Alleles of HLA-DRB1*04 Associated with Pulmonary Tuberculosis in Amazon Brazilian Population

Lima, Dhêmerson Souza de; Ogusku, Maurício Morishi; Santos, M.P.; Silva, Cláudia Maria de Melo; Almeida, Vanessa Alves de; Antunes, Irineide Assumpção; Boechat, Antônio Luiz; Ramasawmy, Rajendranath; Sadahiro, Aya

doi:10.1371/journal.pone.0147543

Cited by 30 publications

(21 citation statements)

References 58 publications

(55 reference statements)

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“…The RRs from the categorical meta-analyses of alcohol use as a risk factor for tuberculosis are presented in table 1 (see also tables S3 and S4 in appendix D for the sex-specific RRs) [ 7 , 23 – 45 ]. Alcohol use was associated with a 35% higher risk of tuberculosis compared to no alcohol use (RR 1.35, 95% CI 1.09–1.68).…”

Section: Resultsmentioning

confidence: 99%

Alcohol consumption as a risk factor for tuberculosis: meta-analyses and burden of disease

et al. 2017

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Meta-analyses of alcohol use, alcohol dosage and alcohol-related problems as risk factors for tuberculosis incidence were undertaken. The global alcohol-attributable tuberculosis burden of disease was also re-estimated.Systematic searches were conducted, reference lists were reviewed and expert consultations were held to identify studies. Cohort and case-control studies were included if there were no temporal violations of exposure and outcome. Risk relations (RRs) were pooled by using categorical and dose-response meta-analyses. The alcohol-attributable tuberculosis burden of disease was estimated by using alcohol-attributable fractions.36 of 1108 studies were included. RRs for alcohol use and alcohol-related problems were 1.35 (95% CI 1.09–1.68; I2: 83%) and 3.33 (95% CI 2.14–5.19; 87%), respectively. Concerning alcohol dosage, tuberculosis risk rose as ethanol intake increased, with evidence of a threshold effect. Alcohol consumption caused 22.02 incident cases (95% CI 19.70–40.77) and 2.35 deaths (95% CI 2.05–4.79) per 100 000 people from tuberculosis in 2014. Alcohol-attributable tuberculosis incidence increased between 2000 and 2014 in most high tuberculosis burden countries, whereas mortality decreased.Alcohol consumption was associated with an increased risk of tuberculosis in all meta-analyses. It was consequently a major contributor to the tuberculosis burden of disease.

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Section: Resultsmentioning

confidence: 99%

Alcohol consumption as a risk factor for tuberculosis: meta-analyses and burden of disease

et al. 2017

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“…Many single-nucleotide polymorphisms (SNPs) in immune response genes are associated with TB ( 5 – 7 ). The most reported are HLA-DRB1, VDR, TIRAP , and NRAMP1 ( 6 , 8 ). Other genes such as toll-like receptors (TLRs), TLR1 , 2, 4, 6, and 9 that are involved in the initial recognition of pathogen-associated molecular patterns to trigger the activation of the effector mechanisms of innate immunity and subsequent targeting of the specific adaptive immune response to Mycobacterium tuberculosis have also been associated with susceptibility or resistance to TB ( 6 , 9 , 10 ).…”

Section: Introductionmentioning

confidence: 99%

Toll-Like Receptor-1 Single-Nucleotide Polymorphism 1805T/G Is Associated With Predisposition to Multibacillary Tuberculosis

et al. 2018

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Tuberculosis (TB), caused by mycobacterial species of the Mycobacterium tuberculosis complex, is a serious global health issue. Brazil is among the 22 countries with the highest number of TB cases, and the state of Amazonas has the highest incidence of TB cases in the country. Toll-like receptors (TLRs) are important pattern recognition receptors of the innate immunity and play a key role in orchestrating an effective immune response. We investigated whether the single-nucleotide polymorphisms (SNPs) 1805T/G TLR1, 2258G/A TLR2, 896A/G and 1196C/T of TLR4, 745T/C TLR6, and −1237A/G and −1486A/G of TLR9 are associated with the predisposition to TB and/or bacillary load. The SNPs genotyping was performed by nucleotide sequencing in 263 TB patients and 232 healthy controls residing in the state of Amazonas. Alleles and genotypes frequencies were similar between patients and healthy individuals for most of the investigated SNPs. Stratification of the TB patients according to their bacillary load showed that the genotype 1805TT TLR1 (rs5743618) was prevalent among paucibacillary patients [odds ratio (OR) = 0.38; 95% confidence interval (CI) = 0.19–0.76; p = 0.009] while the genotype 1805TG was common among multibacillary patients (OR = 3.72; CI = 1.65–8.4; p = 0.004). Comparison of demographic characteristics of patients to controls showed that TB is strongly associated with smoking (OR = 6.55; 95% CI = 3.2–13.6; p < 0.0001); alcohol use disorder (OR = 7.14; 95% CI = 3.7–13.9; p < 0.0001); and male gender (OR = 3.66; 95% CI = 2.52–5.3; p < 0.0001). Multivariate logistic regression demonstrated that alcoholism (OR = 2.93; 95% CI = 1.05–8.16; p = 0.03) and the 1805G allele (OR = 2.75; 95% CI = 1.33–5.7; p = 0.006) are predictive variables for multibacillary TB. Altogether, we suggest that the TLR1 1805G allele may be a relevant immunogenetic factor for the epidemiology of TB together with environmental, sociodemographic, and behavioral factors.

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“…Remarkably, the latter was not significantly associated with pulmonary TB in Croatians (cs/ cn=438/1008), but it was significantly linked to increased risk for the disease in both, Icelandic population (p<3 × 10 -7 , cs/cn=3686/287427) and Russians (p<5 × 10 -4 , cs/cn=5530/5607). Recent case-control studies from other groups, despite using much lower number of individuals, corroborated the role of HLA class II in affecting the risk for TB in Ugandan (HLA DQB1 * 03:03, cs/cn=43/42) [8] and Brasilian Amazon populations (HLA DRB1 * 04, cs/cn=316/306) [9]. Together, the data strongly suggest that poorly-Mycobacterium tuberculosisbinding HLA class II alleles might contribute to developing TB by being one of the many risks among multifactorial genetic hallmarks of tuberculosis.…”

Section: Introductionmentioning

confidence: 94%

Genetic Risk of Tuberculosis is Spread within the Hallmarks of the Disease

Vrbanec¹,

Lederer-Dembic²,

Bulat-Kardum³

et al. 2016

Immunother Open Acc

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Regarding genetic predisposition to tuberculosis, we suggest that the maximal risk for clinical manifestation requires complementation of sub-risks divided among the hallmarks of the disease. Clinical tuberculosis would only be revealed if at least one from each group of the genes encoding putative 5 (perhaps 7) hallmarks of the disease are mutated or changed epigenetically. These mutations/changes could be either sporadic (usually by the influence of the environment like other infection [HIV], nutrition, smoking, radiation etc.) or inherited. Avoidance of the immune attack is one of the hallmarks for TB that is shared with cancer. Perhaps, a similar immunotherapy as the recent one used in treating immunogenic types of cancer (anti-PD1, or/and anti-CTLA4) could be also successful in therapy of (multi-drug) resistant TB.

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Alleles of HLA-DRB1*04 Associated with Pulmonary Tuberculosis in Amazon Brazilian Population

Cited by 30 publications

References 58 publications

Alcohol consumption as a risk factor for tuberculosis: meta-analyses and burden of disease

Alcohol consumption as a risk factor for tuberculosis: meta-analyses and burden of disease

Toll-Like Receptor-1 Single-Nucleotide Polymorphism 1805T/G Is Associated With Predisposition to Multibacillary Tuberculosis

Genetic Risk of Tuberculosis is Spread within the Hallmarks of the Disease

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