A seismological phenomenon preceding the 2017 Ms7.0 Jiuzhaigou earthquake

On 8 August 2017, a Ms7.0 earthquake occurred in Jiuzhaigou in the Sichuan Province of China. In this study, we obtained the vertical continuous data recorded at 12 nearby broadband seismometers from April to December 2017, in order to characterize the temporal and spatial variations in the vertical ground motion prior to the onset of the earthquake. Using the self-mutual information method, we determined that from July to August 2017, the self-mutual information value of the vertical ground motion increased at several stations. The spatiotemporal evolution also shows that the region of highest value migrates from south to north toward the earthquake epicenter. Among them, the change of SPA (the station closest to the epicenter) is the most prominent. We believe that this phenomenon is related to the formation of the Jiuzhaigou earthquake. Our work, in combination with other published works, indicates that the Jiuzhaigou earthquake was caused by the continued eastward movement and obstruction of the Qinghai Tibet Plateau by the Sichuan Basin, and the movement of Longmenshan fault is also one of the causes of the earthquake

A seismological phenomenon preceding the 2017 Ms7.0 Jiuzhaigou earthquake

On 8 August 2017, a Ms7.0 earthquake occurred in Jiuzhaigou in the Sichuan Province of China. In this study, we obtained the vertical continuous data recorded at 12 nearby broadband seismometers from April to December 2017, in order to characterize the temporal and spatial variations in the vertical ground motion prior to the onset of the earthquake. Using the self-mutual information method, we determined that from July to August 2017, the self-mutual information value of the vertical ground motion increased at several stations. The spatiotemporal evolution also shows that the region of highest value migrates from south to north toward the earthquake epicenter. Among them, the change of SPA (the station closest to the epicenter) is the most prominent. We believe that this phenomenon is related to the formation of the Jiuzhaigou earthquake. Our work, in combination with other published works, indicates that the Jiuzhaigou earthquake was caused by the continued eastward movement and obstruction of the Qinghai Tibet Plateau by the Sichuan Basin, and the movement of Longmenshan fault is also one of the causes of the earthquake

Porcine Circovirus 2 Deploys PERK Pathway and GRP78 for Its Enhanced Replication in PK-15 Cells

Porcine circovirus type 2 (PCV2) infection induces autophagy and apoptosis. These cellular responses could be connected with endoplasmic reticulum (ER) stress. It remains unknown if PCV2 induces ER stress and if autophagy or apoptosis is primary to PCV2 infection or secondary responses following ER stress. Here, we demonstrate that PCV2 triggered unfolded protein response (UPR) in PK-15 cells by activating the PERK/eIF2α pathway without concomitant activation of IRE1 or ATF6. Since ATF4 and CHOP were induced later than PERK/eIF2α, it is clear that persistent PCV2 infection could lead to selective activation of PERK via the PERK-eIF2α-ATF4-CHOP axis. Therefore, PERK activation could be part of the pro-apoptotic signaling via induced expression of CHOP by PCV2. Since PERK inhibition by GSK2606414 or RNA silencing or suppression of eIF2α dephosphorylation by salubrinal limited viral replication, we suppose that PCV2 deploys UPR to enhance its replication. Over-expression of GRP78 or treatment with tauroursodeoxycholic acid could enhance viral capsid expression and/or viral titers, indicating that these chaperones, endogenous or exogenous, could help correct folding of viral proteins. Our findings provide the first evidence that ER stress plays a role in the pathogenesis of PCV2 infection probably as part of autophagic and apoptotic responses

DNAJA3 Interacts with PEDV S1 Protein and Inhibits Virus Replication by Affecting Virus Adsorption to Host Cells

Porcine epidemic diarrhea virus (PEDV) infection causes huge economic losses to the pig industry worldwide. DNAJA3, a member of the Hsp40 family proteins, is known to play an important role in the replication of several viruses. However, it remains unknown if it interacts with PEDV. We found that DNAJA3 interacted with PEDV S1, initially with yeast two-hybrid screening and later with Co-IP, GST pull-down, and confocal imaging. Further experiments showed the functional relationship between DNAJA3 and PEDV in the infected IPEC-J2 cells. DNAJA3 overexpression significantly inhibited PEDV replication while its knockdown had the opposite effect, suggesting that it is a negative regulator of PEDV replication. In addition, DNAJA3 expression could be downregulated by PEDV infection possibly as the viral strategy to evade the suppressive role of DNAJA3. By gene silencing and overexpression, we were able to show that DNAJA3 inhibited PEDV adsorption to IPEC-J2 cells but did not affect virus invasion. In conclusion, our study provides clear evidence that DNAJA3 mediates PEDV adsorption to host cells and plays an antiviral role in IPEC-J2 cells