Aspectos generales sobre la estructura del coronavirus del síndrome respiratorio agudo grave 2 (SARS-CoV-2) / General aspects about the structure of Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2)

Introduction: In late 2019, a new coronavirus named Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) that causes respiratory-related illness was reported in Wuhan, China. This virus can attack human lung cells causing a disease called coronavirus disease 2019 (COVID-19), which can lead to pneumonia and acute respiratory distress syndrome. Objective: Describe the structural characteristics of Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2). Methods: A review was written from 47 bibliographic references. Articles and information from national and international journals available in the PubMed, Scopus, Medline, SciELO databases were used. The quality, reliability and validity of the selected articles were analyzed to carry out an adequate review. Analysis-synthesis and logical deduction methods were applied. Development: An introduction to the general aspects of the structure of SARS-CoV-2 is provided by stating the characteristics of the structural and non-structural proteins encoded by the viral genome, which provides the basis for understanding viral entry mechanisms to the host cell, and may be useful to stimulate the search for novel insights and possible therapeutic targets to fight the infection. Conclusions: Knowledge of the structure of the SARS-CoV-2 virus and the characteristics of the structural and non-structural proteins provides the basis for understanding the viral mechanisms of infection and the strategies for developing effective therapeutics(AU)

Introducción: A finales de 2019 se informó el brote de un nuevo coronavirus en Wuhan, China, llamado Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) que causa alteraciones en el aparato respiratorio. Este virus puede atacar las células humanas del pulmón causando una enfermedad denominada enfermedad por coronavirus 2019 (COVID-19), que puede producir neumonía y un síndrome de dificultad respiratoria aguda. Objetivo: Describir las características estructurales del virus SARS-CoV-2. Métodos: Se realizó una revisión bibliográfica a partir de 47 referencias. Se utilizaron artículos e información de revistas nacionales e internacionales disponibles en las bases de datos PubMed, Scopus, Medline, SciELO. Para llevar a cabo una revisión adecuada, se analizaron la calidad, fiabilidad y validez de los artículos seleccionados. Se aplicaron métodos de análisis-síntesis y deducción lógica. Desarrollo: Se proporciona una introducción de los aspectos generales de la estructura del SARS-CoV-2. Se enuncian las características de las proteínas estructurales y no estructurales codificadas por el genoma viral, lo que provee la base para comprender los mecanismos virales de entrada a la célula huésped. El artículo resulta de utilidad para estimular la búsqueda de nuevos conocimientos y posibles objetivos terapéuticos para combatir la infección. Conclusiones: El conocimiento sobre la estructura del virus SARS-CoV-2 y las características de las proteínas estructurales y no estructurales que lo forman ampara significativamente las bases para entender los mecanismos virales de la infección y las estrategias para el desarrollo terapéutico efectivo(AU)

Cell Death Mechanisms in Esophageal Squamous Cell Carcinoma Induced by Vesicular Stomatitis Virus Matrix Protein

OBJECTIVES: Vesicular stomatitis virus (VSV) is under development as an oncolytic virus due to its preferential replication in cancer cells and oncolytic activity, however the viral components responsible have not yet been determined. In this study the effects of VSV wild-type (wt) and M51R-mutant matrix proteins (M51R-mMP) on apoptosis, pyroptosis, necroptosis, and autophagy pathways, in an esophagus cancer cell line (KYSE-30) were investigated. METHODS: The KYSE-30 cells were transfected with pcDNA3.1 plasmids encoding wt or M51R-mMP, and apoptosis, pyroptosis, necroptosis, and autophagy were evaluated 48 and 72 hours after transfection. RESULTS: KYSE-30 cells transfected with VSV wt and M51R-mMPs significantly reduced cell viability to < 50% at 72 hours post-transfection. M51R-MP significantly increased the concentration of caspase-8 and caspase-9 at 48 and 72 hours post-transfection, respectively ( p < 0.05). In contrast, no significant changes were detected following transfection with the VSV wt plasmid. Moreover, VSV wt and M51R-mMP transfected cells did not change the expression of caspase-3. VSV wt and M51R-mMPs did not mMP change caspase-1 expression (a marker of pyroptosis) at 48 and 72 hours post-transfection. However, M51R-mMP and VSV wt transfected cells significantly increased RIP-1 (a marker of necroptosis) expression at 72 hours post-infection ( p < 0.05). Beclin-1, a biomarker of autophagy, was also induced by transfection with VSV wt or M51R-mMPs at 48 hours post-transfection. CONCLUSION: The results in this study indicated that VSV exerts oncolytic activity in KYSE-30 tumor cells through different cell death pathways, suggesting that M51R-mMP may potentially be used to enhance oncolysis.

Zika virus: what do we know about the viral structure, mechanisms of transmission, and neurological outcomes?

Abstract: The Zika virus epidemic that started in Brazil in 2014 has spread to >30 countries and territories in Latin America, leading to a rapid rise in the incidence of microcephalic newborns and adults with neurological complications. At the beginning of the outbreak, little was known about Zika virus morphology, genome structure, modes of transmission, and its potential to cause neurological malformations and disorders. With the advancement of basic science, discoveries of the mechanisms of strain variability, viral transfer to the fetus, and neurovirulence were published. These will certainly lead to the development of strategies to block vertical viral transmission, neuronal invasion, and pathogenesis in the near future. This paper reviews the current literature on Zika virus infections, with the aim of gaining a holistic insight into their etiology and pathogenesis. We discuss Zika virus history and epidemiology in Brazil, viral structure and taxonomy, old and newly identified transmission modes, and neurological consequences of infection.

Role of Toll-like Receptor 3 Variants in Aspirin-Exacerbated Respiratory Disease

PURPOSE: Although the mechanism of virus-induced, aspirin-exacerbated respiratory disease (AERD) is not known fully, direct activation of viral components through Toll-like receptor 3 (TLR3) has been suggested. TLR3 recognizes double-stranded RNA (dsRNA), and activates nuclear factor-kappaB and increases interferon-gamma, which signals other cells to induce airway inflammation in asthma. Considering the association of TLR3 in viral infections and AERD, we investigated whether promoter and non-synonymous variants of TLR3 were associated with AERD. METHODS: The three study groups, 203 with AERD, 254 with aspirin-tolerant asthma (ATA), and 274 normal healthy controls (NC) were recruited from Ajou University Hospital, Korea. Two polymorphisms, -299698G>T and 293391G>A [Leu412Phe], were genotyped using primer extension methods. RESULTS: Genetic associations were examined between two genetic polymorphisms of TLR3 (-299698G>T and 293391G>A [Leu412Phe]) in the three study groups. AERD patients that carried the GG genotype of 293391G>A showed a significantly lower frequency compared with ATA in both co-dominant (P=0.025) and dominant models (P=0.036). Similarly, in the minor allele frequency, the A allele was significantly higher (P=0.023) in AERD compared with ATA for this polymorphism. AERD patients who carried HT2 [GA] showed a significantly higher frequency than other haplotypes in co-dominant (P=0.02) and recessive (P=0.026) models. CONCLUSIONS: Our findings suggest that the -299698G>T and 293391G>A [Leu412Phe] polymorphisms of the TLR3 gene are associated with the AERD phenotype.

Studies on the Development of Viral Detection Markers for the Quality Control of Blood

According to the serological screening methods of antigen-antibody reaction such as ELISA, it has been known that the complete detection of viral infections of HBV, HCV, and HIV-1 viruses in the blood and blood related-products is not much reliable. Therefore, nucleic acid amplification testing methods (NAT) adopted to detect the small quantitative viral nucleic acids could support the basis of using and supplying the blood and its related products safely. This research work is basically designed to describe the simultaneous blood screening system by multiplex or duplex tests for detection of HBV, HCV, and HIV-1 viruses in the blood at one time with low price and labor. It is aimed at easy detection by using the conventional agarose gel electrophoresis. Thus, we tried to detect and identify the viral components in the blood sample according to their different size of PCR products. We decided a set of consensus sequences to recognize each viral DNA fragments after running the multiplex PCR in one tube. This was done by nested RT-PCR using two different RNA viral genomic templates followed by multiplex PCR with addition of viral DNA and their primers after purifying the viral genomic nucleic acids. Those specific primers could be used without any interference to amplify each viral genome in the blood samples. The sensitivities with different viral loads were evaluated on the agarose gel electrophoresis. Three different viral agents in the blood samples could be tested by this multiplex (RT)-PCR with three different primers.