<p>This study evaluated the association of Cytomegalovirus (CMV) infection with miR-155, miR-31, and their target gene TGFBR2 in patients with chronic obstructive pulmonary disease (COPD). A cross-sectional study was conducted on 40 COPD patients in Kermanshah, Iran (Dec 2023–May 2025). COPD diagnosis was based on GOLD criteria, spirometry, radiological findings, and clinical evaluation. Blood samples were collected for molecular analysis. CMV was detected by qPCR. Expression levels of miR-155 and miR-31 were quantified by qRT-PCR and normalized to the kit-provided housekeeping control, whereas TGFBR2 expression was measured by qRT-PCR and normalized to GAPDH. Statistical analyses included t-tests or Mann–Whitney U tests, Pearson or Spearman correlations, and fold-change calculation using the 2<sup>−ΔΔCt</sup> method. CMV infection was detected in 60% of patients (<i>n</i> = 24). CMV-positive COPD patients showed higher miR-155 (3.42 ± 1.18 vs. 1.85 ± 0.64; <i>p</i> = 0.003) and miR-31 (2.78 ± 0.95 vs. 1.42 ± 0.58; <i>p</i> = 0.012) and lower TGFBR2 (0.58 ± 0.24 vs. 1.12 ± 0.38; <i>p</i> = 0.004) compared with CMV-negative patients. MiR-155 and miR-31 were positively correlated (<i>r</i> = 0.724, <i>p</i> &lt; 0.001), and both negatively correlated with TGFBR2 (<i>r</i>=-0.658 and − 0.592, <i>p</i> &lt; 0.001). CMV was also associated with more severe COPD (<i>p</i> = 0.038). CMV infection in COPD patients is linked to upregulation of miR-155/miR-31 and downregulation of TGFBR2, suggesting an association between CMV infection and altered expression of miR-155, miR-31, and TGFBR2, which may reflect shared inflammatory pathways in COPD.</p>

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Association of cytomegalovirus infection with miR-155 and miR-31 and TGFBR2 expression in chronic obstructive pulmonary disease

  • Shahla Shahbazi,
  • Masoud Darabi,
  • Mosayeb Rostamian,
  • Mohsen Moghoofei,
  • Farhad Babaei

摘要

This study evaluated the association of Cytomegalovirus (CMV) infection with miR-155, miR-31, and their target gene TGFBR2 in patients with chronic obstructive pulmonary disease (COPD). A cross-sectional study was conducted on 40 COPD patients in Kermanshah, Iran (Dec 2023–May 2025). COPD diagnosis was based on GOLD criteria, spirometry, radiological findings, and clinical evaluation. Blood samples were collected for molecular analysis. CMV was detected by qPCR. Expression levels of miR-155 and miR-31 were quantified by qRT-PCR and normalized to the kit-provided housekeeping control, whereas TGFBR2 expression was measured by qRT-PCR and normalized to GAPDH. Statistical analyses included t-tests or Mann–Whitney U tests, Pearson or Spearman correlations, and fold-change calculation using the 2−ΔΔCt method. CMV infection was detected in 60% of patients (n = 24). CMV-positive COPD patients showed higher miR-155 (3.42 ± 1.18 vs. 1.85 ± 0.64; p = 0.003) and miR-31 (2.78 ± 0.95 vs. 1.42 ± 0.58; p = 0.012) and lower TGFBR2 (0.58 ± 0.24 vs. 1.12 ± 0.38; p = 0.004) compared with CMV-negative patients. MiR-155 and miR-31 were positively correlated (r = 0.724, p < 0.001), and both negatively correlated with TGFBR2 (r=-0.658 and − 0.592, p < 0.001). CMV was also associated with more severe COPD (p = 0.038). CMV infection in COPD patients is linked to upregulation of miR-155/miR-31 and downregulation of TGFBR2, suggesting an association between CMV infection and altered expression of miR-155, miR-31, and TGFBR2, which may reflect shared inflammatory pathways in COPD.