ABSTRACT
Coronavirus Disease (COVID-19) is an infectious disease that has a high fatality rate and is spreading quickly throughout the world. The WHO claims that SARS-CoV-2, a brandnew coronavirus strain, is to blame for this outbreak (Severe Acute Respiratory Syndrome Corona Virus-2) and that COVID-19 must be treated with both conventional medical therapy and a combination of modern medicine. The technique of this study, a review of the literature, focused on numerous investigations looking at the potential of curcumin molecules from turmeric to cure the COVID-19 disease. Primary data for scientific papers is gathered from national and international journals through searches on electronic search engines like Google Scholar, Sciencedirect, or PubMed and selected publications are assessed, evaluated, and interpreted by authors. Turmeric contains substances that are immune system boosters, anti-inflammatory, antitumor, antiviral, and antioxidants. Curcumin may prevent a number of viral infections, according to evidence. In vitro testing has shown that the SARS-CoV virus is resistant to curcumin's antiviral properties. It's possible that curcumin can halt viral replication. Curcumin has the potential to treat COVID-19 effectively. Curcumin has antiviral activity that can fight the SARS-CoV-two virus. Treatment with curcumin can change the virus top protein structure, preventing the virus from entering the body and from budding. Future study on the use of curcumin as SARS-Cov-2 virus inhibitory agent is necessary in order to employ it as a novel and long-lasting therapy option for Covid-19 patients. © 2022 WITPress. All rights reserved.
ABSTRACT
Remdesivir was recently demonstrated to decrease recovery time in hospitalized patients with SARS-CoV-2 infection. In rhesus macaques, early initiation of remdesivir therapy prevented pneumonia and lowered viral loads in the lung, but viral loads increased in the nasal passages five days after therapy. We developed mathematical models to explain these results. We identified that 1) drug potency is slightly higher in nasal passages than in lungs, 2) viral load decrease in lungs relative to nasal passages during therapy because of infection-dependent generation of refractory cells in the lung, 3) incomplete drug potency in the lung that decreases viral loads even slightly may allow substantially less lung damage, and 4) increases in nasal viral load may occur due to a slight blunting of peak viral load and subsequent decrease of the intensity of the innate immune response, as well as a lack of refractory cells. We also hypothesize that direct inoculation of the trachea in rhesus macaques may not recapitulate natural infection as lung damage occurs more abruptly in this model than in human infection. We demonstrate with sensitivity analysis that a drug with higher potency could completely suppress viral replication and lower viral loads abruptly in the nasal passages as well as the lung. One Sentence SummaryWe developed a mathematical model to explain why remdesivir has a greater antiviral effect on SARS CoV-2 in lung versus nasal passages in rhesus macaques.