Abstract
Reactive oxygen species (ROS) are produced in various cell compartments by an array of enzymes and processes. An excess of ROS production can be hazardous for normal cell functioning, whereas at normal levels, ROS act as vital regulators of many signal transduction pathways and transcription factors. ROS production is affected by a wide range of viruses. However, to date, the impact of viral infections has been studied only in respect to selected ROS-generating enzymes. The role of several ROS-generating and -scavenging enzymes or cellular systems in viral infections has never been addressed. In this review, we focus on the roles of biogenic polyamines and oxidative protein folding in the endoplasmic reticulum (ER) and their interplay with viruses. Polyamines act as ROS scavengers, however, their catabolism is accompanied by H2O2 production. Hydrogen peroxide is also produced during oxidative protein folding, with ER oxidoreductin 1 (Ero1) being a major source of oxidative equivalents. In addition, Ero1 controls Ca2+ efflux from the ER in response to e.g., ER stress. Here, we briefly summarize the current knowledge on the physiological roles of biogenic polyamines and the role of Ero1 at the ER, and present available data on their interplay with viral infections.
Highlights
Viral infections contribute significantly to human disease
It has been clearly shown that polyamine catabolism is associated with production of H2O2 as a by-product
With the exception of human immunodeficiency virus (HIV), it is not known if augmented Reactive oxygen species (ROS) production in infected cells is due to spermine oxidase (SMOX) or PAOX
Summary
Viral infections contribute significantly to human disease. Some viruses cause an acute infection that resolves spontaneously. A number of viruses are oncogenic: HBV and HCV induce hepatocellular carcinoma, EBV causes Burkett or Hodgkin lymphomas, and type 8 herpes virus causes Kaposi sarcoma [4] As a result, both acute and chronic infections may cause permanent or persistent disability and contribute to premature mortality. Many viruses including HBV, HCV, HIV, influenza, respiratory syncytial, rhino, dengue and tick-borne encephalitis viruses enhance ROS production in infected cells [5,6,7,8,9,10,11]. They affect various components of the host’s antioxidant defense system. The interplay between these ROS-producing systems and viral infections will be detailed
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