Background: The leading cause of mutations in the hepatitis B virus (HBV) genome is the high rate of nucleotide misincorporation during reverse transcription. Most mutations were found within the “a” determinant of the S gene’s major hydrophilic region (MHR). They resulted in escape mutants due to amino acid changes in the MHR. However, mutations outside the MHR can also trigger escape mutants. Objectives: This study focused on further molecular studies on the MHR of genotype D of HBV DNA isolated from patients with chronic HBV infection, together with the coexistence of hepatitis B surface antigen (HBsAg) and hepatitis B surface antibodies (anti-HBs) in their serum samples. Methods: In this study, serum samples from 83 patients with chronic HBV infection were analyzed by serological and immunological tests for the concurrence of HBsAg and anti-HBs. In addition, the mutation in the HBV DNA was assessed by nucleotide sequencing of S genes within, upstream, and downstream of the MHR. Results: Among 83 patients with chronic HBV infection, the coexistence of HBsAg and anti-HBs were detected in 11 (13.25%) individuals. Mutations in eight amino acids of seven samples analyzed for nucleotide sequencing were observed at 27 different sites in three locations, namely upstream, within, and downstream of the MHR. The mutations affected the structure of the epitope and the appearance of an escape mutant. Conclusions: The results indicated that mutations downstream and upstream of the MHR play a role in the coexistence of HBsAg and anti-HBs in patients with chronic HBV infection.

Aim: Human respiratory syncytial virus (HRSV) is a common cause of respiratory infections, particularly in infants and the elderly. Ribavirin is the only US FDA-approved antiviral drug for HRSV infection, but it has unwanted side effects. Methods: We engineered an shRNA targeting the HRSV- M gene to antagonize HRSV replication. Results: The results showed that shRNA had a similarly significant reduction in viral load (99.8%) as ribavirin. In addition, combined treatment with ribavirin and M-shRNA resulted in a significant reduction in viral load compared with ribavirin or M-shRNA alone. Conclusion: These results suggest that M-shRNA could be a potential new inhibitor of HRSV replication and could offer a safer and more effective treatment option for HRSV infection in the future.