Reactive oxygen and nitrogen species during viral infections

Abstract

Oxygen and nitrogen radicals are frequently produced during viral infections. These radicals are not only a physiological mechanism for pathogen clearance but also result in many pathological consequences. Low concentrations of radicals can promote viral replication; however, high concentrations of radicals can also inhibit viral replication and are detrimental to the cell due to their mitogenic activity. We reviewed the detailed mechanisms behind oxygen and nitrogen radical production and focused on how viruses induce radical production. In addition, we examined the effects of oxygen and nitrogen radicals on both the virus and host. We also reviewed enzymatic and chemical detoxification mechanisms and recent advances in therapeutic antioxidant applications. Many molecules that modulate the redox balance have yielded promising results in cell and animal models of infection. This encourages their use in clinical practice either alone or with existing therapies. However, since the redox balance also plays an important role in host defence against pathogens, carefully designed clinical trials are needed to assess the therapeutic benefits and secondary effects of these molecules and whether these effects differ between different types of viral infections.

Effects of aging on the male reproductive system

“…In mitochondria, oxygen is converted to highly reactive oxygen molecules called reactive oxygen species (ROS). Low and medium concentrations of ROS are involved in cellular defense against infection agents, signal transduction, and response against mitogens, carboxylation, peroxidation, Pasqualotto et al [28] 0.03 ml [33] and reduction of ribonucleotides; however, high levels of ROS lead to various cellular damage [54][55][56][57][58][59]. ROS induced DNA damage involves base modifications, abasic sites, single strand (ss) and double strand (ds) DNA breaks, and DNA protein cross-links [60][61][62].…”

HIV-1, methamphetamine and astrocytes at neuroinflammatory Crossroads

“…Inducible NO synthase (iNOS) generates NO, which can interact with ROS to form peroxynitrite, a highly RNS (Pacher et al, 2007 ). Low levels of oxidative stress activate anti-oxidant machinery, initiate anti-microbial responses in immune cells and activate endothelial cells (Ma et al, 2014 ; Molteni et al, 2014 ; Salisbury and Bronas, 2015 ). Unchecked oxidative and nitrosative modifications to cellular components, such as the mitochondria, often augment oxidative stress and induce apoptosis (Cossarizza et al, 2002 ; Jou, 2008 ; Indo et al, 2015 ).…”

“…Oxidative stress in the HIV-infected brain, through both the early effects of viral proteins and the later effects on mitochondrial integrity, are well established (Valcour and Shiramizu, 2004 ; Ozdener, 2005 ; Banerjee et al, 2010 ; Uzasci et al, 2013 ). Low ROS levels can promote viral replication and can be induced by viral virulence factors (Molteni et al, 2014 ). HIV-1 gp120, Tat and viral protein R (Vpr) induce ROS in neural cells, including astrocytes (Ferrucci et al, 2013 ; Shah et al, 2013 ).…”

Pharmaconutrition revisited for critically ill patients with coronavirus disease 2019 (COVID-19): Does selenium have a place?

“…It is well established that poor nutritional status of the host increases pathogenicity of viruses, increasing either susceptibility to illness or its severity in nutrient deficient animals [15] . According to the literature, several host nutritional factors have long been associated with an effect on a viral pathogen, specifically by altering its genome, which can impact the viral expression producing a new pathogenic viral phenotype [12] .…”