Oncogenic viruses and host lipid metabolism: a new perspective

Gong, Zaiwu; Zhang, Yan; Wen, Liang; Luo, Bing

doi:10.1099/jgv.0.001861

Cited by 2 publications

(1 citation statement)

References 191 publications

(248 reference statements)

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“…Arginine (Arg) has been proposed to be a key amino acid for viral replication of many DNA and RNA viruses (Tome, 2021). Hijacking of host lipid metabolism by some viruses to improve viral replication has also been suggested (Gong et al, 2023).…”

Section: Mitochondrial Metabolismmentioning

confidence: 99%

Host mitochondria: more than an organelle in SARS-CoV-2 infection

Shoraka,

Samarasinghe,

Ghaemi

et al. 2023

Front. Cell. Infect. Microbiol.

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Since December 2019, the world has been facing viral pandemic called COVID-19 (Coronavirus disease 2019) caused by a new beta-coronavirus named severe acute respiratory syndrome coronavirus-2, or SARS-CoV-2. COVID-19 patients may present with a wide range of symptoms, from asymptomatic to requiring intensive care support. The severe form of COVID-19 is often marked by an altered immune response and cytokine storm. Advanced age, age-related and underlying diseases, including metabolic syndromes, appear to contribute to increased COVID-19 severity and mortality suggesting a role for mitochondria in disease pathogenesis. Furthermore, since the immune system is associated with mitochondria and its damage-related molecular patterns (mtDAMPs), the host mitochondrial system may play an important role during viral infections. Viruses have evolved to modulate the immune system and mitochondrial function for survival and proliferation, which in turn could lead to cellular stress and contribute to disease progression. Recent studies have focused on the possible roles of mitochondria in SARS-CoV-2 infection. It has been suggested that mitochondrial hijacking by SARS-CoV-2 could be a key factor in COVID-19 pathogenesis. In this review, we discuss the roles of mitochondria in viral infections including SARS-CoV-2 infection based on past and present knowledge. Paying attention to the role of mitochondria in SARS-CoV-2 infection will help to better understand the pathophysiology of COVID-19 and to achieve effective methods of prevention, diagnosis, and treatment.

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Section: Mitochondrial Metabolismmentioning

confidence: 99%

Host mitochondria: more than an organelle in SARS-CoV-2 infection

Shoraka,

Samarasinghe,

Ghaemi

et al. 2023

Front. Cell. Infect. Microbiol.

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The interplay of EBV virus and cell metabolism in lung cancer

Wang

2024

J Cellular Molecular Medi

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Epstein–Barr virus infection has been implicated in various cancers, including lung cancer, where it influences cellular metabolism to promote tumorigenesis. This review examines the complex interplay between Epstein–Barr virus and cell metabolism in lung cancer, highlighting viral mechanisms of metabolic reprogramming and their implications for therapeutic strategies. Key viral proteins such as LMP1 and LMP2A manipulate glycolysis, glutaminolysis and lipid metabolism to support viral replication and immune evasion within the tumour microenvironment. Understanding these interactions provides insights into novel therapeutic approaches targeting viral‐induced metabolic vulnerabilities in Epstein–Barr virus‐associated lung cancer.

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Oncogenic viruses and host lipid metabolism: a new perspective

Cited by 2 publications

References 191 publications

Host mitochondria: more than an organelle in SARS-CoV-2 infection

Host mitochondria: more than an organelle in SARS-CoV-2 infection

The interplay of EBV virus and cell metabolism in lung cancer

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