspace.entity.typePublication
hcfmusp.author.externalNASTRI, A. C. S. S.:Univ Sao Paulo, Sch Med, Dept Gastroenterol, BR-05403000 Sao Paulo, Brazil; Univ Sao Paulo, Sch Med, Dept Infect & Parasit Dis, BR-05403000 Sao Paulo, Brazil
hcfmusp.citation.scopus6
hcfmusp.contributor.author-fmusphcFERNANDA DE MELLO MALTA
hcfmusp.contributor.author-fmusphcFERNANDA ROMANO BRUNO
hcfmusp.contributor.author-fmusphcKARINA INACIO LADISLAU DE CARVALHO SALMAZI
hcfmusp.contributor.author-fmusphcJORGE ELIAS KALIL FILHO
hcfmusp.contributor.author-fmusphcFLAIR JOSE CARRILHO
hcfmusp.contributor.author-fmusphcESPER GEORGES KALLAS
hcfmusp.contributor.author-fmusphcJOAO RENATO REBELLO PINHO
hcfmusp.description.beginpage1919
hcfmusp.description.endpage1924
hcfmusp.description.issue11
hcfmusp.description.volume85
hcfmusp.origemWOS
hcfmusp.origem.pubmed23926073
hcfmusp.origem.scopus2-s2.0-84883053961
hcfmusp.origem.wosWOS:000329198500008
hcfmusp.publisher.cityHOBOKEN
hcfmusp.publisher.countryUSA
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hcfmusp.remissive.sponsorshipFAPESP
hcfmusp.remissive.sponsorshipFFM
hcfmusp.remissive.sponsorshipFMUSP
hcfmusp.remissive.sponsorshipFMUSP-HC
hcfmusp.scopus.lastupdate2024-05-10
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