Stress accumulation by confined ice in a temperature gradient.

When materials freeze, they often undergo damage due to ice growth. Although this damage is commonly ascribed to the volumetric expansion of water upon freezing, it is usually driven by the flow of water toward growing ice crystals that feeds their growth. The freezing of this additional water can cause a large buildup of stress. Here, we demonstrate a technique for characterizing this stress buildup with unprecedented spatial resolution. We create a stable ice-water interface in a controlled temperature gradient and measure the deformation of the confining boundary. Analysis of the deformation field reveals stresses applied to the boundary with [Formula: see text](micrometers) spatial resolution. Globally, stresses increase steadily over time as liquid water is transported to more deeply undercooled regions. Locally, stresses increase until ice growth is stalled by the confining stresses. Importantly, we find a strong localization of stresses, which significantly increases the likelihood of damage caused by the presence of ice, even in apparently benign freezing situations. Ultimately, the limiting stress that the ice exerts is proportional to the local undercooling, in accordance with the Clapeyron equation, which describes the equilibrium between a stressed solid and its melt. Our results are closely connected to the condensation pressure during liquid-liquid phase separation and the crystallization pressure for growing crystals. Thus, they are highly relevant in fields ranging from cryopreservation and frost heave to food science, rock weathering, and art conservation.

At the crossroads of epidemiology and biology: Bridging the gap between SARS-CoV-2 viral strain properties and epidemic wave characteristics.

The COVID-19 pandemic has given rise to numerous articles from different scientific fields (epidemiology, virology, immunology, airflow physics …) without any effort to link these different insights. In this review, we aim to establish relationships between epidemiological data and the characteristics of the virus strain responsible for the epidemic wave concerned. We have carried out this study on the Wuhan, Alpha, Delta and Omicron strains allowing us to illustrate the evolution of the relationships we have highlighted according to these different viral strains. We addressed the following questions. 1) How can the mean infectious dose (one quantum, by definition in epidemiology) be measured and expressed as an amount of viral RNA molecules (in genome units, GU) or as a number of replicative viral particles (in plaque-forming units, PFU)? 2) How many infectious quanta are exhaled by an infected person per unit of time? 3) How many infectious quanta are exhaled, on average, integrated over the whole contagious period? 4) How do these quantities relate to the epidemic reproduction rate R as measured in epidemiology, and to the viral load, as measured by molecular biological methods? 5) How has the infectious dose evolved with the different strains of SARS-CoV-2? We make use of state-of-the-art modelling, reviewed and explained in the appendix of the article (Supplemental Information, SI), to answer these questions using data from the literature in both epidemiology and virology. We have considered the modification of these relationships according to the vaccination status of the population.

Risk assessment for long- and short-range airborne transmission of SARS-CoV-2, indoors and outdoors.

Preventive measures to reduce infection are needed to combat the COVID-19 pandemic and prepare for a possible endemic phase. Current prophylactic vaccines are highly effective to prevent disease but lose their ability to reduce viral transmission as viral evolution leads to increasing immune escape. Long-term proactive public health policies must therefore complement vaccination with available nonpharmaceutical interventions aiming to reduce the viral transmission risk in public spaces. Here, we revisit the quantitative assessment of airborne transmission risk, considering asymptotic limits that considerably simplify its expression. We show that the aerosol transmission risk is the product of three factors: a biological factor that depends on the viral strain, a hydrodynamical factor defined as the ratio of concentration in viral particles between inhaled and exhaled air, and a face mask filtering factor. The short-range contribution to the risk, present both indoors and outdoors, is related to the turbulent dispersion of exhaled aerosols by air drafts and by convection (indoors), or by the wind (outdoors). We show experimentally that airborne droplets and CO2 molecules present the same dispersion. As a consequence, the dilution factor, and therefore the risk, can be measured quantitatively using the CO2 concentration, regardless of the room volume, the flow rate of fresh air, and the occupancy. We show that the dispersion cone leads to a concentration in viral particles, and therefore a short-range transmission risk, inversely proportional to the squared distance to an infected person and to the flow velocity. The aerosolization criterion derived as an intermediate result, which compares the Stokes relaxation time to the Lagrangian time-scale, may find application for a broad class of aerosol-borne pathogens and pollutants.