SARS-CoV-2 articles from across Nature Portfolio

Understanding the induced and cross reactive immunity to sarbecoviruses is an important step in rationale and widely applicable vaccine design. Here the authors use a multivalent S2 subunit vaccine and demonstrate protection in female mice against SARS-CoV-2-like and SARS-CoV-1-like coronaviruses.

Identifying mutations in pathogen genomes that confer transmission advantages could improve understanding of viral biology and flag variants for further study. Here, the authors develop a model for identifying mutations that affect transmission rates, validate it in simulations, then apply it to SARS-CoV-2 genomic surveillance data.

Systematic comparison of SARS-CoV-2 spike proteins from pre- and post-Omicron variants in cell lines, primary respiratory epithelial cells and Syrian hamsters show distinct phenotypic trajectories in replication kinetics, cell tropism, cell-to-cell fusion, spike processing, cell entry routes and virulence.

This work reveals how the SARS-CoV-2 spike protein’s membrane-binding domain facilitates viral entry by bridging the viral and host cell membranes. It highlights the role of a specific peptide and cholesterol-rich membranes in enhancing infectivity.

Liu et al. developed a framework called ARNLE to explore host tropism of SARS-CoV-2 and found a shift from weak to strong primate tropism. Key mutations involved in this shift can be analysed to advance research on emerging viruses.

Paper on hydroxychloroquine led by French researcher Didier Raoult is second-most-cited study ever to be withdrawn.

Could human–AI collaborations be the future of interdisciplinary studies?

Confidence that researchers will make decisions in the public interest rose slightly from 2023 to 2024.

A hallmark of post-viral lung disease, including post-acute sequelae of COVID-19, is dysplastic lung repair. CD8⁺ T cells contribute to aberrant repair through induction by IFNγ and TNF of IL-1β in macrophages, halting differentiation of alveolar type 2 cells.

Children under the age of five infected with SARS-CoV-2 produce lower levels of some immune cells than older children and adults do.

The finding comes from a reanalysis of genomic data.