Commentary - International Journal of Clinical Rheumatology (2023) Volume 18, Issue 8

Exploring Rheumatologist Perspectives on Therapy Options for COVID-19

Dimitris Sikivi*

Department of Internal Medicine, Rheumatology Clinic, University of Ioannina, Greece

*Corresponding Author:
Dimitris Sikivi
Department of Internal Medicine, Rheumatology Clinic, University of Ioannina, Greece

Received: 02-Aug-2023, Manuscript No. fmijcr-23-114495; Editor assigned: 04- Aug-2023, Pre-QC No. fmijcr-23-114495 (PQ); Reviewed: 18-Aug-2023, QC No. fmijcr-23-114495; Revised: 22-Aug- 2023, Manuscript No. fmijcr-23-114495 (R); Published: 29-Aug-2023, DOI: 10.37532/1758-4272.2023.18(8).227-230


The clinical movement of the serious intense respiratory example Covid 2 (SARS-CoV-2) to basic disease is related with a foundational and unrestrained dissident reaction of the instill and versatile exemption with the arrival of a plenty of proinflammatory cytokines selected "cytokine storm". Without even a trace of a powerful treatment, various off-marker specialists from the armamentarium of rheumatology are utilized. Then, according to the point of view of a rheumatologist, we will quibble the ongoing medicinal procedures in fundamentally sick cases with SARS-CoV-2 pneumonia. In this manner, we will quibble the specialists that mean to target viral section and its replication into the host cell and those affixing and focusing on the subversive reaction. Numerous agents have been utilized with promising outcomes in this setting, but not all have received approval from international authorities and institutions. SARS-CoV-2 monoclonal antibodies and remdesivir have been approved for use in the first step (viral entry), while corticosteroids and interleukin-6 inhibitors or Janus kinase inhibitors are currently used in the second step.


COVID-19 • Cytokine storm; SARS-CoV-2 • Proinflammatory cytokines


Severe acute respiratory pattern coronavirus- 2 (SARS-COV- 2), the cause of coronavirus complaint 2019 (COVID- 19), surfaced in China at the end of the year and has grown into an epidemic. Keywords: COVID- 19; SARS-CoV- 2 mAbs; Remdesivir; Colchicine; DMARDs; Dexamethasone. The objection has different clinical launches going from asymptomatic, or influenza like example (poor quality fever, sore throat, myalgias, arthralgias, exhaustion), yet additionally to the improvement of reciprocal pneumonia that can advance to hypoxia, dyspnea, respiratory disappointment, thrombotic diathesis, multiorgan disappointment and demise. It is allowed that the vulnerable response of the host plays a significant role in the complaint's pathophysiology and multiorgan dysfunction. Indeed, a systemic unrestrained seditious response of the ingrain and adaptive impunity leading to elevated inflammation known as cytokine release pattern (CRS) are associated with the clinical progression of the infection to critical illness. There's a unique powerless reaction to interferon (IFN) α, β and macrophage (Mφs) actuation, that outcomes in deferred polymorphonuclear (PMN) cell recovery prompting brought down viral simultaneousness. Proinflammatory cytokines like tumor necrosis factor (TNF), interleukin (IL) 1, IL-6, IL-12, IL-18, and chemokines are released as a result of this prolonged vulnerable cell stimulation. D-dimers, C-reactive protein (CRP), ferritin, and fibrinogen are examples of seditious proteins that are produced at high levels as a result. Later, a dysregulation of adaptive impunity with a decrease in CD4 and CD8 lymphocytes may occur. All the underneath may add to the obsessive elements of serious Coronavirus pneumonia communicated with rebellious invasions, verbose alveolar harm and microvascular apoplexy.

Methods and Materials

The SARS-CoV-2 virus is an enveloped contagion with a globular morphology and a genome made of single-stranded RNA (ssRNA). The SARS-CoV-2 genome encodes four primary proteins shaft(S), envelope (E), layer (M), and nucleocapside (N), too asnon- structure and appurtenant proteins. The two subunits S1 and S2 of the shaft protein prevent host cell irruption and attachment. S1 binds to the host cell's angiotensin converting enzyme receptor-2 (ACE2) via its receptor binding sphere (RBD). This starts a conformational change in S2 subunit that outcomes in disease have cell film emulsion and viral section. The viral passage can likewise be through endocytosis [1]. The genome of the contagion patch enters the cytoplasm of the host cell once it leaves the outside environment. By attaching to the ribosomes of the host, the contagion can directly produce its proteins and new genome in the cytoplasm by using its ssRNA, which translates the viral RNA into proteins for RNA polymerase. Through the RNA polymerase, little RNA sea shores are made, which will be perused by the host's ribosomes in the endoplasmic reticulum to assist with making up new underlying elements of the virus. As a result, new viral forms are created that can infect other cells and are released from the host cells via exocytosis. Additionally the disease engendering causes towel injury and initiation of the weak framework. Consequently, signals driven by the SARS-CoV-2(viral RNAs), microorganism related subatomic examples (PAMPs) and harm related atomic examples (DAMPs) (cell trash), follow up on occupant towel cells. In point of fact, the transmission of the virus via ACE2, Risk-Like Receptors (TLRs), and Node- Like Receptors (NLRs) results in the activation of host cells and the production of various pro-inflammatory cytokines. These cytokines follow up on their own receptors in commensurate cells, with farther cell actuation and a swelled item ofproinflammatory cytokines happens, acting in grumbling movement and crumbling [2, 3].

Coronavirus treatment

Coronavirus is another pestilence grievance with deadly issues, at times, and critical overall wellbeing outcomes. Since there are no specific medications to combat SARS-CoV-2 infection, treating COVID-19 is a difficult task for croakers and rheumatologists. As a result, a large number of off-marker medications from the arsenal of rheumatic conditions are now utilized in COVID- 19, and numerous trials have been published and are currently in progress. As portrayed in. There are a number of points that are implicit targets of SARSCoV- 2 infection following the viral entry into the host cell, its viral lifecycle, and cell activation. More specifically, the antiviral treatments in Steps 1 through 3 aim to slow down the viral replication and its cargo. In steps 4 through 8, the drugs are concentrated to reduce cytokine product by inhibiting cytokine cell receptor signaling and activation. Natural remedies and corticosteroids play a crucial role in reducing the seditious response in this setting [4, 5].

The inquiry which emerges' why to utilize these normal and otheranti-provocative specialists in an infectious grumbling? The answer comes from other well-known diseases like mixed cryoglobulineamia and viral hepatitis B and C, both of which are associated with vasculitis, particularly polyarteritis bumps. Here, besides of antiviral specialists, calming and immunomodulatory curatives are utilized. Then again, cases with immune system rheumatic circumstances (ARDs) are likewise portrayed by a dysregulation of the weak framework, where severalpro-fiery cytokines, comparable as TNFα, IL-1, IL-6, IL-17 and others have a huge pathogenetic impact in cases with rheumatoid joint pain (RA), spondyloarthopathies (Exercise center), and dissident entrail objection (IBD) [6, 7]. In terms of treatment, numerous medications have been developed, and the utilization of targeted curatives has made significant progress over the past two decades. The utilization of TNFα obstructions, IL-6 and Janus kinase (JAK) obstacles has upset the treatment of these circumstances. Similarly, cases with ARDs treated with cs, b as well as tsDMARDs, seem not to have an expanded danger of Coronavirus, contrasted with everybody. likewise, cases with ARDs treated with the underneath specialists, when contract SARS-CoV-2 disease, the objection is communicated with lower hospitalization, great issues and appears to be that these prescriptions might reduce the clinical course of Coronavirus [8-10].


In the last twice there has been a huge advancement of logical information, as regards to Coronavirus immunopathology and its treatment. Therefore, there is no evidence to recommend the use of any immunomodulatory or antiviral medication in nonhospitalized COVID-19 cases or in the early stages of the disease. In any case, in named sub gatherings of cases with danger elements of creating extreme Coronavirus, against SARS-CoV-2 mAbs might be thought of. There is no need for immunomodulatory or antiviral treatment in rehabilitated patients with SARSCoV 2 infection who do not require oxygen therapy. In opposite, in restored cases taking supplemental oxygen, on-obtrusive, or mechanical ventilation the utilization of remdesivir in mix with DX, regardless of the utilization of TCZ, or JAK obstructions, particularly BARI is mandatory. From a rheumatology point of view, the following immunomodulatory treatments offer new options for treating severe acute infection conditions that may benefit from them. However, each individual's vulnerable response to SARS-CoV-2 is unique, with distinct clinical phenotypes. Hence, it's a basic to decipher better the weak reaction against SARSCoV- 2 to additionally characterize new healing ways and methodologies.



Conflict of Interest

The authors say that they don't have any financial ties to the subject.


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