Multimodal and Multistimuli 4D-Printed Magnetic Composite Liquid Crystal Elastomer Actuators.

Liquid crystal elastomer (LCE)-based soft actuators are being studied for their significant shape-changing abilities when they are exposed to heat or light. Nevertheless, their relatively slow response compared with soft magnetic materials limits their application possibilities. Integration of magnetic responsiveness with LCEs has been previously attempted; however, the LCE response is typically jeopardized in high volumes of magnetic microparticles (MMPs). Here, a multistimuli, magnetically active LCE (MLCE), capable of producing programmable and multimodal actuation, is presented. The MLCE, composed of MMPs within an LCE matrix, is generated through extrusion-based 4D printing that enables digital control of mesogen orientation even at a 1:1 (LCE:MMPs) weight ratio, a challenging task to accomplish with other methods. The printed actuators can significantly deform when thermally actuated as well as exhibit fast response to magnetic fields. When combining thermal and magnetic stimuli, modes of actuation inaccessible with only one input are achieved. For instance, the actuator is reconfigured into various states by using the heat-mediated LCE response, followed by subsequent magnetic addressing. The multistimuli capabilities of the MLCE composite expand its applicability where common LCE actuators face limitations in speed and precision. To illustrate, a beam-steering device developed by using these materials is presented.

Zika virus employs the host antiviral RNase L protein to support replication factory assembly.

Infection with the flavivirus Zika virus (ZIKV) can result in tissue tropism, disease outcome, and route of transmission distinct from those of other flaviviruses; therefore, we aimed to identify host machinery that exclusively promotes the ZIKV replication cycle, which can inform on differences at the organismal level. We previously reported that deletion of the host antiviral ribonuclease L (RNase L) protein decreases ZIKV production. Canonical RNase L catalytic activity typically restricts viral infection, including that of the flavivirus dengue virus (DENV), suggesting an unconventional, proviral RNase L function during ZIKV infection. In this study, we reveal that an inactive form of RNase L supports assembly of ZIKV replication factories (RFs) to enhance infectious virus production. Compared with the densely concentrated ZIKV RFs generated with RNase L present, deletion of RNase L induced broader subcellular distribution of ZIKV replication intermediate double-stranded RNA (dsRNA) and NS3 protease, two constituents of ZIKV RFs. An inactive form of RNase L was sufficient to contain ZIKV genome and dsRNA within a smaller RF area, which subsequently increased infectious ZIKV release from the cell. Inactive RNase L can interact with cytoskeleton, and flaviviruses remodel cytoskeleton to construct RFs. Thus, we used the microtubule-stabilization drug paclitaxel to demonstrate that ZIKV repurposes RNase L to facilitate the cytoskeleton rearrangements required for proper generation of RFs. During infection with flaviviruses DENV or West Nile Kunjin virus, inactive RNase L did not improve virus production, suggesting that a proviral RNase L role is not a general feature of all flavivirus infections.