The role of host genetic factors in respiratory tract infectious diseases: systematic review, meta-analyses and field synopsis.
Identifieur interne : 000D31 ( PubMed/Checkpoint ); précédent : 000D30; suivant : 000D32The role of host genetic factors in respiratory tract infectious diseases: systematic review, meta-analyses and field synopsis.
Auteurs : Inga Patar I [Croatie] ; Andrea Gelemanovi [Croatie] ; Mirna Kirin [Croatie] ; Ivana Kol I [Croatie] ; Evropi Theodoratou [Royaume-Uni] ; Kenneth J. Baillie [Royaume-Uni] ; Menno D. De Jong [Pays-Bas] ; Igor Rudan [Royaume-Uni] ; Harry Campbell [Royaume-Uni] ; Ozren Polašek [Croatie]Source :
- Scientific reports [ 2045-2322 ] ; 2015.
Descripteurs français
- KwdFr :
- Bases de données factuelles, Chimiokine CCL2 (génétique), Humains, Infections de l'appareil respiratoire (anatomopathologie), Infections de l'appareil respiratoire (génétique), Infections de l'appareil respiratoire (métabolisme), Interleukine-4 (génétique), Polymorphisme de nucléotide simple, Récepteur de type Toll-2 (génétique), Tuberculose (anatomopathologie), Tuberculose (génétique), Tuberculose (mortalité).
- MESH :
- anatomopathologie : Infections de l'appareil respiratoire, Tuberculose.
- génétique : Chimiokine CCL2, Infections de l'appareil respiratoire, Interleukine-4, Récepteur de type Toll-2, Tuberculose.
- mortalité : Tuberculose.
- métabolisme : Infections de l'appareil respiratoire.
- Bases de données factuelles, Humains, Polymorphisme de nucléotide simple.
English descriptors
- KwdEn :
- Chemokine CCL2 (genetics), Databases, Factual, Humans, Interleukin-4 (genetics), Polymorphism, Single Nucleotide, Respiratory Tract Infections (genetics), Respiratory Tract Infections (metabolism), Respiratory Tract Infections (pathology), Toll-Like Receptor 2 (genetics), Tuberculosis (genetics), Tuberculosis (mortality), Tuberculosis (pathology).
- MESH :
- chemical , genetics : Chemokine CCL2, Interleukin-4, Toll-Like Receptor 2.
- genetics : Respiratory Tract Infections, Tuberculosis.
- metabolism : Respiratory Tract Infections.
- mortality : Tuberculosis.
- pathology : Respiratory Tract Infections, Tuberculosis.
- Databases, Factual, Humans, Polymorphism, Single Nucleotide.
Abstract
Host genetic factors have frequently been implicated in respiratory infectious diseases, often with inconsistent results in replication studies. We identified 386 studies from the total of 24,823 studies identified in a systematic search of four bibliographic databases. We performed meta-analyses of studies on tuberculosis, influenza, respiratory syncytial virus, SARS-Coronavirus and pneumonia. One single-nucleotide polymorphism from IL4 gene was significant for pooled respiratory infections (rs2070874; 1.66 [1.29-2.14]). We also detected an association of TLR2 gene with tuberculosis (rs5743708; 3.19 [2.03-5.02]). Subset analyses identified CCL2 as an additional risk factor for tuberculosis (rs1024611; OR = 0.79 [0.72-0.88]). The IL4-TLR2-CCL2 axis could be a highly interesting target for translation towards clinical use. However, this conclusion is based on low credibility of evidence - almost 95% of all identified studies had strong risk of bias or confounding. Future studies must build upon larger-scale collaborations, but also strictly adhere to the highest evidence-based principles in study design, in order to reduce research waste and provide clinically translatable evidence.
DOI: 10.1038/srep16119
PubMed: 26524966
Affiliations:
- Croatie, Pays-Bas, Royaume-Uni
- Hollande-Septentrionale, Écosse
- Amsterdam, Édimbourg
- Université d'Amsterdam, Université d'Édimbourg
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pubmed:26524966Le document en format XML
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<front><div type="abstract" xml:lang="en">Host genetic factors have frequently been implicated in respiratory infectious diseases, often with inconsistent results in replication studies. We identified 386 studies from the total of 24,823 studies identified in a systematic search of four bibliographic databases. We performed meta-analyses of studies on tuberculosis, influenza, respiratory syncytial virus, SARS-Coronavirus and pneumonia. One single-nucleotide polymorphism from IL4 gene was significant for pooled respiratory infections (rs2070874; 1.66 [1.29-2.14]). We also detected an association of TLR2 gene with tuberculosis (rs5743708; 3.19 [2.03-5.02]). Subset analyses identified CCL2 as an additional risk factor for tuberculosis (rs1024611; OR = 0.79 [0.72-0.88]). The IL4-TLR2-CCL2 axis could be a highly interesting target for translation towards clinical use. However, this conclusion is based on low credibility of evidence - almost 95% of all identified studies had strong risk of bias or confounding. Future studies must build upon larger-scale collaborations, but also strictly adhere to the highest evidence-based principles in study design, in order to reduce research waste and provide clinically translatable evidence. </div>
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<Abstract><AbstractText>Host genetic factors have frequently been implicated in respiratory infectious diseases, often with inconsistent results in replication studies. We identified 386 studies from the total of 24,823 studies identified in a systematic search of four bibliographic databases. We performed meta-analyses of studies on tuberculosis, influenza, respiratory syncytial virus, SARS-Coronavirus and pneumonia. One single-nucleotide polymorphism from IL4 gene was significant for pooled respiratory infections (rs2070874; 1.66 [1.29-2.14]). We also detected an association of TLR2 gene with tuberculosis (rs5743708; 3.19 [2.03-5.02]). Subset analyses identified CCL2 as an additional risk factor for tuberculosis (rs1024611; OR = 0.79 [0.72-0.88]). The IL4-TLR2-CCL2 axis could be a highly interesting target for translation towards clinical use. However, this conclusion is based on low credibility of evidence - almost 95% of all identified studies had strong risk of bias or confounding. Future studies must build upon larger-scale collaborations, but also strictly adhere to the highest evidence-based principles in study design, in order to reduce research waste and provide clinically translatable evidence. </AbstractText>
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