Supershear earthquakes with rupture velocity exceeding shear-wave speeds, previously observed in laboratory experiments and large strike-slip events, often have an initial sub-shear stage before they transition to supershear. In this study, integrated geophysical observations of the 2018 Mw 7.5 Palu, Indonesia earthquake, provide robust evidence of an early and persistent supershear rupture speed. Slowness-enhanced back-projection (SEBP) of teleseismic data provides a sharp image of the rupture process, consistently across multiple arrays. The inferred rupture path agrees with the surface rupture trace inferred from the net surface displacement field derived by sub-pixel InSAR image correlation. The SEBP results indicate a sustained rupture velocity of 4.1 km/s from the rupture initiation to the end, despite large fault bends. The persistent supershear speed is further validated by evidence of far-field Rayleigh Mach waves in regional seismograms. The short or absent supershear transition distance can be caused by high initial shear stress or short critical slip-weakening distance, and promoted by fault roughness near the hypocenter. Steady rupture propagation at a supershear speed considered to be unstable, lower than the Eshelby speed, could result from the presence of a damaged fault zone.

BackgroundFoot-and-mouth disease virus (FMDV) causes a severe vesicular disease in domestic and wild cloven-hoofed animals. Because of the limited early protection induced by current vaccines, emergency antiviral strategies to control the rapid spread of FMD outbreaks are needed.Here we constructed multiple microRNAs (miRNAs) targeting the internal ribosome entry site (IRES) element of FMDV and investigated the effect of IRES-specific miRNAs on FMDV replication in baby hamster kidney (BHK-21) cells and suckling mice.ResultsFour IRES-specific miRNAs significantly reduced enhanced green fluorescent protein (EGFP) expression from IRES-EGFP reporter plasmids, which were used with each miRNA expression plasmid in co-transfection of BHK-21 cells. Furthermore, treatment of BHK-21 cells with Bi-miRNA (a mixture of two miRNA expression plasmids) and Dual-miRNA (a co-cistronic expression plasmid containing two miRNA hairpin structures) induced more efficient and greater inhibition of EGFP expression than did plasmids carrying single miRNA sequences.Stably transformed BHK-21 cells and goat fibroblasts with an integrating IRES-specific Dual-miRNA were generated, and real-time quantitative RT-PCR showed that the Dual-miRNA was able to effectively inhibit the replication of FMDV (except for the Mya98 strain) in the stably transformed BHK-21 cells.The Dual-miRNA plasmid significantly delayed the deaths of suckling mice challenged with 50× and 100× the 50% lethal dose (LD50) of FMDV vaccine strains of three serotypes (O, A and Asia 1), and induced partial/complete protection against the prevalent PanAsia-1 and Mya98 strains of FMDV serotype O.ConclusionThese data demonstrate that IRES-specific miRNAs can significantly inhibit FMDV infection in vitro and in vivo.

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The assembly of foot-and-mouth disease virus (FMDV) requires the cleavage of the P12A polyprotein into individual structural proteins by protease 3C. In this study, we constructed a recombinant baculovirus that simultaneously expressed the genes for the P12A and 3C proteins of Asia I FMDV from individual promoters. The capsid proteins expressed in High Five insect cells were processed by viral 3C protease, as shown by Western blotting, and were antigenic, as revealed by their reactivity in an indirect sandwich-ELISA, and by immunofluorescent assay. The empty capsid-like particles were similar to authentic 75S empty capsids from FMDV in terms of their shape, size and sedimentation velocity, as demonstrated by sucrose gradient centrifugation. Both empty capsid-like particles and some small-sized particles (about 10nm in diameter) were also observed using immunoelectron microscopy. Furthermore, the empty capsid-like particles or intermediates induced high levels of FMDV-specific antibodies in guinea pigs following immunization, and neutralizing antibodies were induced in the second week after vaccination. These recombinant, non-infectious, FMDV empty capsids are potentially useful for the development of new diagnostic techniques and vaccines.

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BackgroundSome cell-adapted strains of foot-and-mouth disease virus (FMDV) can utilize heparan sulfate (HS) as a receptor to facilitate viral infection in cultured cells. A number of independent sites on the capsid that might be involved in FMDV-HS interaction have been studied. However, the previously reported residues do not adequately explain HS-dependent infection of two cell-adapted PanAsia-1 strains (O/Tibet/CHA/6/99tc and O/Fujian/CHA/9/99tc) of FMDV serotype O.To identify the molecular determinant(s) for the interaction of O/Tibet/CHA/6/99tc and O/Fujian/CHA/9/99tc with HS receptor, several chimeric viruses and site-directed mutants were generated by using an infectious cDNA of a non-HS-utilizing rescued virus (Cathay topotype) as the genomic backbone. Phenotypic properties of these viruses were determined by plaque assays and virus adsorption and penetration assays in cultured cells.ResultsOnly two of the rescued viruses encoding VP0 of O/Tibet/CHA/6/99tc or VP1 of O/Fujian/CHA/9/99tc formed plaques on wild-type Chinese hamster ovary (WT-CHO; HS+) cells, but not on HS-negative pgsD-677 cells. The formation of plaques by these two chimeric viruses on WT-CHO cells could be abolished by the introduction of single amino acid mutations Gln-2080 → Leu in VP2 of O/Tibet/CHA/6/99tc and Lys-1083 → Glu in VP1 of O/Fujian/CHA/9/99tc, respectively. Nonetheless, the introduced mutation Leu-2080 → Gln in VP2 of O/Fujian/CHA/9/99tc for the construction of expectant recombinant plasmid led to non-infectious progeny virus in baby hamster kidney 21 (BHK-21) cells, and the site-directed mutant encoding Glu-1083 → Lys in VP1 of O/Tibet/CHA/6/99tc did not acquire the ability to produce plaques on WT-CHO cells.Significant differences in the inhibition of the infectivity of four HS-utilizing viruses by heparin and RGD-containing peptide were observed in BHK-21 cells.Interestingly, the chimeric virus encoding VP0 of O/Fujian/CHA/9/99tc, and the site-directed mutant encoding Gln-2080 → Leu in VP2 of O/Tibet/CHA/6/99tc could bind to HS, but there was no expression of the 3A protein of these two viruses in WT-CHO cells.ConclusionThe results suggest that the cooperation of certain specific amino acid residues in the capsid proteins of these two cell-adapted PanAsia-1 strains is essential for viral infectivity, the heparin affinity and the capability on FMDV-HS interaction.