Genetic features of patients with influenza A / H1N1 / 09 complicated by pneumonia

Romanova, E. Yu.; Говорин, А. В.

doi:10.18093/0869-0189-2015-25-4-425-432

Cited by 6 publications

(4 citation statements)

References 3 publications

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“…Through experimental and clinical studies, the systemic inflammatory dysregulation correlating with the disease’s severity and progression has been identified as one of the most important pathogenic mechanisms in infection [ 11 , 12 ]. Cytokine secretion by infected cells is necessary for the initiation of the immune response that controls virus replication [ 13 ]; also, immunopathological mechanisms such as hypercytokinemia (also known as cytokine storm) generally contribute to the more severe evolution of the infection [ 14 , 15 ].…”

Section: Inflammatory Response and Ifitm3 Role In Influenza A Virumentioning

confidence: 99%

Role of the Host Genetic Susceptibility to 2009 Pandemic Influenza A H1N1

Pérez-Rubio

Ponce-Gallegos

Domínguez-Mazzocco

et al. 2021

Viruses

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Influenza A virus (IAV) is the most common infectious agent in humans, and infects approximately 10–20% of the world’s population, resulting in 3–5 million hospitalizations per year. A scientific literature search was performed using the PubMed database and the Medical Subject Headings (MeSH) “Influenza A H1N1” and “Genetic susceptibility”. Due to the amount of information and evidence about genetic susceptibility generated from the studies carried out in the last influenza A H1N1 pandemic, studies published between January 2009 to May 2020 were considered; 119 papers were found. Several pathways are involved in the host defense against IAV infection (innate immune response, pro-inflammatory cytokines, chemokines, complement activation, and HLA molecules participating in viral antigen presentation). On the other hand, single nucleotide polymorphisms (SNPs) are a type of variation involving the change of a single base pair that can mean that encoded proteins do not carry out their functions properly, allowing higher viral replication and abnormal host response to infection, such as a cytokine storm. Some of the most studied SNPs associated with IAV infection genetic susceptibility are located in the FCGR2A, C1QBP, CD55, and RPAIN genes, affecting host immune responses through abnormal complement activation. Also, SNPs in IFITM3 (which participates in endosomes and lysosomes fusion) represent some of the most critical polymorphisms associated with IAV infection, suggesting an ineffective virus clearance. Regarding inflammatory response genes, single nucleotide variants in IL1B, TNF, LTA IL17A, IL8, IL6, IRAK2, PIK3CG, and HLA complex are associated with altered phenotype in pro-inflammatory molecules, participating in IAV infection and the severest form of the disease.

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Section: Inflammatory Response and Ifitm3 Role In Influenza A Virumentioning

confidence: 99%

Role of the Host Genetic Susceptibility to 2009 Pandemic Influenza A H1N1

Pérez-Rubio

Ponce-Gallegos

Domínguez-Mazzocco

et al. 2021

Viruses

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“…Viruses take advantage of SNPs-driven variations in host cytokines that alter the transcriptional activity of their genes as well as association with the possibility of a wide range of influenza viruses [30]. Another challenge is monitoring or classifying people with influenza-like illness [31] that frequently occur after influenza virus vaccination.…”

Section: Introductionmentioning

confidence: 99%

Association of polymorphisms in inflammatory cytokines encoding genes with severe cases of influenza A/H1N1 and B in an Iranian population

Keshavarz

Namdari

Farahmand

et al. 2019

Virol J

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Background The increased levels of blood cytokines is the main immunopathological process that were attributed to severe clinical outcomes in cases of influenza A, influenza B and people with influenza-like illness (ILI). Functional genetic polymorphisms caused by single nucleotide polymorphisms (SNPs) in inflammatory cytokines genes can influence their functions either qualitatively or quantitatively, which is associated with the possibility of severe influenza infections. The aim of the present case-control study was to investigate the association of polymorphisms in inflammatory cytokines genes with influenza patients and ILI group in an Iranian population. Methods Total number of 30 influenza B, 50 influenza A (H1N1) and 96 ILI inpatient individuals were confirmed by Real-time RT-PCR and HI assays. The genotype determination was assessed for defined SNPs in IL-1β, IL-17, IL-10 and IL-28 genes. Results The frequencies of the IL-1β rs16944 ( P = 0.007 ) and IL-17 rs2275913 ( P = 0.006 ) genotypes were associated with severe influenza disease, while the frequencies of IL-10 rs1800872 and IL-28 rs8099917 were not associated with the disease ( P > 0.05 ). Also, the absence of A allele in IL-17 rs2275913 SNP increased the risk of influenza A (H1N1) infection ( P = 0.008 ). Conclusions This study demonstrated that influenza A- (H1N1) and B-infected patients and also ILI controls have different profiles of immune parameters, and individuals carrying the specific cytokine-derived polymorphisms may show different immune responses towards severe outcome.

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“…This could explain the finding reported by a study of patients with influenza pandemic (H1N1) wherein the frequencies of "A" allele and GA genotype were significantly lower while those of the G allele and GG genotype were significantly higher among patients compared with controls [18]. Similarly, another study reported that the patients with influenza-related pneumonia were more frequently homozygous for the G allele of the TNF 308 G/A polymorphism compared with controls [19].…”

Section: Discussionmentioning

confidence: 69%

The role of Tumor necrosis factor alpha −308 G>A promoter polymorphism in pediatric community acquired pneumonia

Gendy

El-Mekkawy

El-Naidany

et al. 2020

Egypt Pediatric Association Gaz

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Background: Tumor necrosis factor alpha (TNF-α) −308 G>A promoter polymorphism might be associated with excessive production of the proinflammatory cytokine TNF-α, modulating host response to pulmonary infections. Our objective was to evaluate the association of TNF-α gene −308 G>A polymorphism with susceptibility to, and severity of, community-acquired pneumonia (CAP).Results: This was a cross-sectional study including 45 Egyptian children hospitalized for CAP in addition to 45 healthy children who served as a control group. Pneumonia severity was assessed on admission by the World Health Organization (WHO) guidelines; Pediatric Respiratory Severity Score (PRESS) score; Predisposition, Infection, Response and Organ failure (PIROm) score; and Respiratory Index of Severity in Children (RISC) score. Genotyping of TNF-α polymorphism was performed to all individuals by polymerase chain reaction and restriction fragment length polymorphism (PCR-RFLP). Patients were monitored till hospital discharge. Frequency of AG genotype was lower among patients compared with control [odds ratio (OR) and 95% confidence interval (CI) = 0.13 (0.03-0.63); p = 0.012]. Prevalence of genotypes AA+AG was lower among patients compared with controls [OR and 95% CI = 0.34 (0.12-0.99); p = 0,048]. The "A" allele prevalence was higher among controls, but no significant association was found with CAP [OR and 95% CI = 0.58 (0.25-1.35); p = 0.21]. When PRESS score was used to classify patients into "severe pneumonia" and "non-severe pneumonia," no significant association of any of the alleles or genotypes with CAP severity was found.Conclusion: TNF-α −308 G>A polymorphism confers protection from pediatric CAP but is not associated with indicators of CAP severity. Larger studies are needed to confirm these findings in pediatric patients from different ethnicities.

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Genetic features of patients with influenza A / H1N1 / 09 complicated by pneumonia

Cited by 6 publications

References 3 publications

Role of the Host Genetic Susceptibility to 2009 Pandemic Influenza A H1N1

Role of the Host Genetic Susceptibility to 2009 Pandemic Influenza A H1N1

Association of polymorphisms in inflammatory cytokines encoding genes with severe cases of influenza A/H1N1 and B in an Iranian population

The role of Tumor necrosis factor alpha −308 G>A promoter polymorphism in pediatric community acquired pneumonia

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