RT Journal Article SR Electronic(1) A1 Feizi, Neda A1 Mehrbod, Parvaneh A1 Romani, Bizhan A1 Soleimanjahi, Hoorieh A1 Bamdad, Taravat A1 Feizi, Amir A1 Jazaeri, Ehsan Ollah A1 Targhi, Hadiseh Shokouhi A1 Saleh, Maryam A1 Jamali, Abbas A1 Fotouhi, Fatemeh A1 Nargesabad, Reza Nasrollahi A1 Abdoli, AsgharYR 2017 T1 Autophagy induction regulates influenza virus replication in a time-dependent manner JF Journal of Medical Microbiology, VO 66 IS 4 SP 536 OP 541 DO https://doi.org/10.1099/jmm.0.000455 PB Microbiology Society, SN 1473-5644, AB Purpose. Autophagy plays a key role in host defence responses against microbial infections by promoting degradation of pathogens and participating in acquired immunity. The interaction between autophagy and viruses is complex, and this pathway is hijacked by several viruses. Influenza virus (IV) interferes with autophagy through its replication and increases the accumulation of autophagosomes by blocking lysosome fusion. Thus, autophagy could be an effective area for antiviral research. Methodology. In this study, we evaluated the effect of autophagy on IV replication. Two cell lines were transfected with Beclin-1 expression plasmid before (prophylactic approach) and after (therapeutic approach) IV inoculation. Results/Key findings. Beclin-1 overexpression in the cells infected by virus induced autophagy to 26 %. The log10haemagglutinin titre and TCID50 (tissue culture infective dose giving 50 % infection) of replicating virus were measured at 24 and 48 h post-infection. In the prophylactic approach, the virus titre was enhanced significantly at 24 h post-infection (P≤0.01), but it was not significantly different from the control at 48 h post-infection. In contrast, the therapeutic approach of autophagy induction inhibited the virus replication at 24 and 48 h post-infection. Additionally, we showed that inhibition of autophagy using 3-methyladenine reduced viral replication. Conclusion. This study revealed that the virus (H1N1) titre was controlled in a time-dependent manner following autophagy induction in host cells. Manipulation of autophagy during the IV life cycle can be targeted both for antiviral aims and for increasing viral yield for virus production., UL https://www.microbiologyresearch.org/content/journal/jmm/10.1099/jmm.0.000455