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The success of angiotensin-converting enzyme 2 (ACE2)-based predictions of severe acute respiratory syndrome-associated virus 2 (SARS-CoV-2) host range stems from phylogenetic correlation, allowing development of scalable models which predict susceptibility to SARS-CoV-2 and other sarbecoviruses without requiring additional ACE2 sequencing.

Common variants of the SARS-CoV-2 Spike protein and its ligand, the human ACE2 receptor, increase the binding affinity, suggesting that they could increase viral transmissibility.

T cell receptor signal strength correlates positively with Th1 generation during acute infection but negatively during chronic infection.

Desensitization of the D2 autoreceptor is reduced following in vivo cocaine exposure due to plasticity in the D2S and not the D2L splice variant.

Rodent herpesvirus Peru overcomes NK ‘missing-self’ killing using a non-classical MHC-I like protein resistant todownregulation by its own ubiquitin ligase that potently sabotages antigen presentation to T-cells.

The reconstitution of a functional envelope protein from an extinct hominid retrovirus reveals its receptor and an ancient host defense that may have led to the extinction of the virus.

The role of C-terminal phosphorylation is critical for the expression of acute desensitization, trafficking and long-term tolerance to morphine.

The intracellular SOCS5 protein has a unique and key role in restraining influenza A infection by regulating epidermal growth factor receptor signaling in airway epithelial cells.

The loss of calcium-dependent D2 autoreceptor desensitization caused by prior in vivo cocaine exposure may be conferred by an unexpected role of the D2L splice variant as an autoreceptor.

A critical role for glycosylation on viral entry and methods to use this knowledge to reduce SARS-CoV-2 infectivity has been demonstrated.