Reactive oxygen species promote heat shock protein 90-mediated HBV capsid assembly

Kim, Yoon Sik; Seo, Hyun Wook; Jung, Guhung

doi:10.1016/j.bbrc.2014.12.110

Cited by 31 publications

(30 citation statements)

References 36 publications

(33 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…There is also evidence that hepatitis B virus X protein (HBx) induces the activation of a set of transcription factors via ROS (oxidative stress), which eventually leads to gene expression in the nucleus (111). ROS can also increase HBV capsid assembly as found in HepG2.2.15 cells (112). Therefore, according to these recently mentioned facts, reducing oxidative stress prior to antiviral treatment may improve treatment outcomes and response rates and possibly lead to viral elimination.…”

Section: Discussionmentioning

confidence: 92%

Hepatitis B and its Relationship With Oxidative Stress

Alavian

Showraki

2016

Hepat Mon

View full text Add to dashboard Cite

ContextDespite the great breakthroughs we have witnessed in the last 50 years in the prevention, diagnosis, and treatment of hepatitis B, we are still far from eradicating or even curing the disease. Achieving further progress in controlling this disease will not be possible without discovering the exact pathogenesis behind it. One prime suspect in the pathogenesis of various diseases is oxidative stress. This review will exclusively explore hepatitis B in the context of oxidative stress to obtain a more comprehensive clinical perspective on its pathogenesis and eventual medical therapy.Evidence AcquisitionWe systematically searched PubMed, Google Scholar, Web of Science, EMBASE, and Scopus using an extensive list of keywords in the following three categories: 1) Hepatitis B and oxidation 2) Hepatitis B and antioxidant system 3) Effects of approved anti-hepatitis B drugs on redox status. All relevant articles were obtained and reviewed carefully after the exclusion criteria were deployed.ResultsThere is great evidence indicating extensive oxidative stress occurs in hepatitis B. This oxidative stress takes place on multiple levels, including lipid peroxidation, DNA oxidation, protein oxidation, and reactive oxygen and nitrogen species production. However, there are also conflicting results with regard to antioxidant therapy and antioxidant status in hepatitis B, some of which may be explained by the concept of “compensatory gaps.” Nevertheless, further studies are indicated to reach a more thorough judgment.ConclusionsDespite the presence of vast oxidative stress in hepatitis B, antioxidant therapy is not always effective as a treatment strategy, especially considering that antioxidants can act as “double-edged swords” or antioxidants; if not used at the right time or place or in the right combination, these substances can easily become pro-oxidants. Therefore, several studies will be needed to determine suitable antioxidant therapies. We propose the “2-step Combined Antioxidant Adjuvant Therapy for hepatitis B (2CAAT Hep B)” as a new strategy for antioxidant adjuvant therapy. We also suggest developing an international platform and database for antioxidant adjuvant therapy in hepatitis B (IPAATH and IDAATH) to canalize this field of research in a standardized direction, especially when complexity is a problem.

show abstract

Section: Discussionmentioning

confidence: 92%

Hepatitis B and its Relationship With Oxidative Stress

Alavian

Showraki

2016

Hepat Mon

View full text Add to dashboard Cite

show abstract

“…Secondly, hydrogen peroxide was shown to promote HBV capsid assembly [310]. This enhancement was revealed in several systems, including cell-free experiments involving Hsp90 protein, thus demonstrating that H 2 O 2 can influence the conformation of the Hsp90/capsid complex.…”

Section: Hepatitis C Virusmentioning

confidence: 99%

Oxidative stress, a trigger of hepatitis C and B virus-induced liver carcinogenesis

et al. 2016

View full text Add to dashboard Cite

Virally induced liver cancer usually evolves over long periods of time in the context of a strongly oxidative microenvironment, characterized by chronic liver inflammation and regeneration processes. They ultimately lead to oncogenic mutations in many cellular signaling cascades that drive cell growth and proliferation. Oxidative stress, induced by hepatitis viruses, therefore is one of the factors that drives the neoplastic transformation process in the liver. This review summarizes current knowledge on oxidative stress and oxidative stress responses induced by human hepatitis B and C viruses. It focuses on the molecular mechanisms by which these viruses activate cellular enzymes/systems that generate or scavenge reactive oxygen species (ROS) and control cellular redox homeostasis. The impact of an altered cellular redox homeostasis on the initiation and establishment of chronic viral infection, as well as on the course and outcome of liver fibrosis and hepatocarcinogenesis will be discussed The review neither discusses reactive nitrogen species, although their metabolism is interferes with that of ROS, nor antioxidants as potential therapeutic remedies against viral infections, both subjects meriting an independent review.

show abstract

“…Complex antioxidants agents maintain homeostasis of aerobic metabolism. Because the pro‐oxidant agents did not exceed the antioxidant systems, there are compensatory mechanisms …”

Section: Discussionmentioning

confidence: 99%

“…Because the pro-oxidant agents did not exceed the antioxidant systems, there are compensatory mechanisms. 23 BRONJ is a condition directly associated with proinflammatory (TNF-a, IL-1b, IL-17) markers and iNOS activity, 24 and it appears that macrophages and the nuclear activity of NF-kB are necessary for the pathogenesis of this condition 4,17 In this study, an increase in the nuclear expression of NF-kB and number of rats showing mononuclear CD68-positive cells were not shown in the "healthy periodontium," but we demonstrated the rise of GSH levels.…”

Section: Discussionmentioning

confidence: 99%