Among the abounding lessons we learned from the SARS-C0V-2 pandemic is the uttermost determinant that people are not equal before the severity of COVID-19. Indeed, the disease course differs with age, gender, ethnicity, underlying clinical conditions and virus variants. Other diseases modifying factors are associated with genetic traits such as those driving the immune response, the blood groups, the coagulation system and the ACE2 receptor variants [1-4].
Related the extremely transmittable abilities of SARS-CoV-2,a harmonious virus to the bat CoV, gets transmitted by three principal processes-- the inhalation of droplets from the SARS-CoV-2 infected person, contacting to the person, and by the surfaces and materials defiled with the virus. Whereupon bat Coronavirus is mostly like the pandemic causing virus SARS-CoV-2, bats are often deliberated and figured out as a possible primary host although no intermediate has not been defined yet in the wherewithal of transmission. The Spike Glycoprotein plays an important role in the case of penetration with the assistance of the ACE2 receptor and the Receptor Binding Domain. In the human body, infiltrating the nucleic acid into host cells, SARS-CoV-2 attacks one cell and one by one into the whole human body; therefore, infected cases are found symptomatic and asymptomatic considering the immune power. Patients with cardiovascular disease or diabetes proceed with their treatment with ACE2 often; therefore, there might be a high chance of getting infected. Whereas the SARS-CoV-2 infects the blood and then lungs, Antigens improvement can be better in order to avoid high-complicated effects. Currently, no vaccination or no accurate cure and treatment has not been defined. An explanation with analysis on SARS-CoV-2 has been performed from the aspect of virology, immunology and molecular biology. Several relevant figures have been included hereby in order to a better understanding of the very concept.
The outbreak of new coronavirus acute respiratory disease (SARS-CoV-2) has been a major global challenge for the scientific community to save humanity. While, the unviability of the vaccine keeps most classes of society, especially African countries, suffer from the healthcare problem. Conventional medicine plants become the alternative method for the therapeutic because it contains valuable bioactive compounds. This brief review devoted the importance of medicinal plants such as Citrus, olive, garlic, ginger, green tea, woad, broad-leaf privet, Japanese torreya, and saffron crocus, by their antiviral effects (anti-SARS coronavirus, anti-HSV, and anti-HIV diseases) and their promising uses as probable boosters of the immune and anti-inflammatory response from SARS-CoV-2 infection. Based on scientific reports, bioactive compounds could inhibit 3-chymotrypsin-like cysteine protease and human protein ACE2, where these facts can be attractive to develop effective drugs.
COVID-19 virus structural components: The 2019-nCoV, also called SARS-CoV-2, was first reported in Wuhan, China in December 2019. The disease was named Coronavirus Disease 2019 (COVID-19) and the virus responsible for it as the COVID-19 virus, respectively, by WHO. The 2019-nCoV has a round, elliptic or pleomorphic form with a diameter of 60–140 nm. It has single-stranded RNA genome containing 29891 nucleotides, a lipid shell, and spike, envelope, membrane and hemagglutinin-esterase (HE) proteins.
Steps in progression of COVID-19 illness: Once inside the airways, the S protein on the viral surface recognizes and mediates the attachment to host ACE-2 receptors and gains access to endoplasmic reticulum. The HE protein facilitates the S protein-mediated cell entry and virus spread through the mucosa, helping the virus to attack the ACE2-bearing cells lining the airways and infecting upper as well as lower respiratory tracts. With the dying cells sloughing down and filling the airways, the virus is carried deeper into the lungs. In addition, the virus is able to infect ACE2-bearing cells in other organs, including the blood vessels, gut and kidneys. With the viral infestation, the activated immune system leads to inflammation, pyrexia and pulmonary edema. The hyperactivated immune response, called cytokine storm in extreme cases, can damage various organs apart from lungs and increases susceptibility to infectious bacteria especially in those suffering from chronic diseases.
The current therapeutics for COVID-19: At present, there is no specific antiviral treatment available for the disease. The milder cases may need no treatment. In moderate to severe cases, the clinical management includes infection prevention and control measures, and symptomatic and supportive care, including supplementary oxygen therapy. In the critically ill patients, mechanical ventilation is required for respiratory failure and hemodynamic support is imperative for managing circulatory failure and septic shock.
Conclusion: Confusion, despair and hopes: There is no vaccine for preexposure prophylaxis or postexposure management. There are no specific approved drugs for the treatment for the disease. A number of drugs approved for other conditions as well as several investigational drugs are being canned and studied in several clinical trials for their likely role in COVID-19 prophylaxis or treatment. The future seems afflicted with dormant therapeutic options as well as faux Espoir or false hopes. As obvious, not all clinical trials will be successful, but having so many efforts in progress, some may succeed and provide a positive solution. Right now, though, confusion and despair prevail.
The infectivity and pathogenesis: SARS-CoV-2, the causative agent of Covid-19, involves Angiotensin-converting enzyme 2 (ACE2) receptors on type II alveolar type 2 (AT2) cells in lungs. Apart from, the upper and lower respiratory tracts, the disease affects the gastrointestinal system prominently, as evidenced by the significant GI symptoms, early in the course of the disease. In addition, the virus infects ACE2-bearing cells in other organs including the heart and blood vessels, brain, and kidneys.
Clinical features and morbidity: The clinical spectrum of COVID-19 varies from asymptomatic or pauci-symptomatic presentation to moderate to severe states characterized by respiratory failure necessitating mechanical ventilation and ICU support and those manifesting critical clinical condition with complications like sepsis, septic shock, and multiple organ dysfunction failure. The CT chest is an important tool for early identification of COVID-19 pneumonia as well as for prognostic purposes.
The recovery and residual damage: The recovery and other outcomes vary depending on age and other aspects including sex, comorbidities, and genetic factors. The outlook for older adults, who account for a disproportionate share of critical disease, is unfavorable, and most of those who survive are unlikely to return to their previous level of functioning. The disease affects their long-term health and quality of life as well as brings in propensity for truncated post-disease survival.
COVID-19 aftermath and follow up: The patients discharged from hospital following severe COVID-19, continue to suffer with lingering impact of the disease as well as that of the emergency treatments that saved their life. The post-infection reduced exercise tolerance and other subtle factors, like post viral fatigue syndrome, post-traumatic stress disorder, impaired concentration, delirium, and disturbed sleep-wake cycle often underly the functional impairment. In fact, there is need of step-down care and later a multidisciplinary support involving regular clinical assessment, respiratory review, physiotherapy, nutritional advice, and psychiatric support.
Conclusion: The life after COVID-19: After recovery from the disease, the virus SARS-CoV-2, may persist for uncertain period. In addition, the chance of reinfection cannot be ruled out. The vitamin D supplementation may be helpful. In general, the quality of life (QOL) in ICU survivors improves but remains lower than general population levels, but most of the patients adapt well to their level of self-sufficiency and QOL. Also, the debility due to co-morbidities may further compromise the activity of daily living and QOL issues. The Age and severity of illness appear to be the major predictors of post-discharge physical functioning.
In late 2019, a pandemic crisis started in Wuhan, China, swept the whole world. The disease is caused by the SARS-CoV-19 virus that belongs to the corona family of viruses. The virus mainly caused failure of respiration, and led to many deaths worldwide. The main focus of research and medicine is to find more about the virus, as well as the development of effective preventive and therapeutic measures. While many trials and opinions have been published, which might support or contradict each other, this article tries to provide a simplified viewpoint about the disease. We highly recommend the therapeutic strategies to include drug combinations that can target the pathogenesis at many levels. For example, a combination of an effective anti-viral Remdesivir, soulable ACE2, and an immune modulator.
A respiratory outbreak of COVID-19 started from Wuhan, China and on 30 January 2020, WHO declared this infection to be epidemic, implementing public health emergency worldwide. On 11th March 2020, observing its prevalence in the whole world and WHO declared as a pandemic. Many countries completely collapse in the grip of this pandemic, as there are no effective treatments available, the precaution is the sole remedy to minimize this infection. The emergence and pandemic of SARS-CoV-2 (since the SARS-CoV in 2002 and MERS-CoV in 2012] manifest the third time outline of highly contagious and pathogenic infection with infect-ability to spread globally in the twentieth-first century. The SARS CoV-2 genome is highly identical to bat coronavirus which is considered to be the perfect natural host. This coronavirus even utilizes the same ACE2 receptor as SARS-CoV and mainly spread the infection to the respiratory tract, which evidently showed that transmission of this virus through interactions and exposures. The death toll of these infected patients is increasing day by day especially when they have prehistory fatal diseases like cardiovascular, diabetics, and respiratory diseases. In this review, we summarized and explained the research progressed and available data on epidemiology, COVID-19 phylogenetic relation and its impact of different fatal disease and their relation and discuss the precautionary methods to combat this pandemic. Moreover, the pieces of evidence of spreading the virus through pets and prevention of being spreading by copper metal endorsement.
Introduction: SARS-CoV-2 life cycle: The disease which reportedly began in Chinese city Wuhan in November-December 2019 manifesting as severe respiratory illness, soon spread to various parts of the world, and was named COVID-19, and declared a pandemic by WHO. The life cycle of SARS-CoV-2 begins with membrane fusion mediated by Spike (S) protein binding to the ACE2 receptors. Following viral entry and release of genome into the host cell cytoplasm there occurs replication and transcription to generate viral structural and non-structural proteins. Finally, VLPs are produced and the mature virions are released from the host cell.
Immunogenicity of the spike protein: The S protein is considered the main antigenic component among structural proteins of SARS-CoV-2 and responsible for inducing the host immune response. The neutralising antibodies (nAbs) targeting the S protein are produced and may confer a protective immunity against the viral infection. Further, the role of the S protein in infectivity also makes it an important tool for diagnostic antigen-based testing and vaccine development. The S-specific antibodies, memory B and circulating TFH cells are consistently elicited following SARS-CoV-2 infection, and COVID-19 vaccine shots in clinical trials.
The emerging SARS-CoV-2 variants: The early genomic variations in SARS-CoV-2 have gone almost unnoticed having lacked an impact on disease transmission or its clinical course. Some of the recently discovered mutations, however, have impact on transmissibility, infectivity, or immune response. One such mutation is the D614G variant, which has increased in prevalence to currently become the dominant variant world-over. Another, relatively new variant, named VUI-202012/01 or B.1.1.7 has acquired 17 genomic alterations and carries the risk of enhanced infectivity. Further, its potential impact on vaccine efficacy is a worrisome issue.
Conclusion: THE UNMET CHALLENGES: COVID-19 as a disease and SARS-CoV-2 as its causative organism, continue to remain an enigma. While we continue to explore the agent factors, disease transmission dynamics, pathogenesis and clinical spectrum of the disease, and therapeutic modalities, the grievous nature of the disease has led to emergency authorizations for COVID-19 vaccines in various countries. Further, the virus may continue to persist and afflict for years to come, as future course of the disease is linked to certain unknown factors like effects of seasonality on virus transmission and unpredictable nature of immune response to the disease.
The ongoing outbreak of Coronavirus Disease 2019 (COVID-19) originally emerged in China during December 2019 and had become a global pandemic by March 2020. COVID-19 is caused by a novel coronavirus, severe acute respiratory syndrome coronavirus type 2 (SARS-CoV-2). Two other coronaviruses have caused world-wide outbreaks in the past two decades, namely SARS-CoV (2002–2003) and Middle East respiratory syndrome coronavirus (MERS-CoV) (2012–present). The surface spike glycoprotein (S), which is critical for virus entry through engaging the host receptor and mediating virus host membrane fusion, is the major antigen of coronaviruses. Recent studies provide molecular insights into antibody recognition of SARS-CoV-2. In this review, we discuss the relationship between the spike glycoprotein of SARS-CoV-2 and its receptor, angiotensin converting enzyme 2 (ACE2) including the latest findings.
COVID-19 is a disease that is caused by SARS-CoV-2 and very speedily spreading all over the world. The blood group’s effect on COVID-19 is not clear. The main aim of this article is to determine the relationship between sensitivity of COVID-19 and ABO blood group. For this study we have observed that the individuals with blood group A are at higher risk of getting COVID-19 because they contain the higher concentration of Angiotensin-converting enzyme-2 that provide the site to virus for entry. But in other blood groups the natural Anti A antibodies block the interaction between host receptor and virus and disturb their interaction. Certain studies show that the infectivity and mortality rate in covid patients is not affected by AB blood group system. But according to research, increased ventilator usage, ICU stay was observed in critically ill patients with AB blood group than of other blood groups. O blood group has proved to be protective against SARS-CoV-2 due to the presence of both anti-A and anti-B antibodies as they prevent the binding of the spike protein S of the virus with the ACE2 receptors which are present on the surface of cells. Moreover, furin also plays a major role in penetration of virus in the host cells. Furin is required for the activation of the spike protein S of the virus and due to the low efficiency of furin cleavage in blood group O it is protected from SARS-CoV-2 and other chronic diseases. Mortality rate of covid 19 depends upon the environmental factors, number of people living in the area and also some economic factors. The different strains of COVID-19 effect the different people differently and as the time passes the strain of COVID-19 has changed and thus according to this the mortality rate of different provinces and areas varies due to environmental factors. Pregnant women have no any kind of transportation of covid to their fetuses but mostly patients of blood group A are being affected by COVID-19 and hence their fetuses are somehow effected. And those pregnant women having blood group O does not have any risk of COVID-19 of severe stages.
Adrhyan Araújo da Silva Oliveira, Ana Maisa Passos da Silva, Jackson Alves da Silva Queiroz, Paulo Ricardo Freitas de Souza, Juan Miguel Villalobos Salcedo and Deusilene Souza Vieira*
Published on: 28th April, 2022
SARS-CoV-2 is a virus that has a positive-sense, single-stranded RNA genome that encodes 4 structural proteins, the main one being the S protein (Spike) responsible for mediating with ACE2 and TMPRSS2 for entry into the host cell. The study of single nucleotide polymorphisms (SNPs) of ACE2 and TMPRSS2 can elucidate their possible intervention in the action of the protein, its activity, and the gene expression of encoding these enzymes, which may increase susceptibility to viral infection. From this, literature searches were carried out until December 2021, listing 11,820 publications for literary analysis on the described genetic variations of these protein structures, as well as their relation and influence on the pathology. It was possible to conclude that there is a great influence exerted by genetic variability in ACE2 and TMPRSS2 increasing the ability of the virus to bind to the host cell and the development of COVID-19 with complications.
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