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Abstract Background & Objective: Hepatitis E virus is one of the most common causes of acute infection in adults. Pregnant and transplant patients are more in risk of HEV infection. Fecal-oral is the main route of HEV transmission but recently transmission by blood transfusion has been observed. This study was aimed to determine the prevalence of HEV-Ab in hemodialysis patients in Gorgan, Iran. Material and Methods: In this cross-sectional descriptive study, we investigated 150 hemodialysis patients of Panje Azar hospital in Gorgan. These patients were evaluated for the presence of HEV total Ab by ELISA method. Results: of 150, 6 patients (4%) are positive for HEV-Ab. There has been no significant relation between anti HEV Ab and variables such as age, gender, ethnicity, duration and number of hemodialysis in a week and (P>0.05). Conclusion: This study, which is the first report from this area, show that the lower prevalence of anti HEV Ab in hemodialysis patients in comparison with pregnant and childbearing age women. Keywords: Hepatitis E Hemodialysis Elisa Gorgan

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Introduction: Respiratory syncytial virus (RSV) is a leading cause of severe lower respiratory tract infections in infants and young children, with disease severity linked to excessive inflammation. A20 (TNFAIP3) is a negative regulator of NF‑κB signalling and may modulate RSV-induced lung inflammation.  Here, we investigated the effect of RSV infection on pulmonary A20 gene expression in a murine model.
Methods: Female BALB/c mice (n=12; 6 per group) were intranasally infected with RSV (3 × 10⁶ PFU) and euthanized on day 5 post‑infection. Lung tissues were collected to analyse the A20 (TNFAIP3) mRNA expression 5 days following RSV infection by Real‑time RT‑PCR.
Results: Quantitative PCR analysis demonstrated a statistically significant upregulation of A20 expression in the lungs of RSV-infected mice compared to the uninfected control group 5 days following infection (p=0.0048).
Conclusions: RSV infection in mice induces A20 expression, suggesting a potential role for A20 in regulating pulmonary inflammation following the virus infection.