Hi Dr.
Please read this paper...
https://www.google.com/url?sa=t&source=web&cd=1&ved=2ahUKEwjxiMvfuoLpAhUJ3qQKHdaJDm8QFjAAegQIBxAC&url=https%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fpmc%2Farticles%2FPMC7138382%2F&usg=AOvVaw2DWh_tPzLQWap4nIH5VTuL
Hi Dr.
With the first reports on coronavirus disease 2019 (COVID-19), which is caused by the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the scientific community working in the field of type III IFNs (IFN-λ) realized that this class of IFNs could play an important role in this and other emerging viral infections. In this Viewpoint, we present our opinion on the benefits and potential limitations of using IFN-λ to prevent, limit, and treat these dangerous viral infections
Good morning Dr.
2/4
Interferon beta-1a, currently in use to treat multiple sclerosis, and interferon alfa-2b are both under investigation as potential treatments for people with COVID-19 coronavirus disease, the deadly respiratory pandemic caused by the SARS-nCoV-2 virus.
Essentially, when confronted with a virus, each cell shoots an emergency flare of interferon to tell the immune system to marshall its defenses.
Interferon Beta 1a, specifically, activates macrophages that engulf antigens and natural killer cells (NK cells), a type of immune T-Cell.
Those cells are integral in the innate immune system.
The theory is, interferon may be able to make the immune system stronger by turning on dormant parts and directing them toward the defense against SARS-nCoV-2's assault.
predicated on the principle of supplementing to compensate for insufficient IFN production or activity that might be actively blocked by the virus.
IFN-I are among the first cytokines produced during a viral infection. They are recognized by the IFNAR receptor present at the plasma membrane in most cell types. Interferon fixation on IFNAR induces the phosphorylation of transcriptional factors such as STAT1 and their relocalization to the nucleus, where they activate interferon-stimulated genes (ISG). Most ISGs are involved in inflammation, signaling and immunomodulation. They interfere with viral replication and spread by several mechanisms such as a slowdown of cell metabolism or secretion of cytokines which promote the activation of the adaptive immunity. ISGs include PRRs, which further sensitize the cell to pathogens, proteins which decrease membrane fluidity, preventing viral egress or membrane fusion, and antivirals that specifically inhibit one step of the viral cycle . IFN-I thus play a major role in antiviral immunity. Because of their immunomodulatory properties, IFN-I are used in the treatment of numerous diseases: for example, subcutaneous injections of IFNβ have been used for more than 20 years for the treatment of patients with multiple sclerosis. The role of IFNβ in the treatment of multiple sclerosis is still debated and likely results partly from the down-regulation of the major histocompatibility complex (MHC) class II expression in antigen-presenting cells, the induction of IL-10 secretion and the inhibition of T-cell migration.
Article Type 1 interferons as a potential treatment against COVID-19
https://www.preprints.org/manuscript/202003.0206/v1
Effective innate immune response against viral infection relies heavily on the interferon (IFN) type I responses and its downstream cascade that culminates in controlling viral
replication and induction of effective adaptive immune response.
https://www.researchgate.net/deref/https%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fpmc%2Farticles%2FPMC7138382%2F
Hi
Article Type 1 interferons as a potential treatment against COVID-19
Hi dear Alaa.
Actually any immune response can lead to a dozens of cytokine Production. In cases of COVID-19 many cytokines seem to be make the infection more woresn and may lead to death in severe and Critical cases and this may called cytokines storm
BR
IFN-I thus play a major role in antiviral immunity. Because of their immunomodulatory properties, IFN-I are used in the treatment of numerous diseases: for example, subcutaneous injections of IFNβ have been used for more than 20 years for the treatment of patients with multiple sclerosis. The role of IFNβ in the treatment of multiple sclerosis is still debated and likely results partly from the down-regulation of the major histocompatibility complex (MHC) class II expression in antigen-presenting cells, the induction of IL-10 secretion and the inhibition of T-cell migration (Jakimovski et al., 2018).
https://www.researchgate.net/publication/340494206_Type_1_interferons_as_a_potential_treatment_against_COVID-19
Article Type 1 interferons as a potential treatment against COVID-19
Dear Dr.
https://www.researchgate.net/publication/340494206_Type_1_interferons_as_a_potential_treatment_against_COVID-19
Hi Dr.
Please read this paper...
https://www.google.com/url?sa=t&source=web&cd=1&ved=2ahUKEwjxiMvfuoLpAhUJ3qQKHdaJDm8QFjAAegQIBxAC&url=https%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fpmc%2Farticles%2FPMC7138382%2F&usg=AOvVaw2DWh_tPzLQWap4nIH5VTuL
there is just a potential role of type 1 interferons in treatment of COVID19.Nothing definite
hello dr
It can protect neighboring cells from infection with the virus
The role of IFNβ in the treatment of multiple sclerosis is still debated and likely results partly from the down-regulation of the major histocompatibility complex (MHC) class II expression in antigen-presenting cells, the induction of IL-10 secretion and the inhibition of T-cell migration
Dear Dr,
Type 1 interferons have a broad antiviral activity in vitro and are currently evaluated in a clinical trial to treat MERS-CoV. In this review, we discuss preliminary data concerning the potential activity of type 1 interferons on SARS-CoV-2, and the relevance of evaluating these molecules in clinical trials for the treatment of COVID-19.
With the first reports on coronavirus disease 2019 (COVID-19), which is caused by the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the scientific community working in the field of type III IFNs (IFN-λ) realized that this class of IFNs could play an important role in this and other emerging viral infections. In this Viewpoint, we present our opinion on the benefits and potential limitations of using IFN-λ to prevent, limit, and treat these dangerous viral infections.
https://pubmed.ncbi.nlm.nih.gov/32289152/
Preprint Therapeutic Approaches for COVID-19 Based on the Dynamics of...
Many interferon play role in preventation of viral infection.
Hi Dr.
I think the following link may help you
https://www.researchgate.net/deref/https%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fpmc%2Farticles%2FPMC7138382%2F
Article Type 1 interferons as a potential treatment against COVID-19
I read paper of dr. Lubna (It’s really good) .. please read it.
Article Type 1 interferons as a potential treatment against COVID-19
Type 1 interferons as a potential treatment against COVID-19
SARS-CoV-2 is a human coronavirus causing the COVID-19 disease. It emerged in China in December 2019 and rapidly propagated in numerous countries, having contaminated more than one million people and killing more than 55,000 up to April 3, 2020. Antiviral treatments are warranted to contain the epidemics. Several candidates are already being investigated, including type 1 interferon (IFN–I) (Martinez, 2020; Belhadi et al., 2020). Indeed, in the context of emerging viral infections, IFN-I are often evaluated (usually in combination with other drugs) before specific treatments are developed, due to their unspecific antiviral effects (Gao et al., 2010; Loutfy et al., 2003; Omrani et al., 2014). We aimed to review the evidence supporting the evaluation of IFN-1 in the treatment of coronaviruses and to discuss its potential in SARS-CoV-2.
Type 1 interferons (IFN–I) designate a group of cytokines comprising the ubiquitous α and β subtypes (themselves subdivided in several isoforms), as well as the ε, ω and κ subtypes (Samuel, 2001). They are secreted by various cell types, notably plasmacytoid dendritic cells, upon recognition of viral components by pattern recognition receptors (PRR) (Liu, 2005). IFN-I are thus among the first cytokines produced during a viral infection. They are recognized by the IFNAR receptor present at the plasma membrane in most cell types. Interferon fixation on IFNAR induces the phosphorylation of transcriptional factors such as STAT1 and their relocalization to the nucleus, where they activate interferon-stimulated genes (ISG). Most ISGs are involved in inflammation, signaling and immunomodulation. They interfere with viral replication and spread by several mechanisms such as a slowdown of cell metabolism or secretion of cytokines which promote the activation of the adaptive immunity. ISGs include PRRs, which further sensitize the cell to pathogens, proteins which decrease membrane fluidity, preventing viral egress or membrane fusion, and antivirals that specifically inhibit one step of the viral cycle (Schneider et al., 2014; Totura and Baric, 2012). IFN-I thus play a major role in antiviral immunity. Because of their immunomodulatory properties, IFN-I are used in the treatment of numerous diseases: for example, subcutaneous injections of IFNβ have been used for more than 20 years for the treatment of patients with multiple sclerosis. The role of IFNβ in the treatment of multiple sclerosis is still debated and likely results partly from the down-regulation of the major histocompatibility complex (MHC) class II expression in antigen-presenting cells, the induction of IL-10 secretion and the inhibition of T-cell migration (Jakimovski et al., 2018).
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https://www.synairgen.com/covid-19/
https://www.medrxiv.org/content/10.1101/2020.04.11.20061473v1
Carly G. K. Ziegler, et al. // SARS-CoV-2 receptor ACE2 is an interferon-stimulated gene in human airway epithelial cells and is detected in specific cell subsets across tissues // Cell, 2020, DOI: 10.1016/j.cell.2020.04.035
Article SARS-CoV-2 Receptor ACE2 Is an Interferon-Stimulated Gene in...
"A very significant discovery by the authors of this work is that the activity of ACE2 gene is stimulated by interferons. The authors showed in vitro experiment that type I and, to a lesser extent, type II interferons activate ACE2 synthesis in the basal cells of the upper respiratory tract, potentially creating new portals for virus penetration. Importantly, interferons are part of some COVID-19 treatment regimens as immune stimulants
In viral infections such as influenza, the expression of the ACE2 gene also increases in the upper respiratory tract cells, probably due to the production of interferons. (The authors have also tested this experiment by examining cells in nasal flushes of infected and uninfected people).
"ACE2 is also crucial to protect humans during various lung injuries," notes Jose Ordovas-Montañez of Boston Children's Hospital, one of the leading authors. - When it gets bigger, it's usually a productive response. But since the virus uses it as a target, we propose a hypothesis that the virus can exploit a normal protective response. (...) It is possible that in some patients, depending on time or dose, interferon may contain the virus, while in others interferon may contribute to infection.
These findings may lead to a number of new studies on angiotensin converting enzyme inhibitors. These drugs are now used to treat hypertension, which is known to increase the likelihood of heavier forms of COVID-19. The role of ACE inhibitors in the development of coronavirus infection is being actively discussed.
Some severe COVID-19 patients develop a cytokine storm, a sharp, potentially lethal reaction of the immune system. "It is possible that the cytokine storm observed is caused by the fact that interferon has not been able to limit the spread of the virus, so the lungs begin to call for help. That's what we're trying to understand now," explains Jose Ordovas-Montañez."
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Cytokine release syndrome (CRS) or cytokine storm syndrome (CSS) is a form of systemic inflammatory response syndrome (SIRS) that can be triggered by a variety of factors such as infections and certain drugs.[3] It occurs when large numbers of white blood cells are activated and release inflammatory cytokines, which in turn activate yet more white blood cells. CRS is also an adverse effect of some monoclonal antibody drugs, as well as adoptive T-cell therapies.[4][5] Severe cases have been called cytokine storms.[2] When occurring as a result of drug administration, it is also known as an infusion reaction.[1]
In addition to adoptive T-cell therapies, severe CRS or cytokine reactions can occur in a number of infectious and non-infectious diseases including graft-versus-host disease (GVHD), coronavirus disease 2019 (COVID-19), acute respiratory distress syndrome (ARDS), sepsis, Ebola, avian influenza, smallpox, and systemic inflammatory response syndrome (SIRS).[15]
Although, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is sufficiently cleared by the early acute phase anti-viral response in most individuals, some progress to a hyperinflammatory condition, often with life-threatening pulmonary involvement. This systemic hyperinflammation results in inflammatory lymphocytic and monocytic infiltration of the lung and the heart, causing ARDS and cardiac failure. Patients with fulminant COVID-19 and ARDS have classical serum biomarkers of CRS including elevated CRP, LDH, IL-6, and ferritin.[16]
https://en.wikipedia.org/wiki/Cytokine_release_syndrome
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Feng Z, et al. // The Use of Adjuvant Therapy in Preventing Progression to Severe Pneumonia in Patients with Coronavirus Disease 2019: A Multicenter Data Analysis. // medRxiv. April 10, 2020; DOI: 10.1101/2020.04.08.20057539
Preprint The Use of Adjuvant Therapy in Preventing Progression to Sev...
