Cannabinoids receptors in Covid-19: Perpetrators and victims.

COVID-19 is caused by SARS-CoV-2 and leads to acute lung injury (ALI), acute respiratory distress syndrome (ARDS), and extrapulmonary manifestations in severely affected cases. However, most of the affected cases are mild or asymptomatic. Cannabinoids (CBs) such as tetrahydrocannabinol (THC) and cannabidiol (CBD), which act on G-protein-coupled receptors called CB1 and CB2, have anti-inflammatory effects. Many published studies show that CBs are effective in various inflammatory disorders, viral infections, and attenuation of ALI and ARDS. Therefore, the aim of the present narrative review was to summarize the possible immunological role of CBs in COVID-19. The effects of CBs are controversial, although they have beneficial effects via CB2 receptors and adverse effects via CB1 receptors against ALI, ARDS, and hyperinflammation, which are hallmarks of COVID-19. The present narrative review has shown that CBs effectively manage ALI and ARDS by suppressing pro-inflammatory cytokines, which are common in COVID-19. Therefore, CBs may be used to manage COVID-19 because of their potent anti-inflammatory effects with suppression of pro-inflammatory cytokines and inhibition of inflammatory signaling pathways.

SARS‐CoV‐2 induced HDL dysfunction may affect the host's response to and recovery from COVID‐19

Introduction Covid‐19 is linked with the development of cardio‐metabolic disorders, including dyslipidemia, dysregulation of high‐density lipoprotein (HDL), and low‐density lipoprotein (LDL). Furthermore, SARS‐Co‐2 infection is associated with noteworthy changes in lipid profile, which is suggested as a possible biomarker to support the diagnosis and management of Covid‐19. Methods This paper adopts the literature review method to obtain information about how Covid‐19 affects high‐risk group patients and may cause severe and critical effects due to the development of acute lung injury and acute respiratory distress syndrome. A narrative and comprehensive review is presented. Results Reducing HDL in Covid‐19 is connected to the disease severity and poor clinical outcomes, suggesting that high HDL serum levels could benefit Covid‐19. SARS‐CoV‐2 binds HDL, and this complex is attached to the co‐localized receptors, facilitating viral entry. Therefore, SARS‐CoV‐2 infection may induce the development of dysfunctional HDL through different mechanisms, including induction of inflammatory and oxidative stress with activation of inflammatory signaling pathways. In turn, the induction of dysfunctional HDL induces the activation of inflammatory signaling pathways and oxidative stress, increasing Covid‐19 severity. Conclusions Covid‐19 is linked with the development of cardio‐metabolic disorders, including dyslipidemia in general and dysregulation of high‐density lipoprotein and low‐density lipoprotein. Therefore, the present study aimed to overview the causal relationship between dysfunctional high‐density lipoprotein and Covid‐19. While Covid‐19 is linked with the development of cardio‐metabolic disorders, including dyslipidemia and dysregulation of high‐density lipoprotein and low‐density lipoprotein, this study aimed to overview the causal relationship between dysfunctional high‐density lipoprotein and Covid‐19.

Potential role of tirzepatide towards Covid-19 infection in diabetic patients: a perspective approach.

In Covid-19, variations in fasting blood glucose are considered a distinct risk element for a bad prognosis and outcome in Covid-19 patients. Tirazepatide (TZT), a dual glucagon-like peptide-1 (GLP-1)and glucose-dependent insulinotropic polypeptide (GIP) receptor agonist may be effective in managing Covid-19-induced hyperglycemia in diabetic and non-diabetic patients. The beneficial effect of TZT in T2DM and obesity is related to direct activation of GIP and GLP-1 receptors with subsequent improvement of insulin sensitivity and reduction of body weight. TZT improves endothelial dysfunction (ED) and associated inflammatory changes through modulation of glucose homeostasis, insulin sensitivity, and pro-inflammatory biomarkers release. TZT, through activation of the GLP-1 receptor, may produce beneficial effects against Covid-19 severity since GLP-1 receptor agonists (GLP-1RAs) have anti-inflammatory and pulmoprotective implications in Covid-19. Therefore, GLP-1RAs could effectively treat severely affected Covid-19 diabetic and non-diabetic patients. Notably, using GLP-1RAs in T2DM patients prevents glucose variability, a common finding in Covid-19 patients. Therefore, GLP-1RAs like TZT could be a therapeutic strategy in T2DM patients with Covid-19 to prevent glucose variability-induced complications. In Covid-19, the inflammatory signaling pathways are highly activated, resulting in hyperinflammation. GLP-1RAs reduce inflammatory biomarkers like IL-6, CRP, and ferritin in Covid-19 patients. Therefore, GLP-1RAs like TZ may be effective in Covid-19 patients by reducing the inflammatory burden. The anti-obesogenic effect of TZT may reduce Covid-19 severity by ameliorating body weight and adiposity. Furthermore, Covid-19 may induce substantial alterations in gut microbiota. GLP-1RA preserves gut microbiota and prevents intestinal dysbiosis. Herein, TZT, like other GLP-1RA, may attenuate Covid-19-induced gut microbiota alterations and, by this mechanism, may mitigate intestinal inflammation and systemic complications in Covid-19 patients with either T2DM or obesity. As opposed to that, glucose-dependent insulinotropic polypeptide (GIP) was reduced in obese and T2DM patients. However, activation of GIP-1R by TZT in T2DM patients improves glucose homeostasis. Thus, TZT, through activation of both GIP and GLP-1, may reduce obesity-mediated inflammation. In Covid-19, GIP response to the meal is impaired, leading to postprandial hyperglycemia and abnormal glucose homeostasis. Therefore, using TZT in severely affected Covid-19 patients may prevent the development of glucose variability and hyperglycemia-induced oxidative stress. Moreover, exaggerated inflammatory disorders in Covid-19 due to the release of pro-inflammatory cytokines like IL-1ß, IL-6, and TNF-α may lead to systemic inflammation and cytokine storm development. Besides, GIP-1 inhibits expression of IL-1ß, IL-6, MCP-1, chemokines and TNF-α. Therefore, using GIP-1RA like TZT may inhibit the onset of inflammatory disorders in severely affected Covid-19 patients. In conclusion, TZT, through activation of GLP-1 and GIP receptors, may prevent SARS-CoV-2-induced hyperinflammation and glucose variability in diabetic and non-diabetic patients.

SARS-COV-2 infection and Parkinson's disease: Possible links and perspectives.

Parkinson's disease (PD) is a neurodegenerative disorder characterized by the progressive loss of dopaminergic neurons in the substantia nigra. The hallmarks are the presence of Lewy bodies composed mainly of aggregated α-synuclein and immune activation and inflammation in the brain. The neurotropism of SARS-CoV-2 with induction of cytokine storm and neuroinflammation can contribute to the development of PD. Interestingly, overexpression of α-synuclein in PD patients may limit SARS-CoV-2 neuroinvasion and degeneration of dopaminergic neurons; however, on the other hand, this virus can speed up the α-synuclein aggregation. The review aims to discuss the potential link between COVID-19 and the risk of PD, highlighting the need for further studies to authenticate the potential association. We have also overviewed the influence of SARS-CoV-2 infection on the PD course and management. In this context, we presented the prospects for controlling the COVID-19 pandemic and related PD cases that, beyond global vaccination and novel anti-SARS-CoV-2 agents, may include the development of graphene-based nanoscale platforms offering antiviral and anti-amyloid strategies against PD.

Mechanistic insight and possible mechanism of seizure in Covid-19: The nuances and focal points.

Coronavirus disease 2019 (COVID-19) is a primary respiratory disease with an alarming impact worldwide. COVID-19 is caused by severe acute respiratory syndrome coronavirus type 2 (SARS-CoV-2) and presents various neurological symptoms, including seizures. SARS-CoV-2 shows neuroinvasive and neurotropic capabilities through a neuronal angiotensin-converting enzyme 2 (ACE2), which is also highly expressed in both neuronal and glial cells. Therefore, SARS-CoV-2 can trigger neuroinflammation and neuronal hyperexcitability, increasing the risk of seizures'. Olfactory neurons could be an exceptional neuronal pathway for the neuroinvasion of respiratory viruses to access the central nervous system (CNS) from the nasal cavity, leading to neuronal injury and neuroinflammation. Although neuronal ACE2 has been widely studied, other receptors for SARS-CoV-2 in the brain have been proposed to mediate viral-neuronal interactions with subsequent neurological squeals. Thus, the objective of the present critical review was to find the association and mechanistic insight between COVID-19 and the risk of seizures.

Mixed storm in SARS‐CoV‐2 infection: A narrative review and new term in the Covid‐19 era

Coronavirus disease 2019 (Covid‐19) is caused by a novel severe acute respiratory syndrome coronavirus virus type 2 (SARS‐CoV‐2) leading to the global pandemic worldwide. Systemic complications in Covid‐19 are mainly related to the direct SARS‐CoV‐2 cytopathic effects, associated hyperinflammation, hypercytokinemia, and the development of cytokine storm (CS). As well, Covid‐19 complications are developed due to the propagation of oxidative and thrombotic events which may progress to a severe state called oxidative storm and thrombotic storm (TS), respectively. In addition, inflammatory and lipid storms are also developed in Covid‐19 due to the activation of inflammatory cells and the release of bioactive lipids correspondingly. Therefore, the present narrative review aimed to elucidate the interrelated relationship between different storm types in Covid‐19 and the development of the mixed storm (MS). In conclusion, SARS‐CoV‐2 infection induces various storm types including CS, inflammatory storm, lipid storm, TS and oxidative storm. These storms are not developing alone since there is a close relationship between them. Therefore, the MS seems to be more appropriate to be related to severe Covid‐19 than CS, since it develops in Covid‐19 due to the intricate interface between reactive oxygen species, proinflammatory cytokines, complement activation, coagulation disorders, and activated inflammatory signaling pathway. SARS‐CoV‐2 infection induces various storm types including cytokine storm (CS), inflammatory storm, lipid storm, thrombotic storm (TS), and oxidative storm. These storms are not developing alone since there is a close relationship between them. Therefore, the mixed storm seems to be more appropriate to be related to severe Covid‐19 than CS, since it develops in Covid‐19 due to the intricate interface between reactive oxygen species, proinflammatory cytokines, complement activation, coagulation disorders, and activated inflammatory signaling pathway

The potential role of scavenger receptor B type I (SR‐BI) in SARS‐CoV‐2 infection

Scavenger receptor type B I (SR‐BI), the major receptor for high‐density lipoprotein (HDL) mediates the delivery of cholesterol ester and cholesterol from HDL to the cell membrane. SR‐BI is implicated as a receptor for entry of severe acute respiratory syndrome coronavirus type 2 (SARS‐CoV‐2). SR‐BI is colocalized with the angiotensin‐converting enzyme 2 (ACE2) increasing the binding and affinity of SARS‐CoV‐2 to ACE2 with subsequent viral internalization. SR‐BI regulates lymphocyte proliferation and the release of pro‐inflammatory cytokines from activated macrophages and lymphocytes. SR‐BI is reduced during COVID‐19 due to consumption by SARS‐CoV‐2 infection. COVID‐19‐associated inflammatory changes and high angiotensin II (AngII) might be possible causes of repression of SR‐BI in SARS‐CoV‐2 infection. In conclusion, the downregulation of SR‐BI in COVID‐19 could be due to direct invasion by SARS‐CoV‐2 or through upregulation of pro‐inflammatory cytokines, inflammatory signaling pathways, and high circulating AngII. Reduction of SR‐BI in COVID‐19 look like ACE2 may provoke COVID‐19 severity through exaggeration of the immune response. Further studies are invoked to clarify the potential role of SR‐BI in the pathogenesis of COVID‐19 that could be protective rather than detrimental. We illustrate that Scavenger receptor type B I (SR‐BI), the major receptor for high‐density lipoprotein (HDL) mediates delivery of cholesterol ester and cholesterol from HDL to the cell membrane. SR‐BI is implicated as a receptor for entry of severe acute respiratory syndrome coronavirus type 2 (SARS‐CoV‐2). Downregulation of SR‐BI in COVID‐19 could be due to direct invasion by SARS‐CoV‐2 or through upregulation of pro‐inflammatory cytokines, inflammatory signaling pathways and high circulating AngII.

Immunological interactions in helminths-SARS CoV-2 coinfection: Could old enemy be a friend today?

Helminths are metazoan parasites affecting about one third of the worldwide population. Chronic helminth infections (CHIs) confer immunological tolerance to harmless and self-antigens mediated by regulatory T cells (Treg) that are up-regulated. In coronavirus disease 2019 (COVID-19), abnormal adaptive immune response and unrestrained innate immune response could result in local and systemic immune-mediated tissue damage. COVID-19 and CHIs establish complicated immune interactions due to SARS-CoV-2-induced immunological stimulation and CHIs-induced immunological tolerance. However, COVID-19 severity in patients with CHIs is mild, as immuno-suppressive anti-inflammatory cytokines counterbalance the risk of cytokine storm. Here, an overview of the interplay between helminths and COVID-19 severity is given. CHIs through helminth-derived molecules may suppress SARS-CoV-2 entry and associated hyperinflammation through attenuation of the TLR4/NF-kB signalling pathway. In addition, CHIs may reduce the COVID-19 severity by reducing the SARS-CoV-2 entry points at ACE2/DPP4/CD147 axis in the initial phase and immunomodulation in the late phase of the disease by suppressing TLR4/NF-kB signalling pathway.

Mixed storm in SARS-CoV-2 infection: A narrative review and new term in the Covid-19 era.

Coronavirus disease 2019 (Covid-19) is caused by a novel severe acute respiratory syndrome coronavirus virus type 2 (SARS-CoV-2) leading to the global pandemic worldwide. Systemic complications in Covid-19 are mainly related to the direct SARS-CoV-2 cytopathic effects, associated hyperinflammation, hypercytokinemia, and the development of cytokine storm (CS). As well, Covid-19 complications are developed due to the propagation of oxidative and thrombotic events which may progress to a severe state called oxidative storm and thrombotic storm (TS), respectively. In addition, inflammatory and lipid storms are also developed in Covid-19 due to the activation of inflammatory cells and the release of bioactive lipids correspondingly. Therefore, the present narrative review aimed to elucidate the interrelated relationship between different storm types in Covid-19 and the development of the mixed storm (MS). In conclusion, SARS-CoV-2 infection induces various storm types including CS, inflammatory storm, lipid storm, TS and oxidative storm. These storms are not developing alone since there is a close relationship between them. Therefore, the MS seems to be more appropriate to be related to severe Covid-19 than CS, since it develops in Covid-19 due to the intricate interface between reactive oxygen species, proinflammatory cytokines, complement activation, coagulation disorders, and activated inflammatory signaling pathway.

The potential role of scavenger receptor B type I (SR-BI) in SARS-CoV-2 infection.

Scavenger receptor type B I (SR-BI), the major receptor for high-density lipoprotein (HDL) mediates the delivery of cholesterol ester and cholesterol from HDL to the cell membrane. SR-BI is implicated as a receptor for entry of severe acute respiratory syndrome coronavirus type 2 (SARS-CoV-2). SR-BI is colocalized with the angiotensin-converting enzyme 2 (ACE2) increasing the binding and affinity of SARS-CoV-2 to ACE2 with subsequent viral internalization. SR-BI regulates lymphocyte proliferation and the release of pro-inflammatory cytokines from activated macrophages and lymphocytes. SR-BI is reduced during COVID-19 due to consumption by SARS-CoV-2 infection. COVID-19-associated inflammatory changes and high angiotensin II (AngII) might be possible causes of repression of SR-BI in SARS-CoV-2 infection. In conclusion, the downregulation of SR-BI in COVID-19 could be due to direct invasion by SARS-CoV-2 or through upregulation of pro-inflammatory cytokines, inflammatory signaling pathways, and high circulating AngII. Reduction of SR-BI in COVID-19 look like ACE2 may provoke COVID-19 severity through exaggeration of the immune response. Further studies are invoked to clarify the potential role of SR-BI in the pathogenesis of COVID-19 that could be protective rather than detrimental.

Long COVID and risk of erectile dysfunction in recovered patients from mild to moderate COVID-19.

Patients with coronavirus disease 2019 (COVID-19) were shown to have reduced serum testosterone levels compared to healthy individuals. Low testosterone levels are linked with the development of erectile dysfunction (ED). In this case-controlled study, 20 healthy controls and 39 patients with ED 3 months after recovering from mild-to-moderate COVID-19 pneumonia were studied. The patients ranged in age from 31 to 47 years. To identify early and late COVID-19 infections, real-time polymerase-chain reaction (RT-PCR) and COVID-19 antibody testing were done. The levels of luteinizing hormone (LH), follicular stimulating hormone (FSH), total testosterone (TT), free testosterone (FT), free androgenic index (FAI), and sex hormone-binding globulin (SHBG) were measured. The sexual health inventory for patients (SHIM) score was used to measure the erectile function of the patients and controls. When compared to the controls, the TT serum level in long COVID-19 (LC) patients with ED was low (p = 0.01). In contrast to controls, FT and FAI were both lower in LC patients with ED. (p = 0.001). FSH serum levels did not significantly differ (p = 0.07), but in ED patients, LH serum levels were elevated. SHIM scores were associated with low TT (p = 0.30), FT (p = 0.09), and high LH (p = 0.76) in LC patients with ED. Male patients with decreased serum levels of LH and testosterone may have hypothalamic-pituitary-gonadal axis dysfunction, which could lead to the development of LC-induced ED. Therefore, an in-depth research is necessary to confirm the causal link between COVID-19 and ED in LC patients.

The potential role of SARS‐CoV‐2 infection in acute coronary syndrome and type 2 myocardial infarction (T2MI): Intertwining spread

Coronavirus disease 2019 (COVID‐19) is a novel pandemic caused by severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2). It has been shown that SARS‐CoV‐2 infection‐induced inflammatory and oxidative stress and associated endothelial dysfunction may lead to the development of acute coronary syndrome (ACS). Therefore, this review aimed to ascertain the link between severe SARS‐CoV‐2 infection and ACS. ACS is a spectrum of acute myocardial ischemia due to a sudden decrease in coronary blood flow, ranging from unstable angina to myocardial infarction (MI). Primary or type 1 MI (T1MI) is mainly caused by coronary plaque rupture and/or erosion with subsequent occlusive thrombosis. Secondary or type 2 MI (T2MI) is due to cardiac and systemic disorders without acute coronary atherothrombotic disruption. Acute SARS‐CoV‐2 infection is linked with the development of nonobstructive coronary disorders such as coronary vasospasm, dilated cardiomyopathy, myocardial fibrosis, and myocarditis. Furthermore, SARS‐CoV‐2 infection is associated with systemic inflammation that might affect coronary atherosclerotic plaque stability through augmentation of cardiac preload and afterload. Nevertheless, major coronary vessels with atherosclerotic plaques develop minor inflammation during COVID‐19 since coronary arteries are not initially and primarily targeted by SARS‐CoV‐2 due to low expression of angiotensin‐converting enzyme 2 in coronary vessels. In conclusion, SARS‐CoV‐2 infection through hypercytokinemia, direct cardiomyocyte injury, and dysregulation of the renin‐angiotensin system may aggravate underlying ACS or cause new‐onset T2MI. As well, arrhythmias induced by anti‐COVID‐19 medications could worsen underlying ACS. SARS‐CoV‐2 infection through hypercytokinemia, direct cardiomyocyte injury, and dysregulation of the renin‐angiotensin system may aggravate acute coronary syndrome (ACS) or cause new‐onset type 2 myocardial infarction. As well, arrhythmias induced by anti‐COVID‐19 medications could worsen ACS.

A perspective study of the possible impact of obeticholic acid against SARS-CoV-2 infection.

The causative agent of CoV disease 2019 is a new coronavirus CoV type 2, affecting the respiratory tract with severe manifestations (SARS-CoV-2). Covid-19 is mainly symptomless, with slight indications in about 85% of the affected cases. Many efforts were done to face this pandemic by testing different drugs and agents to make treatment protocols in different countries. However, the use of these proposed drugs is associated with the development of adverse events. Remarkably, the successive development of SARS-CoV-2 variants which could affect persons even they were vaccinated, prerequisite wide search to find efficient and safe agents to face SARS-CoV-2 infection. Obeticholic acid (OCA), which has anti-inflammatory effects, may efficiently treat Covid-19. Thus, the goal of this perspective study is to focus on the possible medicinal effectiveness in managing Covid-19. OCA is a powerful farnesoid X receptor (FXR) agonist possessing marked antiviral and anti-inflammatory effects. FXR is dysregulated in Covid-19 resulting in hyper-inflammation with concurrent occurrence of hypercytokinemia. Interestingly, OCA inhibits the reaction between this virus and angiotensin-converting enzyme type 2 (ACE2) receptors. FXR agonists control the expression of ACE2 and the inflammatory signaling pathways in this respiratory syndrome, which weakens the effects of Covid-19 disease and accompanied complications. Taken together, FXR agonists like OCA may reveal both direct and indirect impacts in the modulation of immune reaction in SARS-CoV-2 conditions. It is highly recommended to perform many investigations regarding different phases of the discovery of new drugs.

The potential role of SARS-CoV-2 infection in acute coronary syndrome and type 2 myocardial infarction (T2MI): Intertwining spread.

Coronavirus disease 2019 (COVID-19) is a novel pandemic caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). It has been shown that SARS-CoV-2 infection-induced inflammatory and oxidative stress and associated endothelial dysfunction may lead to the development of acute coronary syndrome (ACS). Therefore, this review aimed to ascertain the link between severe SARS-CoV-2 infection and ACS. ACS is a spectrum of acute myocardial ischemia due to a sudden decrease in coronary blood flow, ranging from unstable angina to myocardial infarction (MI). Primary or type 1 MI (T1MI) is mainly caused by coronary plaque rupture and/or erosion with subsequent occlusive thrombosis. Secondary or type 2 MI (T2MI) is due to cardiac and systemic disorders without acute coronary atherothrombotic disruption. Acute SARS-CoV-2 infection is linked with the development of nonobstructive coronary disorders such as coronary vasospasm, dilated cardiomyopathy, myocardial fibrosis, and myocarditis. Furthermore, SARS-CoV-2 infection is associated with systemic inflammation that might affect coronary atherosclerotic plaque stability through augmentation of cardiac preload and afterload. Nevertheless, major coronary vessels with atherosclerotic plaques develop minor inflammation during COVID-19 since coronary arteries are not initially and primarily targeted by SARS-CoV-2 due to low expression of angiotensin-converting enzyme 2 in coronary vessels. In conclusion, SARS-CoV-2 infection through hypercytokinemia, direct cardiomyocyte injury, and dysregulation of the renin-angiotensin system may aggravate underlying ACS or cause new-onset T2MI. As well, arrhythmias induced by anti-COVID-19 medications could worsen underlying ACS.

Dantrolene and ryanodine receptors in COVID-19: The daunting task and neglected warden.

Dantrolene (DTN) is a ryanodine receptor (RyR) antagonist that inhibits Ca2+ release from stores in the sarcoplasmic reticulum. DTN is mainly used in the management of malignant hyperthermia. RyRs are highly expressed in immune cells and are involved in different viral infections, including severe acute respiratory syndrome coronavirus type 2 (SARS-CoV-2), because Ca2+ is necessary for viral replication, maturation and release. DTN can inhibit the proliferation of SARS-CoV-2, indicating its potential role in reducing entry and pathogenesis of SARS-CoV-2. DTN may increase clearance of SARS-CoV-2 and promote coronavirus disease 2019 (COVID-19) recovery by shortening the period of infection. DTN inhibits N-methyl-D-aspartate (NMDA) mediated platelets aggregations and thrombosis. Therefore, DTN may inhibit thrombosis and coagulopathy in COVID-19 through suppression of platelet NMDA receptors. Moreover, DTN has a neuroprotective effect against SARS-CoV-2 infection-induced brain injury through modulation of NMDA receptors, which are involved in excitotoxicity, neuronal injury and the development of neuropsychiatric disorders. In conclusion, DTN by inhibiting RyRs may attenuate inflammatory disorders in SARS-CoV-2 infection and associated cardio-pulmonary complications. Therefore, DNT could be a promising drug therapy against COVID-19. Preclinical and clinical studies are warranted in this regards.

The Potential Effect of Dapsone on the Inflammatory Reactions in Covid-19: Staggering view.

Severe SARS-CoV-2 infection is linked with an overstated immune response with the succeeding release of pro-inflammatory cytokines and progression of the cytokine storm. In addition, severe SARS-CoV-2 infection is associated with the development of oxidative stress and coagulopathy. Dapsone (DPS) is a bacteriostatic antibiotic that has a potent anti-inflammatory effect. Thus, this mini-review aimed to elucidate the potential role of DPS in mitigating inflammatory disorders in Covid-19 patients. DPS inhibits neutrophil myeloperoxidase, inflammation, and neutrophil chemotaxis. Therefore, DPS could be effective against neutrophilia-induced complications in Covid-19. In addition, DPS could be effective in mitigating inflammatory and oxidative stress disorders by suppressing the expression of inflammatory signaling pathways and the generation of reactive oxygen species (ROS) correspondingly. In conclusion, DPS might be effective in the management of Covid-19 through the attenuation of inflammatory disorders. Therefore, preclinical and clinical studies are reasonable in this regard.

COVID-19 and corticosteroids: a narrative review.

It has been reported that corticosteroid therapy was effective in the management of severe acute respiratory syndrome (SARS) and the Middle East Respiratory Syndrome (MERS), and recently in coronavirus disease 2019 (COVID-19). Corticosteroids are potent anti-inflammatory drugs that mitigate the risk of acute respiratory distress syndrome (ARDS) in COVID-19 and other viral pneumonia, despite a reduction of viral clearance; corticosteroids inhibit the development of cytokine storm and multi-organ damage. The risk-benefit ratio should be assessed for critical COVID-19 patients. In conclusion, corticosteroid therapy is an effective way in the management of COVID-19, it reduces the risk of complications primarily acute lung injury and the development of ARDS. Besides, corticosteroid therapy mainly dexamethasone and methylprednisolone are effective in reducing the severity of COVID-19 and associated comorbidities such as chronic obstructive pulmonary diseases (COPD), rheumatoid arthritis, and inflammatory bowel disease (IBD).

Favipiravir in SARS-CoV-2 Infection: Is it Worth it?

Favipiravir is a potential antiviral drug undergoing clinical trials to manage various viral infections, including severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Favipiravir possesses antiviral properties against RNA viruses, including SARS-CoV-2. Unfortunately, these viruses do not have authorized antiviral drugs for the management of diseases resulting from their infection, hence the dire need to accentuate the discovery of antiviral drugs that are efficacious and have a broad spectrum. Favipiravir acts primarily by blocking inward and outward movements of the virus from cells. Favipiravir is a prodrug undergoing intracellular phosphorylation and ribosylation to form an active form, favipiravir-RTP, which binds viral RNA-dependent RNA polymerase (RdRp). Considering the novel mechanism of favipiravir action, especially in managing viral infections, it is vital to pay more attention to the promised favipiravir hold in the management of SARS-CoV-2, its efficacy, and dosage regimen, and interactions with other drugs. In conclusion, favipiravir possesses antiviral properties against RNA viruses, including COVID- 19. Favipiravir is effective against SARS-CoV-2 infection through inhibition of RdRp. Pre-clinical and large-scalp prospective studies are recommended for efficacy and long-term safety of favipiravir in COVID-19.