Abstract
COVID-19 pandemic has now become a challenging global public health concern, having higher risk of developing fatal respiratory disease due to severe inflammatory responses associated with the virus-mediated oxidative stress. The respiratory system is most preferred target organ for this novel virus as the lung is well oxygenated and having large surface area available to the virus for exposure and successively augmenting the health complications. Oxidative stress (OS) is an important factor causing metabolic and physiological alteration and various disease augmentations within the body. Respiratory viral infection has general consociation with cytokine production, inflammation, cell death and other pathophysiological processes which may be the result of perturbed redox balance. Apart from this, the presence of conditions likes aging, diabetes and hypertension and chronic obstructive pulmonary diseases (COPD) are the risk factor for making severity of such infection outcome. It has been well established that an overproduction of reactive oxygen species (ROS) and antioxidant mechanisms deprivation are vital step for viral replica production and consequent release of pro-inflammatory cytokines is also an important factor of the innate immune responses to the pathogens that may result into acute lung damage. Additionally, ROS can damage various vital biological molecules and inactivation of essential enzymes. Oxidative stress is an important factor causing metabolic and other pathophysiological alterations, such as protein oxidations and various associated diseases. Therefore, in this paper, the significant adverse impact of virus on host cell and underlying possible biochemical mechanism has been discussed.
Highlights
Serious health issues and deaths associated from novel COVID-19 pandemic are global public health concern originated from China in 2019
A new approach is required to inhibit the cell pathways that are responsible for viral replication and to combat the serious health issues
The virus-induced oxidative stress through various mechanisms is attributed to the production of proinflammatory cytokines IL-1b and IL-18, which are crucial for host defense to pathogens
Summary
Serious health issues and deaths associated from novel COVID-19 pandemic are global public health concern originated from China in 2019. Corona virus is single stranded RNA virus that affects the respiratory system in human Such notorious viruses exploit the host defense mechanism in various ways for their replication and infections [1] [2]. The main function of this process is to destroy and remove the harmful agent and damaged tissues, enhancing tissue repair Whenever this vital and normally beneficial response takes place in an uncontrolled way, the result is extreme cellular or tissue damage that comes out in the form of chronic inflammation and destruction of normal tissue. Many pro-oxidants such as the superoxide anion one of the important reactive oxygen species (ROS), generated by phagocytes deployed to sites of inflammation, are proposed to be a major cause of the cell and tissue damage, comprising apoptosis, associated with many chronic inflammatory diseases [4] [5]. After entering the host cell through any mucosa, the virus will undergo significant changes such as fusion, endocytosis and cytolysis, which will cause new virions to enter the host cell, resulting in the release of a large amount of pro-inflammatory cytokines and the change of cellular redox status
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