Nonstructural Protein NP1 of Human Bocavirus 1 suppresses the growth of A549 cell by promoting autophagy

Human bocavirus 1 (HBoV1) refers to a human parvovirus causing acute respiratory tract infection in children. Bocaviruses encode an NP1 protein, which has 47% amino acid homology with NP1 of Minute Virus of Canines (MVC) and Bovine Parvovirus (BPV), but not with any protein of other parvoviruses. NP1 was found to induce apoptosis in Hela cells, which does not depend on viral replication and other protein expression. However, whether NP1 induces pulmonary cell death is unclear. In the present study, we investigate the impacts of NP1 on the autophagy and viability of A549 cells by expressing NP1. The plasmid containing NP1 gene was transfected into A549 cells. The apoptosis of A549 was evaluated by apoptosis detection kit and expression of caspase3. Cell viability and cell migration were detected by CCK8 kit and cell scratch test, respectively. The autophagy-related proteins and HMGB1 were detected by Western blot after NP1 expression in transfected cells. The real-time PCR was employed to detect HMGB1 mRNA. The secretory HMGB1 in supernatant of cell culture was measured by ELISA kit. The transient expression of NP1 did not induce apoptosis in A549 cells, but inhibited cell viability and migration. The expression of Beclin1 and LC3 II increased significantly and that of autophagy substrate P62 decreased dramatically upon transfection of NP1. The expression of NP1 reduced both levels of mRNA and protein HMGB1. The NP1 induced A549 autophagy was activated by STAT3 signaling pathway. HBoV1 NP1 induced autophagy in A549 cells by activating phosphorylation of STAT3 signaling pathway and inhibited A549 cell viability. This study provides insight into further elucidating the replication mechanism of HBoV1.