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La pandemia evidenció el bajo nivel de calidad en el que se encontraba el sistema educativo en el Perú y los efectos en salud mental y física, relacionados al estrés en los docentes dentro del contexto de la educación virtual superior. El objetivo de esta investigación fue analizar los principales aportes teóricos del estrés laboral en docentes en el contexto de pandemia. Para el análisis se usó el método cualitativo y diseño tipo documental, recolectando y revisando fuentes científicas relacionadas al tema dentro del periodo que duró el confinamiento. Esto permitió entender que los principales aportes teóricos estaban relacionados al estrés laboral dentro de la educación a distancia, a los factores internos y externos que promueven el estrés, al síndrome de burnout y al tecnoestrés, factores para los que los docentes no estaban preparados. Frente a esta situación, se sumó, la falta de conectividad y el implemento de equipos digitales de última generación. Se pudo concluir entonces la importancia del bienestar integral del docente y el equilibrio de los factores internos y externos determinantes del estrés, para asegurar su adecuado desempeño laboral dentro del contexto de la virtualidad que llevó la pandemia.

High traffic volume is one of the main contributors to wildlife-vehicle collision (WVC) and wildlife mortality on roads. Government shelter-in-place (SIP) orders have been used to help mitigate the spread of COVID-19, resulting in unprecedented reductions in global traffic volumes. Using traffic and collision data from four US states (California, Idaho, Maine, and Washington), we investigated changes in total WVC, following the state and local SIP orders. From mid-March to mid-April 2020, these orders have resulted in up to 71%, 63%, 73%, and 72% reduction in driving, as measured by vehicle miles traveled (VMT), in CA, ID, ME, and WA respectively. The daily WVC rates from the 4 weeks prior to SIP orders going into effect, to the 4 weeks after, declined 34%, with 21, 36, 44, and 33% declines for CA, ID, ME, and WA, respectively. For mountain lions (Puma concolor) in CA, there was a 58% decline in mortality during the traffic reduction. The changes in WVC from 1 month pre-SIP orders to 1 month post-order only occurred in 2020 and not 2015, 2016, 2017, 2018, or 2019, suggesting that the reductions were associated with the reductions in traffic. The measured declines in WVC reversed in ME and WA during May, June and July 2020, paralleling reversals in traffic volumes. A 34% reduction in WVC would potentially equate to 10s of millions fewer vertebrates killed on US roadways during one month of traffic reduction, representing an unintentional conservation action unprecedented in modern times.

Dual purpose systems that treat wastewater and produce lipid rich microalgae biomass have been indicated as an option with great potential for production of biodiesel at a competitive cost. The aim of the present work was to develop a dual purpose system for the treatment of the anaerobic effluents from pig waste utilizing Neochloris oleoabundans and to evaluate its growth, lipid content and lipid profile of the harvested biomass and the removal of nutrients from the media. Cultures of N. oleoabundans were established in 4 L flat plate photobioreactors using diluted effluents from two different types of anaerobic filters, one packed with ceramic material (D1) and another one packed with volcanic gravel (D2). Maximum biomass concentration in D1 was 0.63 g L(-1) which was significantly higher than the one found in D2 (0.55 g L(-1)). Cultures were very efficient at nutrient removal: 98% for NNH4(+) and 98% for PO4(3-). Regarding total lipid content, diluted eflluents from D2 promoted a biomass containing 27.4% (dry weight) and D1 a biomass containing 22.4% (dry weight). Maximum lipid productivity was also higher in D2 compared to D1 (6.27±0.62 mg L(-1) d(-1) vs. 5.12±0.12 mg L(-1) d(-1)). Concerning the FAMEs profile in diluted effluents, the most abundant one was C18:1, followed by C18:2 and C16:0. The profile in D2 contained less C18:3 (linolenic acid) than the one in D1 (4.37% vs. 5.55%). In conclusion, this is the first report demonstrating that cultures of N. oleoabundans treating anaerobic effluents from pig waste are very efficient at nutrient removal and a biomass rich in lipids can be recovered. The maximum total lipid content and the most convenient FAMEs profile were obtained using effluents from a digester packed with volcanic gravel.

The antioxidant effects of tocols (α-tocopherol and α-tocotrienol) and Rosa mosqueta shell extract added to antioxidant-stripped canola oil (TCO) were evaluated and compared with the non-stripped oil (CO) under the same conditions. Seven oil systems were subjected to thermal treatment at 180 °C for 18 h. Polar compounds formation, degradation of tocols and carotenoid pigments were studied. The addition of Rosa mosqueta shell extract gave a great stability to TCO, similar to CO, with a low polar compound formation and a high retention of α-tocopherol compared with other TCO samples, which suggested the protective action of the minor components present in the extract. Alpha-tocopherol showed a higher effectiveness than α-tocotrienol at high temperature. However, an increase in the level of α-tocopherol did not improve its action.

Human respiratory syncytial virus (RSV) is a major cause of severe respiratory illness in children and susceptible adults. RSV blocks the development of the innate antiviral immune response and can grow to high titers in the respiratory tract. Here we demonstrate that immunostimulatory defective viral genomes (iDVGs) that are naturally generated during RSV replication are strong inducers of the innate antiviral response to RSV in mice and humans. In mice, RSV iDVGs stimulated the expression of antiviral genes, restricted viral replication, and prevented weight loss and lung inflammation. In human cells, the antiviral response to RSV iDVGs was dominated by the expression of IFN-λ1 over IFN-β and was driven by rapid intranuclear accumulation of the transcription factor IRF1. RSV iDVGs were detected in respiratory secretions of hospitalized patients, and their amount positively correlated with the level of expression of antiviral genes in the samples. Infection of explanted human lung tissue from different donors revealed that most humans can respond to RSV iDVGs and that the rate of accumulation of iDVGs during infection directly correlates with the quality of the antiviral response. Taken together, our data establish iDVGs as primary triggers of robust antiviral responses to RSV and provide the first evidence for an important biological role for naturally occurring iDVGs during a paramyxovirus infection in humans., Author Summary Respiratory syncytial virus is a major cause of chronic lung damage, asthma exacerbations, and hospitalizations of infants, elders, and high-risk adults. Currently, there is no effective vaccine or treatment available to protect the general population from RSV infection. Here, we demonstrate that defective forms of RSV genomes naturally generated during infection effectively stimulate the antiviral response in vitro and in vivo. In human cells, RSV iDVGs trigger the antiviral response through a mechanism characterized by the potent activation of the transcription factor IRF1 and a dominant expression of the type III IFN gene IFNL1 (IFN-λ1). This study establishes for the first time that naturally occurring iDVGs trigger robust host antiviral responses to RSV in mice and humans and reveals new opportunities to potentiate the host response to RSV infection and minimize viral-induced pathology.

To construct informed conservation plans, researchers must go beyond understanding readily apparent threats such as habitat loss and bush-meat hunting. They must predict subtle and cascading effects of anthropogenic environmental modifications. This study considered a potential cascading effect of deforestation on the howler monkeys (Alouatta pigra) of Balancan, Mexico. Deforestation intensifies flooding. Thus, we predicted that increased flooding of the Usumacinta River, which creates large bodies of water that slowly evaporate, would produce increased lead content in the soils and plants, resulting in lead exposure in the howler monkeys. The average lead levels were 18.18 ± 6.76 ppm in the soils and 5.85 ± 4.37 ppm in the plants. However, the average lead content of the hair of 13 captured howler monkeys was 24.12 ± 5.84 ppm. The lead levels in the animals were correlated with 2 of 15 blood traits (lactate dehydrogenase and total bilirubin) previously documented to be associated with exposure to lead. Our research illustrates the urgent need to set reference values indicating when adverse impacts of high environmental lead levels occur, whether anthropogenic or natural, and the need to evaluate possible cascading effects of deforestation on primates.

Although tree ferns are an important component of temperate and tropical forests, very little is known about their ecology. Their peculiar biology (e.g., dispersal by spores and two-phase life cycle) makes it difficult to extrapolate current knowledge on the ecology of other tree species to tree ferns. In this paper, we studied the effects of negative density dependence (NDD) and environmental heterogeneity on populations of two abundant tree fern species, Cyathea caracasana and Alsophila engelii, and how these effects change across a successional gradient. Species patterns harbor information on processes such as competition that can be easily revealed using point pattern analysis techniques. However, its detection may be difficult due to the confounded effects of habitat heterogeneity. Here, we mapped three forest plots along a successional gradient in the montane forests of Southern Ecuador. We employed homogeneous and inhomogeneous K and pair correlation functions to quantify the change in the spatial pattern of different size classes and a case-control design to study associations between juvenile and adult tree ferns. Using spatial estimates of the biomass of four functional tree types (short- and long-lived pioneer, shade- and partial shade-tolerant) as covariates, we fitted heterogeneous Poisson models to the point pattern of juvenile and adult tree ferns and explored the existence of habitat dependencies on these patterns. Our study revealed NDD effects for C. caracasana and strong environmental filtering underlying the pattern of A. engelii. We found that adult and juvenile populations of both species responded differently to habitat heterogeneity and in most cases this heterogeneity was associated with the spatial distribution of biomass of the four functional tree types. These findings show the effectiveness of factoring out environmental heterogeneity to avoid confounding factors when studying NDD and demonstrate the usefulness of covariate maps derived from mapped communities.

The innate immune response to viruses is initiated when specialized cellular sensors recognize viral danger signals. Here we show that truncated forms of viral genomes that accumulate in infected cells potently trigger the sustained activation of the transcription factors IRF3 and NF-κB and the production type I IFNs through a mechanism independent of IFN signaling. We demonstrate that these defective viral genomes (DVGs) are generated naturally during respiratory infections in vivo even in mice lacking the type I IFN receptor, and their appearance coincides with the production of cytokines during infections with Sendai virus (SeV) or influenza virus. Remarkably, the hallmark antiviral cytokine IFNβ is only expressed in lung epithelial cells containing DVGs, while cells within the lung that contain standard viral genomes alone do not express this cytokine. Together, our data indicate that DVGs generated during viral replication are a primary source of danger signals for the initiation of the host immune response to infection., Author Summary In infections with viruses well adapted to the host virus-encoded proteins that delay the cellular response allow the virus to replicate to high titers prior to host intervention. The mechanisms overcoming viral evasion of the immune system and leading to the production of the primary antiviral cytokine IFNβ are not well established. Here, we demonstrate that truncated forms of viral genomes that are generated in situ during virus replication are a primary source of danger signals for the initiation of the host immune response to respiratory viral infections in vivo. Defective viral genomes (DVGs) are able to function as triggers of the immune response even in the absence of type I IFN signaling and are strong triggers of the host response to infection while overcoming viral antagonism.

Defective viral genomes (DVGs) are generated during virus replication. DVGs bearing complementary ends are strong inducers of dendritic cell (DC) maturation and of the expression of antiviral and pro-inflammatory cytokines by triggering signaling of the RIG-I family of intracellular pattern recognition receptors. Our data show that DCs stimulated with virus containing DVGs have an enhanced ability to activate human T cells and can induce adaptive immunity in mice. In addition, we describe the generation of a short Sendai virus (SeV)-derived DVG RNA (DVG-324) that maintains strong immunostimulatory activity in vitro and in vivo. DVG-324 induced high levels of IFN-β expression when transfected into cells and triggered fast expression of pro-inflammatory cytokines and mobilization of dendritic cells when injected into the footpad of mice. Importantly, DVG-324 enhanced the production of antibodies to a prototypic vaccine after a single intramuscular immunization in mice. Notably, the proinflammatory cytokine profile induced by DVG-324 was different from that induced by poly I:C, the only viral RNA analogue currently used as an immunostimulant in vivo, suggesting a distinct mechanism of action. SeV-derived oligonucleotides represent novel alternatives to be harnessed as potent adjuvants for vaccination.

In this study, we demonstrate the identification of an internal ribosome entry site (IRES) within the 5'-untranslated region (5'-UTR) of the mouse mammary tumor virus (MMTV). The 5'-UTR of the full-length mRNA derived from the infectious, complete MMTV genome was cloned into a dual luciferase reporter construct containing an upstream Renilla luciferase gene (RLuc) and a downstream firefly luciferase gene (FLuc). In rabbit reticulocyte lysate, the MMTV 5'-UTR was capable of driving translation of the second cistron. In vitro translational activity from the MMTV 5'-UTR was resistant to the addition of m(7)GpppG cap-analog and cleavage of eIF4G by foot-and-mouth disease virus (FMDV) L-protease. IRES activity was also demonstrated in the Xenopus laevis oocyte by micro-injection of capped and polyadenylated bicistronic RNAs harboring the MMTV-5'-UTR. Finally, transfection assays showed that the MMTV-IRES exhibits cell type-dependent translational activity, suggesting a requirement for as yet unidentified cellular factors for its optimal function.

In infections with viruses well adapted to the host, virus-encoded proteins that delay the cellular response allow the virus to replicate to high titers prior to host intervention. The mechanisms overcoming viral evasion and leading to the production of the primary antiviral cytokine IFNbeta are not well established. We show that the appearance of defective forms of the viral genome may provide the answer. Defective viral genomes, which were until recently considered an epiphenomenon of in vitro virus replication, accumulate in infected cells at a faster rate than standard viral genomes and potently trigger the sustained activation of the transcription factors IRF3 and NF-kB and the production type I IFNs through a mechanism independent of IFN signaling. Remarkably, our work demonstrates that defective viral genomes are generated naturally during respiratory infections in vivo even in mice lacking the type I IFN receptor, and their appearance coincides with the production of cytokines during infections with Sendai virus or influenza virus. Notably, the hallmark antiviral cytokine IFNβ is only expressed in lung epithelial cells containing defective viral genomes, while cells within the lung that contain standard viral genomes alone do not express this cytokine. Together, our data indicate that defective viral genomes generated naturally during viral replication are a primary source of danger signals for the initiation of the host immune response to infection in vivo.

Viral recognition by specialized cellular sensors is critical for the innate immune response to virus infection. Detection of viral components by these sensors triggers the production of type I interferon (IFN), the earliest hallmark of viral infection, which plays an essential role in inducing an antiviral state in both infected and non-infected cells. Highly pathogenic respiratory viruses replicate in the lungs to high titers before a detectable anti-viral response begins, indicating that the viruses have devised effective mechanisms to avoid the innate anti-viral response. We have shown that dendritic cells can be potently activated in response to Sendai virus that contains a high dose of defective viral genomes (SeV HD) even in the absence of type I IFN signaling. The induction of anti-viral cytokines is driven by a quick and potent activation of IRF3 and NF-κB independently of IRF7. This response depends on the presence of MAVS that is essential for the signaling of the viral RNA sensors RIG-I and MDA5. Interestingly, our study indicates that infection with SeV HD triggers MDA5, but not RIG-I, in a type I IFN independent manner. This supports the hypothesis that the type I IFN-independent up-regulation of MDA5 is involved in the recognition of viral RNA and the subsequent induction of antiviral genes. In conclusion, this study suggests a previously unappreciated type I IFN independent function of MDA5 in the innate immune response to respiratory viruses.

The generation of defective viral genomes (DVGs) during the replication of viruses in vitro has been described for many different viruses including influenza, vesicular stomatitis and rabies. DVGs are truncated forms of the standard virus genome that are unable to replicate due to the lack of a functional viral polymerase. We have shown that DVGs have a potent ability to elicit the activation of dendritic cells in vitro demonstrating their exceptional capacity to trigger innate immunity. The presence of DVGs in viral preparations has been broadly correlated with protection against lethal doses of viruses. It was recently shown that RIG-I predominantly binds DVGs during infections with Sendai virus. The role of DVGs during natural infections is not known. Infection of bone marrow dendritic cells with different strains of Sendai virus showed that DVGs of different sizes are detected in all the viral preparations. In addition, infection with a Sendai virus strain that had been depleted of DVGs results in DVG generation at late points after infection correlating with the peak of viral replication. Interestingly, in mice infected with Sendai virus lacking DVGs we could also detect the appearance of DVGs at late times of infection. Together, these results show that DVGs can arise during the course of a natural virus infection stimulating exciting questions regarding their role stimulating anti-viral immune responses.