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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 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does EBV infection influence metabolism in lung cancer?","Question",{"text":63,"@type":64},"EBV affects cellular metabolic programs to support tumorigenesis by driving metabolic reprogramming that favors cancer cell growth.","Answer",{"name":66,"@type":61,"acceptedAnswer":67},"Which viral proteins are highlighted for metabolic manipulation?",{"text":68,"@type":64},"The review emphasizes viral proteins such as LMP1 and LMP2A, describing how they regulate glycolysis, glutaminolysis, and lipid metabolism.",{"name":70,"@type":61,"acceptedAnswer":71},"What therapeutic implication does the interplay between EBV and metabolism suggest?",{"text":72,"@type":64},"Understanding EBV-driven metabolic vulnerabilities can inform novel therapeutic strategies targeting these metabolic pathways in EBV-associated lung 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I E W  \nThe interplay of EBV virus and cell metabolism in lung cancer  \nHongwei Wang  \nShanxi Province Cancer Hospital/Shanxi Hospital Affiliated to Cancer Hospital, Chinese Academy of Medical Sciences/ Cancer Hospital Affiliated to Shanxi Medical University, Taiyuan, Shanxi, China  \nCorrespondence  \nHongwei Wang, Shanxi Province Cancer Hospital/Shanxi Hospital Affiliated to Cancer Hospital, Chinese Academy Of Medical Sciences/Cancer Hospital Affiliated to Shanxi Medical University, Taiyuan, Shanxi, 030000, China. [Email:](Email: w907300163@126.com)[ w907300163@126.com](Email: w907300163@126.com)  \nAbstract  \nEpstein–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.  \nK E Y WO R D S  \ncell metabolism, Epstein–Barr virus, glycolysis, immune evasion, lung cancer  \n1 | INTRODUCTION  \nLung cancer is the leading cause of cancer-related deaths globally, with approximately 1.8 million deaths annually.1 Despite advancements in detection and treatment, the prognosis for lung cancer patients remains poor, with a 5-year survival rate of less than 17. 8% .2 The heterogeneity of lung cancer, consisting primary of non-small cell lung cancer (NSCLC) and small cell lung cancer (SCLC), presents significant challenges in understanding and managing the disease.3 Epstein–Barr virus (EBV), a ubiquitous gamma-herpesvirus, infects over 90% of the global population, usually establishing a lifelong latent infection in B lymphocytes. While EBV is often asymptomatic in healthy individuals, it is well-recognized for its role in the pathogenesis of several malignancies, including nasopharyngeal carcinoma, Burkitt's lymphoma and certain types of gastric carcinoma. Emerging evidence indicates that EBV may play a role in the aetiology of lung cancer, particularly in the context of immune suppression or genetic predisposition.4  \nThe oncogenic potential of EBV is attributed to its ability to manipulate host cellular processes through the expression of viral proteins such as latent membrane protein 1 (LMP1), latent membrane  \nprotein 2 (LMP2) and Epstein–Barr nuclear antigen 1 (EBNA1) . These proteins interfere with cell signalling pathways, promoting cellular proliferation, inhibiting apoptosis and modulating immune responses.5 The exact mechanisms by which EBV influences lung cancer development, however, remain incompletely understood. A critical aspect of cancer biology is the reprogramming of cellular metabolism to support rapid cell growth and proliferation. Cancer cells exhibit altered metabolic pathways, commonly referred to as the Warburg effect, a metabolic shift where cancer cells predominantly produce energy through glycolysis even in the presence of oxygen, is a hallmark of cancer metabolism. This metabolic reprogramming provides cancer cells with the necessary energy and biosynthetic precursors to sustain their growth.5 The interplay between oncogenic viruses and host cell metabolism has garnered increasing attention, as viruses like EBV can hijack host metabolic pathways to facilitate their replication and promote oncogenesis.6 This review aims to elucidate the intricate relationship between EBV infection and metabolic reprogramming in lung cancer. By examining the molec","cbCaigc1vHJwQf5D","https://ap.wps.com/l/cbCaigc1vHJwQf5D","pdf",288949,"English","# Introduction\n## Biology of EBV","[{\"question\":\"How does EBV infection influence metabolism in lung cancer?\",\"answer\":\"EBV affects cellular metabolic programs to support tumorigenesis by driving metabolic reprogramming that favors cancer cell growth.\"},{\"question\":\"Which viral proteins are highlighted for metabolic manipulation?\",\"answer\":\"The review emphasizes viral proteins such as LMP1 and LMP2A, describing how they regulate glycolysis, glutaminolysis, and lipid metabolism.\"},{\"question\":\"What therapeutic implication does the interplay between EBV and metabolism suggest?\",\"answer\":\"Understanding EBV-driven metabolic vulnerabilities can inform novel therapeutic strategies targeting these metabolic pathways in EBV-associated lung cancer.\"}]","The interplay of EBV virus and cell metabolism in lung cancer | PDF",1790017646,18]