Evolving understanding of antibody-dependent enhancement (ADE) of SARS-CoV-2.

Since immune system and internal environment in vivo are large and complex, the interpretation of the observed immune effect from the perspective of a single immune cell or antibody seems a little feeble. Many studies have shown that specific antibodies against " former" viruses have a reduced ability to neutralize "new" mutant strains. However, there is no comprehensive and clear view of whether there will be Antibody-dependent enhancement (ADE). We review the latest relevant studies, hoping to explain the ADE of SARS-CoV-2 infection sometimes observed in some patients.

The mammalian endocytic cytoskeleton.

Clathrin-mediated endocytosis (CME) is the major route through which cells internalise various substances and recycle membrane components. Via the coordinated action of many proteins, the membrane bends and invaginates to form a vesicle that buds off-along with its contents-into the cell. The contribution of the actin cytoskeleton to this highly dynamic process in mammalian cells is not well understood. Unlike in yeast, where there is a strict requirement for actin in CME, the significance of the actin cytoskeleton to mammalian CME is variable. However, a growing number of studies have established the actin cytoskeleton as a core component of mammalian CME, and our understanding of its contribution has been increasing at a rapid pace. In this review, we summarise the state-of-the-art regarding our understanding of the endocytic cytoskeleton, its physiological significance, and the questions that remain to be answered.