A novel coronavirus strain has been testing the capabilities of our modern world and suffocating health care systems, while bringing together scientist's researches and governmental powers, to fight off its robust viral disease.A new zoonotic pathogenic member of the human coronaviruses, that was first documented in Wuhan, China, has crossed the species barrier to infect humans and caused an outbreak of viral pneumonia.In this brief review, we'll discuss the virology of SARS-CoV-2, the virus that causes COVID-19, covering the general structure of the virus, its genetics and its process of replication.SARS-CoV-2 gets into the cell through the recognition of the angiotensinconverting enzyme 2 (ACE2) receptors by the spike glycoprotein, with the aid of the priming protein transmembrane serine protease 2 (TMPRSS2), which is important for its activation, and replicates as a result of a complex process that involves RNA synthesis, proofreading and capping.
SARS-CoV-2 is the seventh zoonotic pathogenic novel member of the human coronaviruses and the third coronavirus to cause a large-scale epidemic in the twenty-first century, highly contagious, spreading quickly around the world and affecting all individuals, especially the elderly, those with diverse genetic and immunological backgrounds, also those with multiple underlying disorders and varied demographics like sex and environmental conditions.This work introduces the virology of the novel virus, reveals its possible origin and describes how it spreads via the diverse routes of infection, showing the biological characteristics related to its risk of causing a pandemic, and the kind of diagnostic tools used to identify it.The virus pandemic rapidly progressed worldwide and is still ongoing; the numbers of affected and those deceased are increasing, with devastating societal, economic and political impacts.
Angiotensin II levels in COVID-19 are controversial.We studied 12 hospitalized patients, including their baseline levels of peripheral lymphocyte subsets (via flow cytometry) and plasma angiotensin II (via radioimmunoassay).Controls comprised radioimmunoassay's 124 healthy subjects.Angiotensin II levels (pg/ml) were elevated among patients versus controls (Mean ± standard deviation: 98.8 ± 146.9 versus 23.7 ± 15.6, p < 0.0001; Median, interquartile range: 27, 20 to 116 versus 22, 14 to 28).Half the patients had lymphocytopenia (< 1000 cells/mm 3 ), and the CD3+/CD4+ counts were negatively associated with body mass index, viral load, hospital stay and non-home discharge.Angiotensin II imbalance appears to be a biomarker for COVID-19 morbidity and merits further investigation.
The aim of this work is to identify the clinical features of pediatric COVID-19 and to relate them with laboratory findings on potential markers of poorer outcomes, such as evidence of organ dysfunction and of superimposed bacterial infection. We performed a systematic literature review with meta-analysis using the data bases Pubmed, Scopus, SciELO, Cochrane Library, Web of Science, EMBASE and Google Scholar. Only pediatric cases with COVID-19 confirmed by rRT-PCR were selected. Demographical and clinical characteristics, laboratory and imaging features, complications, exposure setting, and outcomes were evaluated. After screening, 90 articles were selected for full-text assessment, 42 being included for qualitative and quantitative analyses. Additionally, 31 case reports were included and analyzed separately. For 4210 patients, fever (48.6%, 95% CI: 43.5-53.7%) and cough (44.2%, 95% CI: 39.1-49.3%) were the most prevalent clinical features. 29.7% (95% CI: 23.3-35.5%) of the children did not report any symptom. 66.4% (95% CI: 60.2-72.1%) of children had abnormal radiologic findings. Among the patients, 5.1% (95% CI: 2.7-9.3%) required intensive care unit and 27.5% (95% CI: 19.0-38.1%) presented secondary infections. The pediatric cases of COVID-19 are generally asymptomatic, with fever and cough, however, being the most frequently observed symptoms. The radiologic images often show ground glass opacities. The overall laboratory biomarkers show a scenario of inflammation. Children presented high co-infection rate, particularly with Mycoplasma.
Fil: Chinestra, Silvia Carolina. Consejo Nacional de Investigaciones Cientificas y Tecnicas. Centro Cientifico Tecnologico Conicet - Bahia Blanca. Centro de Recursos Naturales Renovables de la Zona Semiarida. Universidad Nacional del Sur. Centro de Recursos Naturales Renovables de la Zona Semiarida; Argentina
It is widely accepted that an effective HIV-1 preventative vaccine must elicit antibodies that can block virus acquisition. Although, anti-HIV-1 broadly neutralizing antibodies (bnAbs) have been isolated, unfortunately, no vaccine immunogens have been designed that can elicit these bnAbs in uninfected at-risk individuals. Some studies have suggested that other antibody functionalities, besides neutralization, such as antibody-dependent cellular cytotoxicity (ADCC), may prevent HIV-1 acquisition. In contrast to bnAbs, ADCC-inducing antibodies may be more amenable to elicitation by current vaccine technologies. This review will provide clarity about the role of nAbs and ADCC-inducing antibodies in preventing transmission, highlight mechanisms that potentially explain how ADCC-mediating antibodies may work, and speculate about the generation of these novel protective antibodies. Anti-HIV-1 ADCC-inducing antibodies may provide a new avenue for developing an effective HIV-1 vaccine.
Self-inactivating retroviruses are an attractive vector choice for long term and stable expression of therapeutic genes because of their ability to integrate into the host genome. However, their ut ...
A central obstacle to the design of a global HIV vaccine is viral diversity. Antigenic differences in envelope proteins result in distinct HIV serotypes, operationally defined such that antibodies raised against envelope from one serotype will not bind envelope molecules from a different serotype. The existence of serotypes has presented a similar challenge to vaccine development against other pathogens. In such cases, antigenic diversity has been addressed by vaccine design: for example, the poliovirus vaccine includes 3 serotypes of poliovirus, and Pneumovax® presents a cocktail of 23 pneumococcal variants to the immune system. It is likely that a successful vaccine for HIV must also comprise a cocktail of antigens. Here, data relevant to the development of cocktail vaccines, designed to harness diverse, envelope-specific B-cell and T-cell responses, are reviewed.
