Highlights d SARS-CoV-2 spike protein interacts with heparan sulfate and ACE2 through the RBD d Heparan sulfate promotes Spike-ACE2 interaction d SARS-CoV-2 infection is co-dependent on heparan sulfate and ACE2 d Heparin and non-anticoagulant derivatives block SARS-CoV-2 binding and infection

We present a comprehensive study of the evolution of the nematic electronic structure of FeSe using high resolution angle-resolved photoemission spectroscopy (ARPES), quantum oscillations in the normal state and elastoresistance measurements. Our high resolution ARPES allows us to track the Fermi surface deformation from four-fold to two-fold symmetry across the structural transition at ~87 K which is stabilized as a result of the dramatic splitting of bands associated with dxz and dyz character. The low temperature Fermi surface is that a compensated metal consisting of one hole and two electron bands and is fully determined by combining the knowledge from ARPES and quantum oscillations. A manifestation of the nematic state is the significant increase in the nematic susceptibility as approaching the structural transition that we detect from our elastoresistance measurements on FeSe. The dramatic changes in electronic structure cannot be explained by the small lattice effects and, in the absence of magnetic fluctuations above the structural transition, points clearly towards an electronically driven transition in FeSe stabilized by orbital-charge ordering.Comment: Latex, 8 pages, 4 figure

Cd3As2 is a candidate three-dimensional Dirac semi-metal which has exceedingly high mobility and nonsaturating linear magnetoresistance that may be relevant for future practical applications. We report magnetotransport and tunnel diode oscillation measurements on Cd3As2, in magnetic fields up to 65 T and temperatures between 1.5 K to 300 K. We find the non-saturating linear magnetoresistance persist up to 65 T and it is likely caused by disorder effects as it scales with the high mobility, rather than directly linked to Fermi surface changes even when approaching the quantum limit. From the observed quantum oscillations, we determine the bulk three-dimensional Fermi surface having signatures of Dirac behaviour with non-trivial Berry's phase shift, very light effective quasiparticle masses and clear deviations from the band-structure predictions. In very high fields we also detect signatures of large Zeeman spin-splitting (g ∼ 16).

We show that SARS-CoV-2 spike protein interacts with cell surface heparan sulfate and angiotensin converting enzyme 2 (ACE2) through its Receptor Binding Domain. Docking studies suggest a putative heparin/heparan sulfate-binding site adjacent to the domain that binds to ACE2. In vitro, binding of ACE2 and heparin to spike protein ectodomains occurs independently and a ternary complex can be generated using heparin as a template. Contrary to studies with purified components, spike protein binding to heparan sulfate and ACE2 on cells occurs codependently. Unfractionated heparin, non-anticoagulant heparin, treatment with heparin lyases, and purified lung heparan sulfate potently block spike protein binding and infection by spike protein-pseudotyped virus and SARS-CoV-2 virus. These findings support a model for SARS-CoV-2 infection in which viral attachment and infection involves formation of a complex between heparan sulfate and ACE2. Manipulation of heparan sulfate or inhibition of viral adhesion by exogenous heparin may represent new therapeutic opportunities.

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