Ultraviolet-A light increases mitochondrial anti-viral signaling protein in confluent human tracheal cells via cell-cell signaling.

Mitochondrial antiviral signaling (MAVS) protein mediates innate antiviral responses, including responses to certain coronaviruses such as severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2). We have previously shown that ultraviolet-A (UVA) therapy can prevent virus-induced cell death in human ciliated tracheal epithelial cells (HTEpC) infected with coronavirus-229E (CoV-229E), and results in increased intracellular levels of MAVS. In this study, we explored the mechanisms by which UVA light can activate MAVS, and whether local UVA light application can activate MAVS at locations distant from the light source (e.g. via cell-to-cell communication). MAVS levels were compared in HTEpC exposed to 2 mW/cm2 narrow band (NB)-UVA for 20 min and in unexposed controls at 30-40% and at 100% confluency, and in unexposed HTEpC treated with supernatants or lysates from UVA-exposed cells or from unexposed controls. MAVS was also assessed in different sections of confluent monolayer plates where only one section was exposed to NB-UVA. Our results showed that UVA increases the expression of MAVS protein. Further, cells in a confluent monolayer exposed to UVA conferred an elevation in MAVS in cells adjacent to the exposed section, and also in cells in the most distant sections which were not exposed to UVA. In this study, human ciliated tracheal epithelial cells exposed to UVA demonstrate increased MAVS protein, and also appear to transmit this influence to confluent cells not exposed to UVA, likely via cell-cell signaling.

Percolation clusters of organics in interstellar ice grains as the incubators of life.

Biomolecules can be synthesized in interstellar ice grains subject to UV radiation and cosmic rays. I show that on time scales of ≳106 years, these processes lead to the formation of large percolation clusters of organic molecules. Some of these clusters would have ended up on proto-planets where large, loosely bound aggregates of clusters (superclusters) would have formed. The interior regions of such superclusters provided for chemical micro-environments that are filtered versions of the outside environment. I argue that models for abiogenesis are more likely to work when considered inside such micro-environments. As the supercluster breaks up, biochemical systems in such micro-environments gradually become subject to a less filtered environment, allowing them to get adapted to the more complex outside environment. A particular system originating from a particular location on some supercluster would have been the first to get adapted to the raw outside environment and survive there, thereby becoming the first microbe. A collision of a microbe-containing proto-planet with the Moon could have led to fragments veering off back into space, microbes in small fragments would have been able to survive a subsequent impact with the Earth.