Current and future chemical treatments to fight biodeterioration of outdoor building materials and associated biofilms: Moving away from ecotoxic and towards efficient, sustainable solutions.

All types of building materials are rapidly colonized by microorganisms, initially through an invisible and then later a visible biofilm that leads to their biodeterioration. Over centuries, this natural phenomenon has been managed using mechanical procedures, oils, or even wax. In modern history, many treatments such as high-pressure cleaners, biocides (mainly isothiazolinones and quaternary ammonium compounds) are commercially available, as well as preventive ones, such as the use of water-repellent coatings in the fabrication process. While all these cleaning techniques offer excellent cost-benefit ratios, their limitations are numerous. Indeed, building materials are often quickly recolonized after application, and microorganisms are increasingly reported as resistant to chemical treatments. Furthermore, many antifouling compounds are ecotoxic, harmful to human health and the environment, and new regulations tend to limit their use and constrain their commercialization. The current state-of-the-art highlights an urgent need to develop innovative antifouling strategies and the widespread use of safe and eco-friendly solutions to biodeterioration. Interestingly, innovative approaches and compounds have recently been identified, including the use of photocatalysts or natural compounds such as essential oils or quorum sensing inhibitors. Most of these solutions developed in laboratory settings appear very promising, although their efficiency and ecotoxicological features remain to be further tested before being widely marketed. This review highlights the complexity of choosing the adequate antifouling compounds when fighting biodeterioration and proposes developing case-to-case innovative strategies to raise this challenge, relying on integrative and multidisciplinary approaches.

Methyl Potassium Siliconate and Siloxane Inhibit the Formation of Multispecies Biofilms on Ceramic Roof Tiles: Efficiency and Comparison of Two Common Water Repellents.

Ceramic roof tiles are widespread marketed building materials, rapidly colonized by microorganisms that form multispecies biofilms on their surface and play crucial roles in biodeterioration processes. Coating tiles with water repellents is a pervasive industrial strategy employed to prevent liquid water penetration and slow biodeterioration. Very few studies have examined the links between the characteristics of water-repellent coatings and biofilm colonization patterns. Our work aims to compare the effects of coating tiles with two common water repellents (siliconate and siloxane) on the growth of colonizing microbes. We combined in situ exposure of tiles for over six years and macroscopic and microscopic observations with in vitro biotests, relying on the use of algal and fungal models. Our data showed that (1) tiles coated with water repellents were macroscopically less colonized by lichens (2) a significant fungal biofilm development at the microscopic scale (3) water repellents had very contrasting effects on our model strains. These data reinforce the great interest for industry to conduct more studies linking the nature of the water repellents with the composition of colonizing multispecies biofilms. The long-term objective is to improve the available water repellents and better adapt their selection to the nature of microbial colonization.

The NSs Protein Encoded by the Virulent Strain of Rift Valley Fever Virus Targets the Expression of Abl2 and the Actin Cytoskeleton of the Host, Affecting Cell Mobility, Cell Shape, and Cell-Cell Adhesion.

Rift Valley fever virus (RVFV) is a highly pathogenic zoonotic arbovirus endemic in many African countries and the Arabian Peninsula. Animal infections cause high rates of mortality and abortion among sheep, goats, and cattle. In humans, an estimated 1 to 2% of RVFV infections result in severe disease (encephalitis, hepatitis, or retinitis) with a high rate of lethality when associated with hemorrhagic fever. The RVFV NSs protein, which is the main virulence factor, counteracts the host innate antiviral response to favor viral replication and spread. However, the mechanisms underlying RVFV-induced cytopathic effects and the role of NSs in these alterations remain for the most part unknown. In this work, we have analyzed the effects of NSs expression on the actin cytoskeleton while conducting infections with the NSs-expressing virulent (ZH548) and attenuated (MP12) strains of RVFV and the non-NSs-expressing avirulent (ZH548ΔNSs) strain, as well as after the ectopic expression of NSs. In macrophages, fibroblasts, and hepatocytes, NSs expression prevented the upregulation of Abl2 (a major regulator of the actin cytoskeleton) expression otherwise induced by avirulent infections and identified here as part of the antiviral response. The presence of NSs was also linked to an increased mobility of ZH548-infected cells compared to ZH548ΔNSs-infected fibroblasts and to strong changes in cell morphology in nonmigrating hepatocytes, with reduction of lamellipodia, cell spreading, and dissolution of adherens junctions reminiscent of the ZH548-induced cytopathic effects observed in vivo Finally, we show evidence of the presence of NSs within long actin-rich structures associated with NSs dissemination from NSs-expressing toward non-NSs-expressing cells.IMPORTANCE Rift Valley fever virus (RVFV) is a dangerous human and animal pathogen that was ranked by the World Health Organization in 2018 as among the eight pathogens of most concern for being likely to cause wide epidemics in the near future and for which there are no, or insufficient, countermeasures. The focus of this work is to address the question of the mechanisms underlying RVFV-induced cytopathic effects that participate in RVFV pathogenicity. We demonstrate here that RVFV targets cell adhesion and the actin cytoskeleton at the transcriptional and cellular level, affecting cell mobility and inducing cell shape collapse, along with distortion of cell-cell adhesion. All these effects may participate in RVFV-induced pathogenicity, facilitate virulent RVFV dissemination, and thus constitute interesting potential targets for future development of antiviral therapeutic strategies that, in the case of RVFV, as with several other emerging arboviruses, are presently lacking.