Dataset Information

Revealing an association between HPV and systemic lupus erythematosus: A bidirectional two-sample Mendelian randomization study.

ABSTRACT:

Background

An increasing number of studies have focused on the association between Human papillomavirus (HPV) infection and systemic lupus erythematosus (SLE). However, current evidence is largely based on retrospective studies, which are susceptible to confounding factors and cannot establish causation.

Methods

A bidirectional two-sample Mendelian randomization (MR) design was used to evaluate the causal relationship between HPV and SLE. Mononucleoside polymers (SNPS) with strong evidence for genome-wide association studies (GWAS) were selected from the HPV exposure dataset and used as an instrumental variable (IV) for this study. For the MR Analysis results, the MR-Egger intercept P test, MR-Presso global test, CochranQ test and leave-one test were used for sensitivity analysis.

Results

Based on the evidence of MR Analysis, this study finally determined that there was no causal association between HPV16 and HPV18 and SLE.

Conclusions

Possible regulation of HPV infection is not significantly associated with regulation of SLE. These findings provide new insights into the underlying mechanisms of HPV and SLE and need to be validated by further studies.

SUBMITTER: Pan F

PROVIDER: S-EPMC11305866 | biostudies-literature | 2024 Aug

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Revealing an association between HPV and systemic lupus erythematosus: A bidirectional two-sample Mendelian randomization study.

Pan Fangfang F Shen Huiliang H Wang Ben B Wang Jian J

Skin research and technology : official journal of International Society for Bioengineering and the Skin (ISBS) [and] International Society for Digital Imaging of Skin (ISDIS) [and] International Society for Skin Imaging (ISSI) 20240801 8

<h4>Background</h4>An increasing number of studies have focused on the association between Human papillomavirus (HPV) infection and systemic lupus erythematosus (SLE). However, current evidence is largely based on retrospective studies, which are susceptible to confounding factors and cannot establish causation.<h4>Methods</h4>A bidirectional two-sample Mendelian randomization (MR) design was used to evaluate the causal relationship between HPV and SLE. Mononucleoside polymers (SNPS) with strong ...[more]

PMID: 39112437

Similar Datasets

Project description:Background: Although observational studies have demonstrated that blood lipids were associated with systemic lupus erythematosus (SLE), the causality of this association remains elusive as traditional observational studies were prone to confounding and reverse causality biases. Here, this study attempted to reveal the potential causal link between SLE and the levels of four blood lipids (HDL cholesterol, LDL cholesterol, TG, and TC). Methods: Bidirectional two-sample Mendelian randomization (MR) was employed to explore the unconfounded causal associations between the four blood lipids and SLE. In addition, regression-based Multivariate MR (MVMR) to quantify the possible mediation effects of blood lipids on SLE. After a rigorous evaluation of the quality of studies, the single-nucleotide polymorphisms (SNPs) associated with the four blood lipids were selected from the Global Lipids Genetic Consortium (GLGC) consisted of 188,577 individuals of European ancestry, and the SNPs related to SLE were selected from a large-scale genome-wide association study (GWAS) database named IEU GWAS. Subsequently, MR analyses were conducted with inverse-variance weighted (IVW), weighted median, weighted mode, simple mode, and MR-Egger regression. Sensitivity analyses were performed to verify whether heterogeneity and pleiotropy led to bias in the MR results. Results: Bidirectional two-sample MR results demonstrated that there was no significant causal association between SLE and the four blood lipids (When setting SLE as outcome, HDL cholesterol and SLE, IVW OR: 1.32, 95% CI: 1.05∼1.66, p = 1.78E-02; LDL cholesterol and SLE, IVW OR: 1.26, 95% CI: 1.04∼1.53, p = 2.04E-02; TG and SLE, IVW OR: 1.04, 95% CI: 0.71∼1.51, p = 8.44E-01; TC and SLE, IVW OR: 1.07, 95% CI: 0.89∼1.29, p = 4.42E-01; When setting SLE as exposure, SLE and HDL cholesterol, IVW OR: 1.00, 95% CI: 0.99∼1.01, p = 9.51E-01; SLE and LDL cholesterol, IVW OR: 0.99, 95% CI: 0.98∼1.00, p = 3.14E-01; SLE and TG, IVW OR: 0.99, 95% CI: 0.98∼1.00, p = 1.30E-02; SLE and TC, IVW OR: 0.99, 95% CI: 0.98∼1.00, p = 1.56E-01). Our MVMR analysis also provided little evidence that genetically determined lipid traits were significantly associated with the risk of SLE (HDL cholesterol and SLE, p = 9.63E-02; LDL cholesterol and SLE, p = 9.63E-02; TG and SLE, p = 8.44E-01; TC and SLE, p = 4.42E-01). Conclusion: In conclusion, these data provide evidence that genetic changes in lipid traits are not significantly associated with SLE risk in the European population.

Project description:BackgroundPrevious observational studies have suggested that the causal role of systemic lupus erythematosus (SLE) in the risk of cardiovascular diseases (CVDs) remained inconsistent. In this study, we aimed to investigate the causal relationship between SLE and CVDs by two-sample Mendelian randomization (MR) analysis.MethodsGenetic instruments for SLE were obtained from a public genome-wide association study (GWAS) with 4,036 patients with SLE and 6,959 controls. Summary statistical data for CVDs, including coronary artery disease (CAD), myocardial infarction (MI), atrial fibrillation (AF), ischemic stroke (IS), and its subtypes, were identified from other available GWAS meta-analyses. The inverse-variance weighted (IVW) method was used as the primary method to estimate the causal effect. The simple- and weighted-median method, MR-Egger method, and MR pleiotropy residual sum and outlier (MR-PRESSO) were provided as a supplement to the IVW method. Besides, we performed sensitivity analyses, including Cochran's Q test, MR-Egger intercept test, and leave-one-out analysis, to evaluate the robustness of the results.ResultsA total of 15 single-nucleotide polymorphisms (SNPs) were identified after excluding linkage disequilibrium (LD) and potential confounding factors. According to the IVW results, our MR study indicated that genetically predicted SLE was not causally connected with the risk of CVDs [CAD: odds ratio (OR) = 1.005, 95% confidence interval (CI) = 0.986-1.024, p-value = 0.619; MI: OR = 1.002, 95% CI = 0.982-1.023, p-value = 0.854; AF: OR = 0.998, 95% CI = 0.982-1.014, p-value = 0.795; IS: OR = 1.006, 95% CI = 0.984-1.028, p-value = 0.621; cardioembolic stroke (CES): OR = 0.992, 95% CI = 0.949-1.036, p-value = 0.707; small vessel stroke (SVS): OR = 1.014, 95% CI = 0.964-1.067, p-value = 0.589; large artery stroke (LAS): OR = 1.030, 95% CI = 0.968-1.096, p-value = 0.352]. Analogical findings could be observed in supplementary MR methods. Sensitivity analyses suggested that the causal estimates were robust.ConclusionOur two-sample MR analysis provided no evidence that genetically determined SLE was causally associated with the risk of CVDs.

Dataset Information

Revealing an association between HPV and systemic lupus erythematosus: A bidirectional two-sample Mendelian randomization study.

Background

Methods

Results

Conclusions

Publications

Revealing an association between HPV and systemic lupus erythematosus: A bidirectional two-sample Mendelian randomization study.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets