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With the onset of the COVID-19 pandemic and its negative effect on economic activity, a decrease in remittances was expected. However, on the contrary, remittances have increased in countries like Mexico. Using a fixed-effect model with information at the state level, this study finds evidence that the increase in COVID-19 cases was associated with a higher level of remittances to Mexican states, allowing some degree of insurance against the pandemic. However, remittances did not respond to the decrease in employment caused by the pandemic in local economies. A portion of the observed increases in remittances during the pandemic can be explained by factors at the national level. © 2023, Oviedo University Press. All rights reserved.
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Background: The Interferon (IFN)-gamma pathway, including its receptor subunits (IFNAR1 and IFNAR2), is related to hyperinflammation and lower viral clearance in COVID-19. IFNAR2 and the soluble form of the protein have been associated with COVID-19 severity. Aim(s): We aimed to evaluate the association of the IFNAR2 rs2236757, rs1051393, rs3153, rs2834158, and rs2229207 with the clinical outcome (survivors and non-survivors) of patients with severe COVID-19. Method(s): The study included 1,136 patients (67% males, median 56 years old) with severe COVID-19, hospitalized in the Instituto Nacional de Enfermedades Respiratorias, a tertiary care hospital in Mexico. Variants were assessed using Taqman assays. The association study was performed using PLINK v2. Result(s): Four hundred and fifteen patients died during the hospital stay (36.5%). We found higher minor allele frequencies of the rs2236757, rs3153, and rs2834158 among non-survivors compared with survivors. The analyses of genotypes also showed associations of the dominant model for the three variants (Table 1). The rs2834158 was also associated with a logistic regression model adjusted for age (p= 0.038). Conclusion(s): IFNAR2 variants contribute to the genetic risk for mortality in patients with severe COVID-19. (Table Presented).
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Background: TNF and its receptors (TNFR1 and TNFR2) have been implicated in the severity of COVID-19. But it has not been explored the association of genetic variants with cytokine levels. Aim(s): We assessed the association of TNF (rs1800629, rs361525), TNFRSF1A (rs767455, rs1800693), and TNFRSF1B (rs1061622, rs3397) single nucleotide variants with TNF, TNFR1, and TNFR2 plasma levels in patients with severe COVID-19. Method(s): The study included 334 severe COVID-19 hospitalized patients in Mexico's Instituto Nacional de Enfermedades Respiratorias. Blood sampling was performed among the first seven days since patients' admission. Cytokine levels were determined using ELISA and Taqman assays for genotyping. Kruskal-Wallis test was performed in RStudio v.1.3.1073. Result(s): Patients with TT or GT genotype (TNFRSF1B rs1061622) exhibited higher sTNFR1 levels than those carrying GG (1,580 and 1,499 pg/ml vs 1,031 pg/mL). For TNF rs1800629 and rs361525 the higher TNFR2 levels were observed among patients homozygous for the common allele (rs1800629 GG=3,993 pg/mL vs AG+AA=2,881 pg/mL;rs361525 GG=3,996 pg/mL, AG=3,919 pg/mL, and AA=1,935 pg/mL). Higher levels of both receptors were related with more severe forms of COVID-19. Conclusion(s): TNFRSF1B rs1061622, and TNF rs1800629 and rs361525 affect the TNFR1 and TNFR2 levels implicated in the severity of COVID-19.
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The endocytic pathway is a common strategy that several highly pathogenic viruses use to enter into the cell. To demonstrate the usefulness of this pathway as a common target for the development of broad-spectrum antivirals, the inhibitory effect of drug compounds targeting endosomal membrane proteins were investigated. This study entailed direct comparison of drug effectiveness against animal and human pathogenic viruses, namely Ebola (EBOV), African swine fever virus (ASFV), and the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). A panel of experimental and FDA-approved compounds targeting calcium channels and PIKfyve at the endosomal membrane caused potent reductions of entry up to 90% in SARS-CoV-2 S-protein pseudotyped retrovirus. Similar inhibition was observed against transduced EBOV glycoprotein pseudovirus and ASFV. SARS-CoV-2 infection was potently inhibited by selective estrogen receptor modulators in cells transduced with pseudovirus, among them Raloxifen inhibited ASFV with very low 50% inhibitory concentration. Finally, the mechanism of the inhibition caused by the latter in ASFV infection was analyzed. Overall, this work shows that cellular proteins related to the endocytic pathway can constitute suitable cellular targets for broad range antiviral compounds.