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Assays for the Specific Growth Rate and Cell-binding Ability of Rotavirus
Published on: January 28, 2019
Inflammatory and oxidative stress in rotavirus infection
Carlos A Guerrero1, Orlando Acosta1
1Carlos A Guerrero, Orlando Acosta, Department of Physiological Sciences, Faculty of Medicine, Universidad Nacional de Colombia, Bogotá 111311, Colombia.
Abstract:
Rotaviruses are the single leading cause of life-threatening diarrhea affecting children under 5 years of age. Rotavirus entry into the host cell seems to occur by sequential interactions between virion proteins and various cell surface molecules. The entry mechanisms seem to involve the contribution of cellular molecules having binding, chaperoning and oxido-reducing activities. It appears to be that the receptor usage and tropism of rotaviruses is determined by the species, cell line and rotavirus strain. Rotaviruses have evolved functions which can antagonize the host innate immune response, whereas are able to induce endoplasmic reticulum (ER) stress, oxidative stress and inflammatory signaling. A networking between ER stress, inflammation and oxidative stress is suggested, in which release of calcium from the ER increases the generation of mitochondrial reactive oxygen species (ROS) leading to toxic accumulation of ROS within ER and mitochondria. Sustained ER stress potentially stimulates inflammatory response through unfolded protein response pathways. However, the detailed characterization of the molecular mechanisms underpinning these rotavirus-induced stressful conditions is still lacking. The signaling events triggered by host recognition of virus-associated molecular patterns offers an opportunity for the development of novel therapeutic strategies aimed at interfering with rotavirus infection. The use of N-acetylcysteine, non-steroidal anti-inflammatory drugs and PPARγ agonists to inhibit rotavirus infection opens a new way for treating the rotavirus-induced diarrhea and complementing vaccines.
Insights
Rotaviruses cause severe diarrhea in young children by inducing cellular stress. Novel therapies targeting these stress pathways, like N-acetylcysteine, offer new treatment options beyond vaccines.
Area of Science:
- Virology
- Immunology
- Cellular Biology
Background:
- Rotaviruses are a primary cause of severe diarrhea in children under five globally.
- Rotavirus infection involves complex interactions with host cell surface molecules for entry.
- Rotaviruses possess mechanisms to evade the host immune system and induce cellular stress.
Purpose of the Study:
- To elucidate the molecular mechanisms of rotavirus-induced endoplasmic reticulum (ER) stress, oxidative stress, and inflammation.
- To explore the interplay between ER stress, inflammation, and oxidative stress during rotavirus infection.
- To identify potential therapeutic targets for rotavirus-induced diarrhea.
Main Methods:
- The study reviews existing literature on rotavirus entry mechanisms and host-pathogen interactions.
- It discusses the signaling pathways involved in rotavirus-induced cellular stress, including ER and mitochondrial function.
- The review examines potential therapeutic interventions based on interfering with these stress pathways.
Main Results:
- Rotavirus entry is mediated by sequential interactions with host cell molecules, with receptor usage varying by strain and host.
- Rotaviruses induce ER stress, oxidative stress, and inflammatory signaling, potentially through calcium release and ROS generation.
- A network involving ER stress, inflammation, and oxidative stress is proposed, contributing to disease pathogenesis.
Conclusions:
- Understanding rotavirus-induced stress signaling provides a basis for developing novel therapeutic strategies.
- Compounds like N-acetylcysteine, NSAIDs, and PPARγ agonists show promise in inhibiting rotavirus infection.
- These agents offer a potential complementary approach to vaccination for managing rotavirus diarrhea.
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