Abstract
BackgroundSome patients have a greater response to viral infection than do others having a similar level of viral replication. Hypercytokinemia is the principal immunopathological mechanism that contributes to a severer clinical course in cases of influenza A/H1N1. The benefit produced, or damage caused, by these cytokines in severe disease is not known. The genes that code for these molecules are polymorphic and certain alleles have been associated with susceptibility to various diseases. The objective of the present study was to determine whether there was an association between polymorphisms of TNF, LTA, IL1B, IL6, IL8, and CCL1 and the infection and severity of the illness caused by the pandemic A/H1N1 in Mexico in 2009.MethodsCase–control study. The cases were patients confirmed with real time PCR with infection by the A/H1N1 pandemic virus. The controls were patients with infection like to influenza and non-familial healthy contacts of the patients with influenza. Medical history and outcome of the disease was registered. The DNA samples were genotyped for polymorphisms TNF rs361525, rs1800629, and rs1800750; LTA rs909253; IL1B rs16944; IL6 rs1818879; IL8 rs4073; and CCL1 rs2282691. Odds ratio (OR) and the 95% confidence interval (95% CI) were calculated. The logistic regression model was adjusted by age and severity of the illness in cases.ResultsInfection with the pandemic A/H1N1 virus was associated with the following genotypes: TNF rs361525 AA, OR = 27.00; 95% CI = 3.07–1248.77); LTA rs909253 AG (OR = 4.33, 95% CI = 1.82–10.32); TNF rs1800750 AA (OR = 4.33, 95% CI = 1.48–12.64); additionally, LTA rs909253 AG showed a limited statistically significant association with mortality (p = 0.06, OR = 3.13). Carriers of the TNF rs1800629 GA genotype were associated with high levels of blood urea nitrogen (p = 0.05); those of the TNF rs1800750 AA genotype, with high levels of creatine phosphokinase (p=0.05). The IL1B rs16944 AA genotype was associated with an elevated number of leukocytes (p <0.001) and the IL8 rs4073 AA genotype, with a higher value for PaO2 mm Hg.ConclusionThe polymorphisms of genes involved in the inflammatory process contributed to the severity of the clinical behavior of infection by the pandemic influenza A/H1N1 virus.
Highlights
Some patients have a greater response to viral infection than do others having a similar level of viral replication
Because we think that genetic factors of the host may influence the nature and intensity of the inflammatory immune response, the objective of this study was to determine whether the polymorphisms of genes that are associated with inflammation may be associated with the development of the infection and with the clinical severity in Mexican mestizo patients with influenza A/H1N1
A total of 44 patients were positive for the influenza A/H1N1 virus (A/H1N1 group); the remaining 50 patients who had tested negative for the influenza A/H1N1 virus, were diagnosed as having influenza-like illness (ILI)
Summary
Some patients have a greater response to viral infection than do others having a similar level of viral replication. The genes that code for these molecules are polymorphic and certain alleles have been associated with susceptibility to various diseases. The objective of the present study was to determine whether there was an association between polymorphisms of TNF, LTA, IL1B, IL6, IL8, and CCL1 and the infection and severity of the illness caused by the pandemic A/H1N1 in Mexico in 2009. The majority of those infected by the influenza A/H1N1 virus presented mild symptoms that were self-limiting, a subgroup of patients followed an adverse clinical course, requiring a greater level of medical attention and more aggressive management [2]. Some co-morbidities (e.g., immunosuppression, pre-existing pulmonary disease, cardiac disease, diabetes, asthma that requires regular medical attention, smoking, and obesity) have been demonstrated to increase the risk of hospitalization for infection with influenza A/H1N1 [4,5]. The results of certain laboratory tests (e.g., lactate dehydrogenase (LDH), >600 IU/L; hypoxemia (PaO2,
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
