Your browser doesn't support javascript.
Show: 20 | 50 | 100
Results 1 - 3 de 3
J Mol Liq ; 367: 120566, 2022 Dec 01.
Article in English | MEDLINE | ID: covidwho-2069492


A key step to inhibit severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection is to prevent the entry of the virus into the host cells. The receptor-binding domains (RBDs) of spike proteins of SARS-CoV and other human coronaviruses utilize heparan sulfate proteoglycans (HSPGs) as the primary receptors for their accumulation on the cell surface and then scan for binding to the main entry receptor angiotensin-converting enzyme 2 (ACE2). SARS-CoV and SARS-CoV-2 share structurally similar RBDs and therefore, it is possible that SARS-COV-2 primarily binds to HSPGs followed by binding to the ACE2 receptors. A promising strategy to inhibit virus infection is to circulate exogenous bioactive moieties structurally mimicking cellular HSPG and ACE2 which act as decoy receptors binding to SARS-CoV-2 and competitively inhibit virus entry to the host cells mediated by cellular-bound HSPG and ACE2. Using a molecular docking tool, we identified carboxymethyl benzyl amide sulfonate (CMBS) and polyanetholesulfonic acid (PAS) as the suitable HSPG mimicking ligands, and Paenibacillus sp. B38-derived carboxypeptidase (B38-CAP) and Bacillus subtilis-derived carboxypeptidase (BS-CAP) as the potential ACE2-like enzymes having a strong binding affinity to the spike proteins as that of cellular HSPG and ACE2. Further, the binding stability and compactness of these moieties with SARS-CoV-2 were analyzed through molecular dynamics (MD) simulations, and the results indicated that these moieties form well-stable complexes with the RBD of spike proteins. The identified moieties could be conjugated to the surfaces of non-toxic nanoparticles to provide multiple interactions to efficiently shield SARS-CoV-2, and inhibit viral entry to the host cells.

Horm Mol Biol Clin Investig ; 42(1): 63-68, 2021 Feb 19.
Article in English | MEDLINE | ID: covidwho-1088785


After the global outbreak of coronaviruses caused diseases such as Middle East Respiratory Syndrome (MERS) and Severe Acute Respiratory Syndrome (SARS), an outbreak due to these viruses occurred in December, 2019 in Wuhan, Hubei Province, China and led to a worldwide spread. Coronavirus 2019 disease (COVID-19) has emerged as a serious global health emergency and spread from a person to another who has the virus. But the scope of an intermediate host is not known. Population at higher risk includes individuals in higher age group (>60 years) or with comorbidities such as diabetes, hypertension, cardiovascular disease and weaker immune system. Many unknown and underestimate risk factors could be responsible for adverse outcomes in COVID-19. These risk factors should be appropriately identified, addressed and necessary actions should be taken to mitigate the effect of COVID-19 pandemic. Bhopal gas tragedy was one of the world's worst industrial chemical leak disaster. The survivors of this incident still suffer from the various complications such as increased rate of cancers, chronic illness like tuberculosis, respiratory diseases, birth defects, nerve injury, growth retardations, gynecological illness and many more. The survivors of Bhopal gas tragedy are at higher risk of developing COVID-19 related adverse outcome. One of the possible explanations can be long term effect of methyl isocyanate (MIC). MIC exposure can lead to possible toxic effect on genetic, epigenetic and non-genetic factors. In this review, we aim to establish the scientific basis for adverse outcome in COVID-19 patients who are also victims of Bhopal gas tragedy.

Bhopal Accidental Release , COVID-19 , Disaster Victims , SARS-CoV-2/physiology , Survivors , Aged , Aged, 80 and over , COVID-19/diagnosis , COVID-19/epidemiology , COVID-19/etiology , COVID-19/virology , China/epidemiology , Comorbidity , Disaster Victims/rehabilitation , Disaster Victims/statistics & numerical data , Disasters , Humans , India/epidemiology , Middle Aged , Pandemics , SARS-CoV-2/isolation & purification , Survivors/statistics & numerical data
Horm Mol Biol Clin Investig ; 42(1): 77-85, 2021 Feb 04.
Article in English | MEDLINE | ID: covidwho-1067449


COVID-19 has resulted in an ongoing global pandemic, which spread largely among people who have had close contact with the infected person. The immunopathology of the SARS-CoV-2 virus includes the production of an excess amount of pro-inflammatory cytokines "a cytokine-storm". The respiratory system (main), cardiovascular system and the gastrointestinal tract are the most affected body systems during viral infection. It has been found that most of the patients who require admission to hospital are elderly or have chronic underlying diseases. Higher cases of malnutrition and co-morbidities like diabetes mellitus and cardiovascular diseases are reported in elderly patients due to which, the immune system weakens and hence, the response to the virus is diminished in magnitude. A deficiency of micronutrients results in impaired immune responses leading to improper secretion of cytokines, alterations in secretory antibody response and antibody affinity which increases susceptibility to viral infection. The deficiency of various micronutrients in COVID-19 patient can be treated by appropriate nutritional supplements, prescribed after evaluating the patients' nutritional status. Here we aim to highlight the role of a few particular nutrients namely Vitamin D, Vitamin C, Omega-3 fatty acids, Zinc and Magnesium along with the synergistic roles they play in enhancing immunity and thus, maintaining homeostasis.

COVID-19/epidemiology , Malnutrition/epidemiology , Ascorbic Acid/physiology , COVID-19/complications , COVID-19/immunology , COVID-19/therapy , Dietary Supplements , Fatty Acids, Omega-3/physiology , Humans , Immune System/physiology , Magnesium/physiology , Malnutrition/complications , Malnutrition/immunology , Malnutrition/therapy , Micronutrients/physiology , Nutritional Status/physiology , Pandemics , SARS-CoV-2/physiology , Vitamin D/physiology , Zinc/physiology