Clinical and genetic markers associated with tuberculosis, HIV-1 infection, and TB/HIV-immune reconstitution inflammatory syndrome outcomes.


Journal

BMC infectious diseases
ISSN: 1471-2334
Titre abrégé: BMC Infect Dis
Pays: England
ID NLM: 100968551

Informations de publication

Date de publication:
20 Jan 2020
Historique:
received: 13 03 2019
accepted: 09 01 2020
entrez: 22 1 2020
pubmed: 22 1 2020
medline: 9 4 2020
Statut: epublish

Résumé

Tuberculosis (TB) and AIDS are the leading causes of infectious disease death worldwide. In some TB-HIV co-infected individuals treated for both diseases simultaneously, a pathological inflammatory reaction termed immune reconstitution inflammatory syndrome (IRIS) may occur. The risk factors for IRIS are not fully defined. We investigated the association of HLA-B, HLA-C, and KIR genotypes with TB, HIV-1 infection, and IRIS onset. Patients were divided into four groups: Group 1- TB+/HIV+ (n = 88; 11 of them with IRIS), Group 2- HIV+ (n = 24), Group 3- TB+ (n = 24) and Group 4- healthy volunteers (n = 26). Patients were followed up at INI/FIOCRUZ and HGNI (Rio de Janeiro/Brazil) from 2006 to 2016. The HLA-B and HLA-C loci were typed using SBT, NGS, and KIR genes by PCR-SSP. Unconditional logistic regression models were performed for Protection/risk estimation. Among the individuals with TB as the outcome, KIR2DS2 was associated with increased risk for TB onset (aOR = 2.39, P = 0.04), whereas HLA-B*08 and female gender were associated with protection against TB onset (aOR = 0.23, P = 0.03, and aOR = 0.33, P = 0.01, respectively). Not carrying KIR2DL3 (aOR = 0.18, P = 0.03) and carrying HLA-C*07 (aOR = 0.32, P = 0.04) were associated with protection against TB onset among HIV-infected patients. An increased risk for IRIS onset was associated with having a CD8 count ≤500 cells/mm

Sections du résumé

BACKGROUND BACKGROUND
Tuberculosis (TB) and AIDS are the leading causes of infectious disease death worldwide. In some TB-HIV co-infected individuals treated for both diseases simultaneously, a pathological inflammatory reaction termed immune reconstitution inflammatory syndrome (IRIS) may occur. The risk factors for IRIS are not fully defined. We investigated the association of HLA-B, HLA-C, and KIR genotypes with TB, HIV-1 infection, and IRIS onset.
METHODS METHODS
Patients were divided into four groups: Group 1- TB+/HIV+ (n = 88; 11 of them with IRIS), Group 2- HIV+ (n = 24), Group 3- TB+ (n = 24) and Group 4- healthy volunteers (n = 26). Patients were followed up at INI/FIOCRUZ and HGNI (Rio de Janeiro/Brazil) from 2006 to 2016. The HLA-B and HLA-C loci were typed using SBT, NGS, and KIR genes by PCR-SSP. Unconditional logistic regression models were performed for Protection/risk estimation.
RESULTS RESULTS
Among the individuals with TB as the outcome, KIR2DS2 was associated with increased risk for TB onset (aOR = 2.39, P = 0.04), whereas HLA-B*08 and female gender were associated with protection against TB onset (aOR = 0.23, P = 0.03, and aOR = 0.33, P = 0.01, respectively). Not carrying KIR2DL3 (aOR = 0.18, P = 0.03) and carrying HLA-C*07 (aOR = 0.32, P = 0.04) were associated with protection against TB onset among HIV-infected patients. An increased risk for IRIS onset was associated with having a CD8 count ≤500 cells/mm

Identifiants

pubmed: 31959123
doi: 10.1186/s12879-020-4786-5
pii: 10.1186/s12879-020-4786-5
pmc: PMC6971853
doi:

Substances chimiques

Genetic Markers 0
HLA-B Antigens 0
HLA-C Antigens 0
KIR2DS2 protein, human 0
Receptors, KIR 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

59

Subventions

Organisme : Conselho Nacional de Desenvolvimento Científico e Tecnológico
ID : 404573/2012-6
Organisme : France Recherche Nord & Sud Sida-HIV Hépatites - ANRS
ID : ANRS12274

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Auteurs

Nathalia Beatriz Ramos de Sá (NBR)

Laboratory of AIDS & Molecular Immunology, Oswaldo Cruz Institute, FIOCRUZ. Av. Brasil 4365, Leonidas Deane Building, room 401, Rio de Janeiro, 21040-360, Brazil.

Marcelo Ribeiro-Alves (M)

Laboratory of Clinical Research on STD/AIDS, National Institute of Infectious Diseases Evandro Chagas, FIOCRUZ, Rio de Janeiro, Brazil.

Tatiana Pereira da Silva (TP)

Laboratory of AIDS & Molecular Immunology, Oswaldo Cruz Institute, FIOCRUZ. Av. Brasil 4365, Leonidas Deane Building, room 401, Rio de Janeiro, 21040-360, Brazil.

Jose Henrique Pilotto (JH)

Laboratory of AIDS & Molecular Immunology, Oswaldo Cruz Institute, FIOCRUZ. Av. Brasil 4365, Leonidas Deane Building, room 401, Rio de Janeiro, 21040-360, Brazil.
Nova Iguaçu General Hospital, Nova Iguaçu, Rio de Janeiro, Brazil.

Valeria Cavalcanti Rolla (VC)

Clinical Research Laboratory on Mycobacteria, National Institute of Infectious Diseases Evandro Chagas, FIOCRUZ, Rio de Janeiro, Brazil.

Carmem B W Giacoia-Gripp (CBW)

Laboratory of AIDS & Molecular Immunology, Oswaldo Cruz Institute, FIOCRUZ. Av. Brasil 4365, Leonidas Deane Building, room 401, Rio de Janeiro, 21040-360, Brazil.

Daniel Scott-Algara (D)

Unité de Biologie Cellulaire des Lymphocytes, Institut Pasteur, Paris, France.

Mariza Gonçalves Morgado (MG)

Laboratory of AIDS & Molecular Immunology, Oswaldo Cruz Institute, FIOCRUZ. Av. Brasil 4365, Leonidas Deane Building, room 401, Rio de Janeiro, 21040-360, Brazil. mmorgado@ioc.fiocruz.br.

Sylvia Lopes Maia Teixeira (SLM)

Laboratory of AIDS & Molecular Immunology, Oswaldo Cruz Institute, FIOCRUZ. Av. Brasil 4365, Leonidas Deane Building, room 401, Rio de Janeiro, 21040-360, Brazil.

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Classifications MeSH