Development of an Algorithm for Calculating the Moisture Content and Time of Forest Fire Maturation of Forest Combustible Materials for Determining Forest Fire Hazards

Nowadays, forests play an important role in stabilizing the ecological balance, being one of the most important components of the biosphere. Due to the vital activity of forests, the gas composition of the atmosphere is normalized. Mass forest fires have the opposite effect. They cause irreparable damage to flora and fauna, contribute to the melting of Arctic ice, an increase in the Earth’s temperature, and destabilization of the carbon balance. The purpose of this study is to develop an algorithm for calculating the moisture content and time of forest fire maturation of forest combustible materials. To achieve this goal, the main factors determining a forest fire hazard have been studied, as well as a review of existing methods for assessing forest fire danger and scientific papers on forest pyrology. As a result of the analysis of the research aimed at studying the rate of drying of forest combustible materials (FCM), depending on the physical properties and environmental parameters, a dependency of changes in moisture content over time was obtained. With its help, knowing the initial moisture content of FCM, it is possible to calculate the periods of fire maturation for each component of the forest plantation. Cooperative use of the resulting algorithm with a digital twin of a forest stand makes it possible to identify the most fire-hazard forest areas and estimate the period of their fire-prone maturation

Coxsackievirus A7 and Enterovirus A71 Significantly Reduce SARS-CoV-2 Infection in Cell and Animal Models

In this study, we investigated the features of co-infection with SARS-CoV-2 and the enterovirus vaccine strain LEV8 of coxsackievirus A7 or enterovirus A71 for Vero E6 cells and Syrian hamsters. The investigation of co-infection with SARS-CoV-2 and LEV-8 or EV-A71 in the cell model showed that a competitive inhibitory effect for these viruses was especially significant against SARS-CoV-2. Pre-infection with enteroviruses in the animals caused more than a 100-fold decrease in the levels of SARS-CoV-2 virus replication in the respiratory tract and more rapid clearance of infectious SARS-CoV-2 from the lower respiratory tract. Co-infection with SARS-CoV-2 and LEV-8 or EV-A71 also reduced the severity of clinical manifestations of the SARS-CoV-2 infection in the animals. Additionally, the histological data illustrated that co-infection with strain LEV8 of coxsackievirus A7 decreased the level of pathological changes induced by SARS-CoV-2 in the lungs. Research into the chemokine/cytokine profile demonstrated that the studied enteroviruses efficiently triggered this part of the antiviral immune response, which is associated with the significant inhibition of SARS-CoV-2 infection. These results demonstrate that there is significant viral interference between the studied strain LEV-8 of coxsackievirus A7 or enterovirus A71 and SARS-CoV-2 in vitro and in vivo

Human Adenovirus and Influenza A Virus Exacerbate SARS-CoV-2 Infection in Animal Models

In this study, we investigated the features of the infectious process by simulating co-infection with SARS-CoV-2 and human adenovirus type 5 (HAdV-5) or influenza A virus (IAV) in vitro and in vivo. The determination of infectious activity of viruses and digital PCR demonstrated that during simultaneous and sequential HAdV-5 followed by SARS-CoV-2 infection in vitro and in vivo, the HAdV-5 infection does not interfere with replication of SARS-CoV-2. The hamsters co-infected and mono-infected with SARS-CoV-2 exhibited nearly identical viral titers and viral loads of SARS-CoV-2 in the lungs. The hamsters and ferrets co-infected by SARS-CoV-2- and IAV demonstrated more pronounced clinical manifestations than mono-infected animals. Additionally, the lung histological data illustrate that HAdV-5 or IAV and SARS-CoV-2 co-infection induces more severe pathological changes in the lungs than mono-infection. The expression of several genes specific to interferon and cytokine signaling pathways in the lungs of co-infected hamsters was more upregulated compared to single infected with SARS-CoV-2 animals. Thus, co-infection with HAdV-5 or IAV and SARS-CoV-2 leads to more severe pulmonary disease in animals