a b s t r a c t SARS-CoV-2 causes the recent global COVID-19 public health emergency. ACE2 is the receptor for both SARS-CoV-2 and SARS-CoV. To predict the potential host range of SARS-CoV-2, we analyzed the key residues of ACE2 for recognizing S protein. We found that most of the selected mammals including pets (dog and cat), pangolin and Circetidae mammals remained the most of key residues for association with S protein from SARS-CoV and SARS-CoV-2. The interaction interface between cat/dog/pangolin/Chinese hamster ACE2 and SARS-CoV/SARS-CoV-2 S protein was simulated through homology modeling. We identified that N82 in ACE2 showed a closer contact with SARS-CoV-2 S protein than M82 in human ACE2. Our finding will provide important insights into the host range of SARS-CoV-2 and a new strategy to design an optimized ACE2 for SARS-CoV-2 infection.Please cite this article as: J. Luan et al., Spike protein recognition of mammalian ACE2 predicts the host range and an optimized ACE2 for SARS-CoV-2 infection, Biochemical and Biophysical Research Communications, https://doi.

Background & Aims-The generation of oxidative stress and TGF-β1 production play important roles in liver fibrogenesis. We have previously shown that HCV increases hepatocyte TGF-β1 expression. However, the mechanisms by which this induction occurs have not been well studied. We explored the possibility that HCV infection regulates TGF-β1 expression through generation of reactive oxygen species (ROS), which act through one or more of the p38 MAPK, ERK, JNK, and NFκB signaling pathways to induce TGF-β1 expression.

Proteins critical for vesicle formation by the Coat Protein I (COPI) complex are being identified, but less known has been the role of specific lipids. Brefeldin-A ADP-Ribosylated Substrate (BARS) acts in the fission step of COPI vesicle formation. Here, we show that BARS induces membrane curvature in cooperation with phosphatidic acid (PA). This revelation has allowed us to further delineate COPI vesicle fission into two sub-stages: i) an earlier stage of bud neck constriction, in which BARS and other COPI components are needed, and ii) a later stage of bud neck scission, in which PA generated by phospholipase D2 (PLD2) is needed additionally. Moreover, in contrast to the disruption of the Golgi seen upon perturbing the core COPI components (such as coatomer), inhibition of PLD2 results in milder disruptions, predicting that such COPI components have additional role(s) in maintaining Golgi structure other than through COPI vesicle formation.