#preprint

Abstract Despite safety concerns regarding the toxicity of tattoo ink, no studies have reported the consequences of tattooing on the immune response. In this work, we have characterized the transport and accumulation of different tattoo inks in the lymphatic system using a murine model. Upon quick lymphatic drainage, we observed that macrophages mainly capture the ink in the lymph node (LN). An initial inflammatory reaction at local and systemic levels follows ink capture. Notably, the inflammatory process is maintained over time as we observed clear signs of inflammation in the draining LN two months following tattooing. In addition, the capture of ink by macrophages was associated with the induction of apoptosis in both human and murine models. Furthermore, the ink accumulated in the LN altered the immune response against a COVID-19 vaccine. We observed a reduced antibody response following vaccination with a mRNA-based SARS-CoV-2 vaccine, which was associated with a decreased expression of the Spike protein in macrophages in the draining LN. Considering the unstoppable trend of tattooing in the population, our results are crucial in informing the toxicology programs, policymakers, and the general public regarding the potential risk of the tattooing practice associated with an altered immune response.

Abstract Understanding the transmission dynamics of SARS-CoV-2, particularly its transfer from contaminated surfaces (fomites) to human skin, is crucial for mitigating the spread of COVID-19. While extensive research has examined the persistence of SARS-CoV-2 on various surfaces, there is limited understanding of how efficiently it transfers to human skin, and how long it survives on the skin. This study investigates two key aspects of SARS-CoV-2 transmission: (1) the transfer efficiency of SARS-CoV-2 from non-porous (plastic and metal) and porous (cardboard) surfaces to a 3D human skin model (LabSkin), and (2) the survival of SARS-CoV-2 on the skin under different temperature conditions. First, we validated LabSkin as a suitable surrogate for human skin by comparing the transfer efficiency of the bacteriophage Phi 6 from surfaces to LabSkin and to human volunteers fingers. No significant differences were observed, confirming LabSkin's suitability for these studies. Subsequently, the transfer of SARS-CoV-2 from surfaces to LabSkin was assessed, showing that plastic and metal surfaces had similar transfer efficiencies (~13%), while no transfer occurred from cardboard once the inoculum had dried on the surface. Finally, the survival of SARS-CoV-2 on skin was assessed, showing a rapid decay at higher temperatures, with a half-life ranging from 2.8 to 17.8 hours depending on the temperature. These findings enhance our understanding of viral transmission via fomites and inform public health strategies to reduce the risk of SARS-CoV-2 transmission through surface contact.

Post-acute sequelae of COVID (PASC) persist in many patients for weeks and months after recovery from initial SARS-CoV-2 infection. Recent evidence suggests that pathological changes in skeletal muscle may contribute significantly to ongoing pain and fatigue, particularly post-exertional malaise. This study aimed to investigate the underlying mechanisms of PASC-related fatigue by examining skeletal muscle function and circulating factors in affected individuals. We conducted a cross-sectional case-control study of patients with fatigue-associated PASC who had experienced mild to moderate COVID-19 without hospitalization. Skeletal muscle biopsies revealed reduced mitochondrial respiration and content in PASC participants compared to healthy controls. This lower respiratory capacity was accompanied by markedly elevated circulating levels of soluble IL-2 receptor alpha subunit (sIL2R), a T cell-specific receptor. In vitro experiments demonstrated that sIL2R directly impairs mitochondrial oxygen consumption and reduces mitochondrial complex III subunit protein levels in cultured muscle cells. These findings suggest a mechanism linking systemic immune dysregulation to muscle-specific mitochondrial dysfunction in PASC. This work provides new insights into the pathophysiology of PASC identifying sIL2R as a promising therapeutic target for addressing mitochondrial deficits in PASC-related fatigue and opening avenues for developing targeted interventions.