COVID-19 Central Research Database
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  • Potential effects of curcumin in the treatment of COVID-19 infection

    The main clinical manifestation of COVID-19 is the presence of respiratory symptoms, but some patients develop severe cardiovascular and renal complications. There is an urgency to understand the mechanism by which this virus causes complications so as to develop treatment options. Curcumin, a natural polyphenolic compound, could be a potential treatment option for patients with coronavirus disease. In this study, we review some of the potential effects of curcumin such as inhibiting the entry of virus to the cell, inhibiting encapsulation of the virus and viral protease, as well as modulating various cellular signaling pathways. This review provides a basis for further research and development of clinical applications of curcumin for the treatment of newly emerged SARS-CoV-2. CONCLUSION AND CHALLENGES In this review, we have attempted an overview of the potential antiviral effects of curcumin that can be helpful for researchers to further investigate the potency of curcumin against the new emerging SARSCoV-2 infection. The ability of curcumin to modulate a wide range of molecular targets makes it a suitable candidate for the management of coronavirus infection. Curcumin may have beneficial effects against COVID-19 infection via its ability to modulate the various molecular targets that contribute to the attachment and internalization of SARS-CoV-2 in many organs, including the liver, cardiovascular system, and kidney. Curcumin could also modulate cellular signaling pathways such as inflammation, apoptosis, and RNA replication. Curcumin may also suppress pulmonary edema and fibrosis-associated pathways in COVID-19 infection. Despite the potential beneficial effects and safety profile of curcumin against various diseases, the limited bioavailability of this turmericderived compound, especially via oral administration may be a problematic issue (Anand, Kunnumakkara, Newman, & Aggarwal, 2007). Yang et al. demonstrated that intravenous administration of curcumin (10 mg/kg) resulted in better bioavailability in comparison to oral administration with a higher dose (500 mg/kg) (K. Y. Yang, Lin, Tseng, Wang, & Tsai, 2007). Several clinical trials have shown that the issue regarding the bioavailability of curcumin can be mitigated by administering higher concentrations within non-toxic limits (Kunnumakkara et al., 2019). In addition, many studies have suggested various ways to improve the bioavailability of curcumin such as manipulation and encapsulation of curcumin into micelles, liposomes, phospholipid complexes, exosomes, or polymeric nanocarrier formulation and also utilization of curcumin in combination with cellulosic derivatives, natural antioxidants, and a hydrophilic carrier (Jäger et al., 2014; Moballegh Nasery et al., 2020). Moreover, several studies have reported the synergistic therapeutic effects of curcumin in combination with other natural or synthetic compounds (Singh et al., 2013). Overall, the welldocumented anti-inflammatory and immunomodulatory effects of curcumin along with the evidence on the anti-fibrotic and pulmonoprotective effects of this phytochemical on the lung tissue make it a promising candidate for the treatment of COVID-19. Since curcumin is known to have strong inhibitory effects on NF-κB and several pro-inflammatory cytokines, it can be particularly helpful as an adjunct in reversing the fatal cytokine storm that occurs in serious cases of COVID-19. 6 ZAHEDIPOUR ET AL. To sum up, this review shows that curcumin as an antiviral and anti-inflammatory agent can be helpful for both prevention and treatment of new emerging coronavirus. However, well-designed clinical trials are needed to demonstrate the potential efficacy of curcumin against SARS-CoV-2 infection and its ensuing complications. Reference & Source Information: https://onlinelibrary.wiley.com/ Read more on :

  • Vaccine For Coronavirus Likely to be Available by September, Says Oxford Expert Sarah Gilbert

    Professor Sarah Gilbert, an expert of mediconology at the University of Oxford, said she is confident of a vaccine for novel coronavirus being available by September this year. Her claims comes in contradiction of most pharmaceutical wizards predicting an 18-month time frame to find either a vaccine or a cure to the COVID-19 disease. COVID-19 Ten Times Worse Than Swine Flu, Vaccine Needed to Fully Halt Disease: WHO.Londo: Professor Sarah Gilbert, an expert of mediconology at the University of Oxford, said she is confident of a vaccine for novel coronavirus being available by September this year. Her claims comes in contradiction of most pharmaceutical wizards predicting an 18-month time frame to find either a vaccine or a cure to the COVID-19 disease. COVID-19 Ten Times Worse Than Swine Flu, Vaccine Needed to Fully Halt Disease: WHO. Gilbert, while speaking to BBC Radio on Monday, said trials are being conducted across the world at an "unprecedented rate". In the University of Oxford as well, the process to screen over 500 volunteers - aged between 18 to 55 - for the ChAdOx1 nCoV-19 vaccine has been expedited, she said. The manufacturers should be ready to produce the vaccine in bulk, she said, adding that billions across the globe would have to be vaccinated against the disease. The process to initiate manufacturing should not be kept on hold till the vaccine is confirmed to be successful, the professor added. "We need to start manufacturing large amounts of the vaccine. It is not uncommon for companies to start manufacturing a new vaccine before they really know for certain it works”, she told the radio channel during the morning show. The Oxford team, which was successful with its rapid vaccine response tests for Ebola in 2014, is hopeful of repeating the success with its coronavirus vaccine trials. The clinical tests are expected to begin next week, Gilbert said. She had last week told a leading magazine that her team is "80 percent sure" of developing the vaccine. Globally, the COVID-19 pandemic infected more than 1,900,000 persons by the time this report was published. The death toll climbed to 118,497. The worst-affected is the United States, where over 600,000 are infected and the death toll has crossed the 23,000-mark. Italy and Spain have recorded over 20,000 and more than 17,000 deaths, respectively. Source www.nytimes.com

  • Indian researchers from JNCASR develops novel anti-microbial coating

    Bengaluru based Jawaharlal Nehru Centre for Advanced Scientific Research (JNCASR), an autonomous institution under the Department of Science and Technology, has developed a one-step curable anti-microbial coating which, when coated on different surfaces such as textile, plastic and so on could kill a range of virus types including COVID 19. JNCASR is an autonomous institution under the Department of Science and Technology. According to the researchers, “till date, to the best of our knowledge, there is no covalent coating strategy which can kill all viruses, bacteria and fungi.” This covalent coating, the research paper about which has been accepted in the journal Applied Material and Interfaces, has been found to completely kill influenza virus as well as resistant pathogenic bacteria and fungi, including methicillin-resistant Staphylococcus aureus and fluconazole-resistant C. albicans spp. The molecules developed have an ability to chemically cross-link with different surfaces upon UV irradiation. Upon the formation of the coating, it has been shown to permeabilize the membranes of pathogens (i.e. bacteria) leading to their inactivation. Microbial attachment and their colony formation on different surfaces play a major role in the transmission of deadly infections in the community as well as healthcare settings. Keeping this in mind, an easy approach was developed to coat a wide range of substrates used in daily life as well as in clinical settings. Molecules were designed, keeping in mind their optimum solubility in a wide range of solvents (such as water, ethanol, chloroform). The coating can be fabricated on a variety of surfaces, and its ease and robustness eliminate the necessity of skilled personnel for procurement of the coating. Coronavirus, like influenza, is also an enveloped virus. Therefore, it is anticipated that the coating may inactivate SARS-CoV-2 upon contact and can help prevent contamination if coated on various surfaces. Considering the current outbreak, if shown to be active, the molecule can be synthesised in large scale through a CRO (Contract Research Organisation) and can be coated on various personal protective tools such as masks, gloves and gowns in collaboration with the private organisations. The molecules can also be coated on other medical devices and tools to avoid hospital-acquired or nosocomial infections. Currently, the frontline health workers are at the biggest risk currently. The molecules were then immobilised on different substrates such as cotton, polyurethane, polypropylene, polystyrene, etc., which construct majority of the objects we see around us. After coating, the surfaces were evaluated for their antibacterial, antifungal, and antiviral activity. References: BioSpectrum, https://www.biospectrumindia.com/news/58/16098/jncasr-develops-novel-anti-microbial-coating.html The Tribune, https://www.tribuneindia.com/news/nation/indian-researchers-develop-coating-that-kills-covid-64274

  • Contribution of monocytes and macrophages to the local tissue inflammation & cytokine storm in COVID-19.

    The COVID -19 -, SARS - and MERS -related coronaviruses share many genomic and structural similarities. However, the SARS -CoV -2 is less pathogenic than SARS -CoV and MERS -CoV. Despite some differences in the cytokine patterns, it seems that the cytokine storm plays a crucial role in the pathogenesis of COVID - 19 -, SARS - and MERS. Monocytes and macrophages may be infected by SARS - CoV -2 through ACE2 -dependent and ACE2 -independent pathways. SARS -CoV -2 can effectively suppress the anti -viral IFN response in monocytes and macrophages. Since macrophages and dendritic cells (DCs ) act as antigen presenting cells (APCs ), the infection of these cells by SARS -CoV -2 impair s the adaptive immune responses against the virus. Upon infection, monocytes migrate to the tissue s where they become infected resident macrophages, allowing viruses to spread through all organs and tissues. The SARS -CoV - 2 -infected monocytes and macrophages can produce large amounts of numerous types of pro - inflammatory cytokines and chemokines, which contribute to local tissue inflammation and a dangerous systemic inflammatory response called cytokine storm. Both local tissue inflammation and the cytokine storm play a fundamental role in the development COVID -19 -related complications, such as acute respiratory distress syndrome (ARDS), which is a main cause of death in COVID - 19 patients. Here, we describe the monocytes and macrophage responses during Journal Pre-proof Journal Pre-proof - 3 - Jafarzadeh A. et al. severe coronavirus infections, while highlighting potential therapeutic interventions to attenuate macrophage -related inflammatory reactions in possible approaches for COVID -19 treatment. In mucosal respiratory infections, alveolar macrophages serve as the first anti -viral defense through production type I IFNs. Monocytes/macrophages are the principal leukocytes attracted to the alveolar space in the initial response to respiratory viral infection. Monocytes and macrophages may be directly infected by SARS -CoV -2 through ACE2 -dependent process or indirectly infected via ACE2 -independent pathways using L -SIGN, DC -SIGN, CD147, ADE, and phagocytosis of virus - containing apoptotic bodies. SARS -CoV -2 can effectively suppress the anti -viral IFN response in monocytes and macrophages. As DCs, monocytes, and macrophages can act as APCs, the SARS -CoV -2 infection of these cells impairs the anti -viral adaptive immune responses. Upon infection, monocytes migrate to tissues where they become infected resident macrophages, allowing viruses to spread through all organs and tissues. Both infected - and uninfected macrophages can be found in the lungs of patients with COVID -19. Monocytes and macrophages can communicate with other cell types via direct cell -cell contacts, leading to the virus dissemination. The SARS -CoV - 2 -infected monocytes and macrophages can produce large amounts of numerous types of pro -inflammatory cytokines and chemokines , which contribute to the local tissue inflammation and Journal Pre-proof Journal Pre-proof - 32 - Jafarzadeh A. et al. dangerous systemic inflammatory response as named cytokine storm. Low expression of ACE2 by monocytes/macrophages of COVID -19 patients may also promote pathological reactions due to pro -inflammatory properties of angiotensin II and dysfunction of the renin -angiotensin system (RAS). Both local tissue inflammation and cytokine storm play a fundamental role in the development of COVID -19 -related complications, such ARDS, which is the main cause of death in SARS -CoV - 2 -infected patients (Figure 3B) . Although the modulation of macrophage activation may be considered as a promising therapeutic approach for COVID -19, a better understanding of macrophage polarization and heterogeneity during COVID -19 is required. Moreover, the patterns of the macrophage polarization may vary during the different stages of the COVID -19 and need to be clarified in future researches. Various types of macrophages can perform a decisive role in the outcome of the COVID -19. Since macrophage polarization is a reversible process, it is necessary to clarify the factors affecting macrophage plasticity during COVID -19 and how to manipulate macrophage plasticity in a favourable direction. Moreover, macrophages from different organs may express different markers. The better understanding of which subsets of monocytes/macrophages drive disease pathology is important for the development of proper therapeutic interventions [103]. Reference & Source information: https://www.sciencedirect.com Read More on :

  • The role of chest computed tomography in the management of COVID-19: A review of results and recommendation

    The use of chest computed tomography (CT) has been indicated as an important tool for the detection and management of COVID-19. The use of chest CT has been recommended as an effective form of initial screening and monitoring of the disease progression, due to the primary involvement of the respiratory system. Chest CT is a routine imaging tool for the diagnosis of pneumonia and is a simple test that is widely available and provides a fast diagnosis. The goal of this study is to evaluate this potential by reviewing the role of chest CT thus far in the detection and management of COVID-19. Numerous studies reviewed in this paper largely concur in their findings that the early hallmarks of COVID-19 infection are ground-glass opacities (GGOs), often with a bilateral and peripheral lung distribution. In addition, most studies demonstrated similar CT findings related to the progression of the disease, starting with GGOs in early disease, followed by the development of crazy paving in middle stages and finally increasing consolidation in the later stages of the disease. Studies have reported a low rate of misdiagnosis by chest CT, as well as a high rate of misdiagnosis by the rRT-PCR tests. Specifically, chest CT provides more accurate results in the early stages of COVID-19, when it is critical to begin treatment as well as isolate the patient to avoid the spread of the virus. While rRT-PCR will probably remain the definitive final test for COVID-19, until it is more readily available and can consistently provide higher sensitivity, the use of chest CT for early-stage detection has proven valuable in avoiding misdiagnosis as well as monitoring the progression of the disease. With the understanding of the role of chest CT, researchers are beginning to apply deep learning and other algorithms to differentiate between COVID-19 and non-COVID-19 CT scans, to determine the severity of the disease to guide the course of treatment, and investigate numerous additional COVID-19 applications. Most studies demonstrated similar CT findings related to the progression of the disease, starting with GGOs in early disease, followed by the development of crazy paving in middle stages and finally increasing consolidation in the later stages of the disease. Finally, studies agree in the absence of ancillary chest CT findings such as lymphadenopathy, pleural effusions, pulmonary nodules, and lung cavitation. Studies have reported a low rate of misdiagnosis by chest CT, as well as a high rate of misdiagnosis by the rRT-PCR tests. Specifically, chest CT provides more accurate results in the early stages of COVID-19, when it is critical to begin treatment as well as isolate the patient to avoid the spread of the virus. While rRT-PCR will probably remain the definitive final test for COVID-19 until it is more readily available and can consistently provide higher sensitivity, the use of chest CT for early-stage diagnosis and isolation has proven valuable in avoiding misdiagnosis and controlling the spread as well as monitoring the progression of the disease. To further the role of chest CT and the computer-assisted detection process, researchers are beginning to apply deep learning and other algorithms to differentiate between COVID-19 and non-COVID-19 CT scans, determine the severity of the disease to guide the course of treatment, and investigate numerous additional COVID-19 applications. The goal of this review-in-brief is to facilitate the research in imaging technology development to benefit the detection and monitoring of COVID-19. Reference & source information: https://journals.sagepub.com Read More on :

  • Interaction of the Coronavirus Nucleoprotein with Nucleolar Antigens and the Host Cell

    The interaction of viral proteins with nucleolar antigens may account for why viral proteins have been observed in the nucleolus and may also explain the viral exploitation of nucleolar function, leading to alterations in host cell transcription, translation, and disruption of the host cell cycle to facilitate viral replication. In this study we wanted to investigate whether coronavirus N proteins interacted with two nucleolar antigens, fibrillarin and nucleolin. Interaction with either or both of these antigens might explain our previous observations that coronavirus N proteins localized to the nucleolus (26, 64). Because proteins that localize to the nucleolus have been implicated in cell growth and the cell cycle (11, 40, 41), we also wished to investigate whether coronavirus N proteins affect cell division. Our data indicated that rather than adopting its normal (globular) Christmas tree-like appearance (5), in infected cells fibrillarin was distributed throughout the nucleolus and was possibly more concentrated in the nucleolar periphery. Transfection of either HeLa or Vero cells with plasmids that expressed either the IBV (type III coronavirus) or MHV (type II coronavirus) N proteins also resulted in a change in distribution of fibrillarin, in a similar manner to that observed in virus-infected cells. However, unlike HIV Rev protein, which localizes to the nucleolus with a pattern similar to fibrillarin (16) (determined by confocal microscopy), the coronavirus N protein localized uniformly throughout the nucleolus (see, e.g., Fig. 3F) (26, 64). The redistribution of fibrillarin, as a consequence of virus infection, is not unique to coronaviruses. Infection of cells with adenovirus also resulted in the redistribution of fibrillarin (46). To our knowledge this is the first time this has been demonstrated for an RNA virus. The reason for reorganization of fibrillarin to the perinucleolar region is unknown; however, the perinucleolar compartment has been implicated to play a role in transcription and in RNA metabolism in the host cell (28). To investigate whether the coronavirus N protein also associates with fibrillarin in the cytoplasm, experiments with a GFP-fibrillarin fusion protein indicated that both fibrillarin and IBV or MHV N protein colocalized in the perinuclear region and nucleolus (e.g., Fig. 6C and 7C, respectively). The nucleolar functions of fibrillarin are well established and include a role in ribosome assembly (60) and, as a factor of the nucleolus, in cell cycle regulation (11). Experiments that blocked fibrillarin with antibody prevented the translocation of fibrillarin to the nucleoli and resulted in the reduction or inhibition of PolI transcription (19); by redistributing fibrillarin N protein might have a similar effect. Alternatively, by interacting with fibrillarin, N protein could potentially affect ribosomal biogenesis and, therefore, have a concomitant effect on host cell translation. During MHV infection, host cell translation is decreased, although translation of viral mRNAs is either unaffected or upregulated (24, 55). N protein may therefore interact with nucleolar components to improve translation of virus mRNAs, perhaps by sequestering ribosomes (or parts thereof) to viral mRNAs (26). Unfortunately, from the point of view of this study, the monoclonal antibody against nucleolin, used in immunofluorescence, only recognized human nucleolin (in accordance with the manufacturer’s guidelines [Leinco Technologies]), and this limited the study of possible redistribution of nucleolin by N protein to HeLa cells which expressed MHV N protein. While our data suggested that nucleolin was not reorganized in these cells, it is not possible to conclude that this does not occur in virus-infected cells or with other coronavirus N proteins expressed in species-specific cell types. For example, nucleolin is retained in the cytoplasm in poliovirus-infected cells (62), probably because cytoplasmic-nuclear trafficking is prevented (23), and adenovirus infection results in the redistribution of nucleolin to the cytoplasm (38). Binding studies with purified immobilized phosphorylated or nonphosphorylated IBV N protein and nuclear extracts prepared from Vero cells indicated that there was a direct interaction between N protein and nucleolin (Fig. 8E, lanes 1 and 3, respectively). Two recombinant His-tagged proteins were used to investigate the specificity of nucleolin binding to N protein, HIV core (p24) protein, and DcuR, a DNA-binding protein isolated from E. coli (22). Nucleolin did not bind to either of these immobilized proteins or to the NTA beads in the absence of protein, indicating that nucleolin specifically interacted with N protein. Interestingly, the data indicated that immobilized Nphos protein bound more nucleolin than Nnonphos protein, a finding that is contrary to what would be predicted if the protein associated by electrostatic charge alone. Reference & Source information: https://www.ncbi.nlm.nih.gov/ Read more on :

  • Vital Information on Mitigating the Spread of COVID-19

    The virus is not a living organism, but a protein molecule (DNA) covered by a protective layer of lipid (fat), which, when absorbed by the cells of the ocular, nasal or buccal mucosa, changes their genetic code. (mutation) and convert them into aggressors and multiplier cells. Since the virus is not a living organism but a protein molecule, it is not killed, but decays on its own. The disintegration time depends on the temperature, humidity and type of material where it lies. The virus is very fragile; the only thing that protects it is a thin outer layer of fat. That is why any soap or detergent is the best remedy, because the foam CUTS the FAT (that is why you have to rub so much: for 20 seconds or more, to make a lot of foam). By dissolving the fat layer, the protein molecule disperses and breaks down on its own. The virus CANNOT go through healthy skin. HEAT melts fat; this is why it is so good to use water above 25 degrees Celsius for washing hands, clothes and everything. In addition, hot water makes more foam and that makes it even more useful. Alcohol or any mixture with alcohol over 65% DISSOLVES ANY FAT, especially the external lipid layer of the virus. Any mix with 1 part bleach and 5 parts water directly dissolves the protein, breaks it down from the inside. Oxygenated water helps long after soap, alcohol, and chlorine because peroxide dissolves the virus protein, but you have to use it pure and it hurts your skin. NO BACTERICIDE SERVES. The virus is not a living organism like bacteria; they cannot kill what is not alive with antibiotics, but quickly disintegrate its structure with everything said. NEVER shake used or unused clothing, sheets or cloth. While it is glued to a porous surface, it is very inert and disintegrates only between 3 hours (fabric and porous), 4 hours (copper, because it is naturally antiseptic; and wood, because it removes all the moisture and does not let it peel off and disintegrates), 24 hours (cardboard), 42 hours (metal) and 72 hours (plastic). But if you shake it or use a feather duster, the virus molecules float in the air for up to 3 hours and can lodge in your nose. The virus molecules remain very stable in external cold, or artificial as air conditioners in houses and cars. They also need moisture to stay stable, and especially darkness. Therefore, dehumidified, dry, warm and bright environments will degrade it faster. UV LIGHT on any object that may contain it breaks down the virus protein. For example, to disinfect and reuse a mask is perfect. Be careful, it also breaks down collagen (which is protein) in the skin, eventually causing wrinkles and skin cancer. Vinegar is NOT useful because it does not break down the protective layer of fat. NO SPIRITS, NOR VODKA, serve. The strongest vodka is 40% alcohol, and you need 65%. LISTERINE IF IT SERVES! It is 65% alcohol. The more confined the space, the more concentration of the virus there can be. The more open or naturally ventilated, the less is the concentration. This is super said, but you have to wash your hands before and after touching mucosa, food, locks, knobs, switches, remote control, cell phone, watches, computers, desks, TV, etc and when using the bathroom. You have to HUMIDIFY HANDS DRY from so much washing them because the molecules can hide in the micro cracks. The thicker the moisturizer, the better. Also, keep your NAILS SHORT so that the virus does not hide there. Sources: John Hopkins University, Harvard University Studies, Harvard Society of Fellows.

  • Potential effects of curcumin in the treatment of COVID-19 infection

    Punitha It's a wonderful article and Thank you so much for sharing this information Keep it up 😊

  • Investigation into SARS-CoV-2 Resistance of Compounds in Garlic Essential Oil

    Eighteen active substances, including 17 organosulfur compounds found in garlic essential oil (T), were identified by GC−MS analysis. For the first time, using the molecular docking technique, we report the inhibitory effect of the considered compounds on the host receptor angiotensin-converting enzyme 2 (ACE2) protein in the human body that leads to a crucial foundation about coronavirus resistance of individual compounds on the main protease (PDB6LU7) protein of SARS-CoV-2. The results show that the 17 organosulfur compounds, accounting for 99.4% contents of the garlic essential oil, have strong interactions with the amino acids of the ACE2 protein and the main protease PDB6LU7 of SARS-CoV2. The strongest anticoronavirus activity is expressed in allyl disulfide and allyl trisulfide, which account for the highest content in the garlic essential oil (51.3%). Interestingly, docking results indicate the synergistic interactions of the 17 substances, which exhibit good inhibition of the ACE2 and PDB6LU7 proteins. The results suggest that the garlic essential oil is a valuable natural antivirus source, which contributes to preventing the invasion of coronavirus into the human body. Conclusion This study proposes a potential approach to the use of natural essential oils, in general, and garlic essential oil, in particular, to tackle the current pandemic SARS-CoV-2. The compounds in the garlic essential oil inhibit the ACE2 protein, leading the virus to lose the host receptor and attacking the PDB6LU7protein—the main protease of SARS-CoV-2—at the same time. This prevents protein maturation of the virus and the spread of infection. Docking simulation suggests the active binding site of most active compounds in garlic essential oil with the ACE2 protein and the PDB6LU7protein. From the analysis of the docking data, it is revealed that 17 (T1–T17) out of 18 compounds of the garlic essential oil are capable of inhibiting ACE2 and resisting SARS-CoV-2 and that the total content of these 17 compounds accounts for 99.4% composition of the garlic essential oil. The docking score (DS) energy of compounds for the ACE2 protein ranges from −14.06 to −7.89 kcal·mol–1, and the DS energy of compounds for the PDB6LU7protein of SARS-CoV-2 ranges from −15.32 to −11.68 kcal·mol–1. The order of active compounds inhibiting the ACE2 protein is as follows:T5 = T11 > T1 = T2 > T4 > T8 > T9 > T12 > T13 > T14 > T15 > T3 > T7 > T10 > T16 > T17 > T6. Meanwhile, the order of active compounds resisting SARS-CoV-2 isT2 = T1 > T5 > T4 > T11 > T15 > T8 > T16 > T9 > T12 > T13 > T3 > T6 > T7 > T10 > T14 > T17. The synergistic interactions of 17 substances of the garlic essential oil exhibited good inhibition on the ACE2 protein (host receptor of the virus) and the PDB6LU7protein of the virus. This study opens the door toward the use of the garlic essential oil in discovering and treating SARS-CoV-2 to prevent the current pandemic. Reference & Source Information: https://pubs.acs.org/ Read more on :

  • Potential effects of curcumin in the treatment of COVID-19 infection

    Traditional Methods of tackling Covid-19. Thanks for Sharing