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New evidence of brain proinflammatory cascades supports post-acute sequelae of SARS-CoV-2 infection, ultimately promoting the onset and progression of Alzheimer's disease as a function of age.

SARS-CoV-2 host-shutoff inhibits innate NK surveillance by suppressing activating ligands, however ADCC provides a potent NK stimulus that is mediated by antibodies targeting Nucleocapsid, ORF3a, and Membrane, with those targeting Spike being significantly weaker.

Multi-omic analyses reveal that the chromatin-associated microrchidia protein, MORC (PF3D7_1468100), at the blood stage of the human malaria parasite, Plasmodium falciparum, interacts with a range of nuclear proteins.

Lys417 regulates the opening and closing of SARS-CoV-2 spike protein, allowing SARS-CoV-2 to maintain a delicate balance between infectiousness and evading host immune response.

A novel, overlapping, putatively functional gene in SARS-CoV-2, ORF3d, is absent from close relatives of SARS-CoV-2 and may have contributed to the biology, emergence, or spread of the virus.

SARS-CoV-2 infection in hamsters causes cardiovascular pathologies.

SARS coronaviruses encode several mysterious proteins such as Orf3a and, in contrast to what has been claimed, Orf3a is not an ion channel but rather disrupts cellular trafficking by binding to the protein sorting complex known as HOPS.

Cell culture adaptation of SARS-CoV-2 is prevented on human airway cells with an active serine protease-mediated entry pathway, allowing the production of genetically stable virus stocks for laboratory experiments.

Cross-reactive T cell immunity against the SARS-CoV-2 is severely compromised in HIV viremic individual.

The use of within-host pathogen genomic sequence data can be used to improve phylogenetic and transmission estimates.