SARS-CoV-2 mutations affect antigen processing by the proteasome to alter CD8 T cell responses.

Mutations within viral epitopes can result in escape from T cells, but the contribution of mutations in flanking regions of epitopes in SARS-CoV-2 has not been investigated. Focusing on two SARS-CoV-2 nucleoprotein CD8 epitopes, we investigated the contribution of these flanking mutations to proteasomal processing and T cell activation. We found decreased NP-B*27:05 CD8 T cell responses to the NP-Q7K mutation, likely due to a lack of efficient epitope production by the proteasome, suggesting immune escape caused by this mutation.

Evaluation of T cell responses to naturally processed variant SARS-CoV-2 spike antigens in individuals following infection or vaccination.

Most existing studies characterizing severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)-specific T cell responses are peptide based. This does not allow evaluation of whether tested peptides are processed and presented canonically. In this study, we use recombinant vaccinia virus (rVACV)-mediated expression of SARS-CoV-2 spike protein and SARS-CoV-2 infection of angiotensin-converting enzyme (ACE)-2-transduced B cell lines to evaluate overall T cell responses in a small cohort of recovered COVID-19 patients and uninfected donors vaccinated with ChAdOx1 nCoV-19.

T cells are ready for the fight against monkeypox.

In this issue of Cell Host & Microbe, Grifoni et al. provide reassuring evidence that the majority of epitopes induced by vaccinia virus vaccines are conserved in monkeypox virus and can elicit memory T cell responses, while also providing an extensive list of potential T cell epitopes.

Improving the quality of family meeting documentation in the ICU at the end of life.

Objective: Improve documentation quality of end-of-life family meetings in a tertiary intensive care unit (ICU).

Design: Before-and-after interventional quality improvement project between October 2018 and February 2020 utilising an electronic pro-forma record.

Setting: Australian, University affiliated, mixed medical-surgical 22 bed adult ICU.

IFITM3 restricts virus-induced inflammatory cytokine production by limiting Nogo-B mediated TLR responses.

Interferon-induced transmembrane protein 3 (IFITM3) is a restriction factor that limits viral pathogenesis and exerts poorly understood immunoregulatory functions. Here, using human and mouse models, we demonstrate that IFITM3 promotes MyD88-dependent, TLR-mediated IL-6 production following exposure to cytomegalovirus (CMV). IFITM3 also restricts IL-6 production in response to influenza and SARS-CoV-2.