The Right to Protest During a Pandemic: Using Public Health Ethics to Bridge the Divide Between Public Health Goals and Human Rights.

Public protest continued to represent a prominent form of social activism in democratic societies during the COVID-19 pandemic. In Australia, a lack of specific legislation articulating protest rights has meant that, in the context of pandemic restrictions, such events have been treated as illegal mass gatherings. Numerous large protests in major cities have, indeed, stirred significant public debate regarding rights of assembly during COVID-19 outbreaks. The ethics of infringing on protest rights continues to be controversial, with opinion divided as to whether public health goals or human rights should take precedence. This paper applies public health ethical theory to an in-depth analysis of arguments on both sides of the debate. Using the Nuffield Council on Bioethics framework as a backdrop, proportionality and necessity of restrictions are understood as key concepts that are common to both public health and human rights perspectives. The analysis presented here finds a middle-ground between the prevailing arguments on opposing sides and is further able to rationalize the use of protest itself as an important element of a mature public health ethics response to restrictive policy. Thus, this paper aims to influence public health policy and legislation regarding protest rights during public health emergencies.

Single-cell analysis of human glioma and immune cells identifies S100A4 as an immunotherapy target.

A major rate-limiting step in developing more effective immunotherapies for GBM is our inadequate understanding of the cellular complexity and the molecular heterogeneity of immune infiltrates in gliomas. Here, we report an integrated analysis of 201,986 human glioma, immune, and other stromal cells at the single cell level. In doing so, we discover extensive spatial and molecular heterogeneity in immune infiltrates. We identify molecular signatures for nine distinct myeloid cell subtypes, of which five are independent prognostic indicators of glioma patient survival. Furthermore, we identify S100A4 as a regulator of immune suppressive T and myeloid cells in GBM and demonstrate that deleting S100a4 in non-cancer cells is sufficient to reprogram the immune landscape and significantly improve survival. This study provides insights into spatial, molecular, and functional heterogeneity of glioma and glioma-associated immune cells and demonstrates the utility of this dataset for discovering therapeutic targets for this poorly immunogenic cancer.