Polymorphisms in HLA-C and KIR alleles are not associated with HAM/TSP risk in HTLV-1-infected subjects

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dc.contributor Sistema FMUSP-HC: Faculdade de Medicina da Universidade de São Paulo (FMUSP) e Hospital das Clínicas da FMUSP
dc.contributor.author ASSONE, Tatiane FMUSP-HC
SMID, Jerusa
OLIVEIRA, Augusto Cesar Penalva de
GONCALVES, Fernanda de Toledo FMUSP-HC
LUIZ, Olinda do Carmo FMUSP-HC
NORRIS, Philip J.
dc.date.issued 2018
dc.identifier.citation VIRUS RESEARCH, v.244, Special Issue, p.71-74, 2018
dc.identifier.issn 0168-1702
dc.identifier.uri http://observatorio.fm.usp.br/handle/OPI/26589
dc.description.abstract Introduction: Several genetic polymorphisms may be related to susceptibility or resistance to viral disease outcomes. Immunological or genetic factors may act as major triggers of the immune pathogenesis of HAM/TSP. This study investigated the association of immune related genetic polymorphisms with viral and immunological markers. Methods: 247 HTLV-1-infected volunteers, drawn from a larger group of HTLV-infected subjects followed at the Institute of Infectious Diseases ""Emilio Ribas"" (IIER) for up to 19 years, participated in this study, which ran from June 2011 to July 2016. The subjects were classified according to their neurological status into two groups: Group 1 (160 asymptomatic individuals) and Group 2 (87 HAM/TSP patients). Samples were tested for spontaneous lymphocyte proliferation (LPA) and HTLV-1 proviral load (PVL) and for IFN-lambda 4, HLA-C and KIR genotypes using qPCR. Results: We found associations between LPA (p = 0.0001) with HAM/TSP and confirmed the IFN-lambda 4 polymorphism rs8099917, allele GG, as a protective factor using a recessive model (OR = 3.22, CI = 1.10-9.47). Polymorphisms in HLA-C and KIR alleles were not associated with risk of developing HAM/TSP. Conclusion: We demonstrated that age, LPA and an IFN-lambda 4 polymorphism were associated with progression to HAM/TSP. Understanding HAM/TSP pathogenesis can provide important markers of prognostic value for clinical management, and contribute to the discovery of new therapeutic interventions in the future.
dc.description.sponsorship · CNPq [134001/2011-7]
· FAPESP [2012/23397-0, 2014/22827-7]
dc.language.iso eng
dc.relation.ispartof Virus Research
dc.rights restrictedAccess
dc.subject Polymorphisms; Interferons; HTLV-1; HLA antigens
dc.subject.other myelopathy/tropical spastic paraparesis; virus type-i; htlv-1 proviral load; cd8(+) t-cells; real-time pcr; type-1 htlv-1; infection; pathogenesis; disease; therapy
dc.title Polymorphisms in HLA-C and KIR alleles are not associated with HAM/TSP risk in HTLV-1-infected subjects
dc.type article
dc.rights.holder Copyright ELSEVIER SCIENCE BV
dc.description.group LIM/07
dc.description.group LIM/38
dc.description.group LIM/40
dc.description.group LIM/56
dc.identifier.doi 10.1016/j.virusres.2017.11.010
dc.identifier.pmid 29129607
dc.type.category original article
dc.type.version publishedVersion
hcfmusp.author ASSONE, Tatiane:IMT:
hcfmusp.author MALTA, Fernanda M.:HC:ICHC
hcfmusp.author PAIVA, Arthur M.:IMT:
hcfmusp.author GONCALVES, Fernanda de Toledo:FM:
hcfmusp.author LUIZ, Olinda do Carmo:FM:
hcfmusp.author FONSECA, Luiz Augusto M.:HC:ICHC
hcfmusp.author CASSEB, Jorge:IMT:DVCIENT-83
hcfmusp.author.external · BAKKOUR, Sonia:Blood Syst Res Inst, San Francisco, CA USA
· MONTALVO, Leilani:Blood Syst Res Inst, San Francisco, CA USA
· SMID, Jerusa:Inst Infect Dis Emilio Ribas IIER, Sao Paulo, Brazil
· OLIVEIRA, Augusto Cesar Penalva de:Inst Infect Dis Emilio Ribas IIER, Sao Paulo, Brazil
· NORRIS, Philip J.:Blood Syst Res Inst, San Francisco, CA USA; Univ Calif San Francisco, San Francisco, CA 94143 USA
hcfmusp.origem.id WOS:000425575400009
hcfmusp.origem.id 2-s2.0-85033383931
hcfmusp.publisher.city AMSTERDAM
hcfmusp.publisher.country NETHERLANDS
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dc.description.index MEDLINE
dc.identifier.eissn 1872-7492
hcfmusp.citation.scopus 5
hcfmusp.citation.wos 5
hcfmusp.affiliation.country Brasil
hcfmusp.affiliation.country Estados Unidos

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