SARS-CoV-2 and the Possible Role of Raf/MEK/ERK Pathway in Viral Survival: Is This a Potential Therapeutic Strategy for COVID-19?

Ghasemnejad Berenji, M and Pashapour, S (2021) SARS-CoV-2 and the Possible Role of Raf/MEK/ERK Pathway in Viral Survival: Is This a Potential Therapeutic Strategy for COVID-19? Pharmacology, 106. pp. 119-121.

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Abstract

In late 2019, a sudden rise in respiratory-related disease cases in China triggered the identification of its source as a novel corona virus, termed severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The disease caused by novel SARS-CoV-2 is named as CO- VID-19 by the World Health Organization [1]. The culprit virus belongs to the Coronaviridae family of coronaviruses that caused 2 other outbreaks, namely, severe acute respiratory syndrome (SARS) in 2002 [2] and Middle East respiratory syndrome in 2012 [3]. As the survival of every virus depends on its host cell, the understanding of cellular functions such as signaling pathways that are essential for viral replication may be suitable to define targets for antiviral therapy and pave the way toward effective drugs against essential cellular activities supporting viral replication [4]. In this regard, we have focused on the Raf/ MEK/ERK signaling pathway, which is probably one of the most well-known signal transduction pathways among biologists because of its implication in a wide variety of cellular functions such as cell proliferation, cell cycle arrest, and apoptosis [5]. The mechanism of this pathway is initiated by G protein-coupled receptors, which leads to the phosphorylation of downstream molecules and activates the serine threonine kinase Raf (dual specificity kinase MEK and MAPK/ERK). ERK phosphorylates various substrates, transforms the signals, and follows different functions in cells [6]. Hence, it is not surprising that several DNA and RNA viruses inherit this pathway, apart from an initial activation upon viral attachment, for various steps in the viral life cycle [7]. Consequently, the kinetic of pathway activation is highly dynamic [8]. For example, herpes simplex type-1 virus-induced activation of the Raf/MEK/ERK pathway is used for cytoskeleton rearrangement during entry [9], JC polyomavirus requires ERK activation for viral transcription [10], and influenza A virus hijacks Raf/MEK/ERK activity for efficient viral ribonucleoprotein export [11, 12]. Ebola virus glycoprotein-induced cytotoxicity

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