Geodetic Constraints on San Francisco Bay Area Fault Slip Rates and Potential Seismogenic Asperities on the Partially Creeping Hayward Fault

The Hayward fault in the San Francisco Bay Area (SFBA) is sometimes considered unusual among continental faults for exhibiting significant aseismic creep during the interseismic phase of the seismic cycle while also generating sufficient elastic strain to produce major earthquakes. Imaging the spatial variation in interseismic fault creep on the Hayward fault is complicated because of the interseismic strain accumulation associated with nearby faults in the SFBA, where the relative motion between the Pacific plate and the Sierra block is partitioned across closely spaced subparallel faults. To estimate spatially variable creep on the Hayward fault, we interpret geodetic observations with a three-dimensional kinematically consistent block model of the SFBA fault system. Resolution tests reveal that creep rate variations with a length scale of \u3c15 km are poorly resolved below 7 km depth. In addition, creep at depth may be sensitive to assumptions about the kinematic consistency of fault slip rate models. Differential microplate motions result in a slip rate of 6.7 ± 0.8 mm/yr on the Hayward fault, and we image along-strike variations in slip deficit rate at ∼15 km length scales shallower than 7 km depth. Similar to previous studies, we identify a strongly coupled asperity with a slip deficit rate of up to 4 mm/yr on the central Hayward fault that is spatially correlated with the mapped surface trace of the 1868 MW = 6.9–7.0 Hayward earthquake and adjacent to gabbroic fault surfaces

Why are there different dynamics in the selection of drug resistance in HIV and hepatitis B and C viruses?

The arrival of new antiviral drugs to treat chronic hepatitis B virus (HBV) and hepatitis C virus (HCV) infections has given rise to great expectations along with concerns regarding the selection of drug-resistant variants. Many lessons learnt from HIV therapeutics can be helpful for designing adequate treatment strategies against viral hepatitis, the avoidance of sequential weak monotherapies being one of them. Although HIV, HBV and HCV share many biological features, including very rapid viral dynamics, distinctive characteristics explain why the speed of selection of drug resistance differs substantially between these viruses, being faster for HCV than for HIV and slower for HBV