bims-mevinf 2025-11-09 papers

bims-mevinf

Biomed News

on Metabolism in viral infections

Issue of 2025–11–09
eleven papers selected by
Alexander V. Ivanov, Engelhardt Institute of Molecular Biology

Porcine reproductive and respiratory syndrome virus activates the pentose phosphate pathway via the ROS/HIF-1α/G6PD axis to promote viral replication.
Fatty acid synthase may facilitate the trafficking of bovine alpha herpesvirus 1 out of the Golgi apparatus, potentially promoting viral infection.
Comparative plasma metabolomics of Delta and Omicron SARS-CoV-2 variants: insights into variant-specific pathogenesis and therapeutic implications.
Hepatitis B virus is a stealth virus that minimizes proteomic and secretomic changes in primary human hepatocytes.
Validation of Lung [18F]FDG Uptake as a Quantitative PET Biomarker for Influenza-Associated Pulmonary Inflammation.
Parechovirus-3 infection disrupts immunometabolism and leads to glutamate excitotoxicity in neural organoids.
Impaired natural killer cell migration in HIV-infected individuals is caused by TIGIT-mediated inhibition of HIF-1α-dependent glycolysis.
Transcriptomics-driven antiviral drug screening identifies ATF6 as a homeostatic regulator of ER stress and innate immunity.
PEDV NSP8 inhibits IFN-III production induced by MAVS through downregulation of PEX13.
Assessment of Oxidative Stress Biomarkers in Felines Infected with Calicivirus.
Study on Differential Metabolites Between Human Papillomavirus Infection and Cervical Cancer Based on Non-Targeted Metabolomics.

Virulence. 2025 Dec;16(1): 2585639

Porcine reproductive and respiratory syndrome virus activates the pentose phosphate pathway via the ROS/HIF-1α/G6PD axis to promote viral replication.

Ying-Xian Ma, Jia-Ming Yang, Hang-Tian Mei, Lei Zeng, Guo-Yu Yang, Jiang Wang, Sheng-Li Ming, Bei-Bei Chu.

  Porcine reproductive and respiratory syndrome virus (PRRSV), a highly contagious pathogen in swine, poses significant economic challenges to global pork production. This study elucidated the regulatory interplay between PRRSV infection and the pentose phosphate pathway (PPP), a critical metabolic axis for anabolism. Comparative metabolomic profiling of porcine alveolar macrophages (PAMs) pre- and post-PRRSV infection demonstrated marked upregulation of PPP activity, concomitant with elevated levels of nucleotide biosynthesis. This metabolic shift was driven by PRRSV-induced upregulation of glucose-6-phosphate dehydrogenase (G6PD), the PPP's rate-limiting enzyme. Mechanistic investigations revealed that PRRSV infection stimulated hypoxia-inducible factor 1α (HIF-1α) expression, which transcriptionally activates G6PD. Genetic silencing of HIF-1α abolished PRRSV-mediated G6PD induction. Furthermore, reactive oxygen species (ROS) accumulation was identified as the upstream regulator of HIF-1α activation during PRRSV infection. Pharmacological ROS scavenging disrupted the ROS/HIF-1α/G6PD signaling cascade, diminished NADPH and reduced glutathione production, and consequently attenuated viral proliferation. These results established that PRRSV exploited the ROS/HIF-1α axis to reprogram host glucose metabolism through PPP potentiation, creating a biosynthetic environment conducive to viral propagation.

Keywords:  G6PD; HIF-1α; PPP; PRRSV; ROS

DOI:  https://doi.org/10.1080/21505594.2025.2585639
Microbiol Spectr. 2025 Nov 06. e0138825

Fatty acid synthase may facilitate the trafficking of bovine alpha herpesvirus 1 out of the Golgi apparatus, potentially promoting viral infection.

Xiaozhen Ma, Wenyuan Gu, Xuan Li, Xiuyan Ding, Liqian Zhu.

  The lipogenic enzyme fatty acid synthase (FASN) is essential for the de novo synthesis of fatty acids, and its aberrant expression has been implicated in the development of various diseases. However, the interaction between BoAHV-1 infection and FASN remains to be fully elucidated. In this study, we observed that both viral acute infection and latency in bovine trigeminal ganglia (TG) neurons, as well as virus productive infection at later stages in Neuro-2A and MDBK cells, significantly reduced FASN protein levels. Notably, a subset of FASN protein co-localized with the viral glycoprotein gD, as revealed by confocal microscopy in these cell cultures. Knockdown of FASN protein expression using siRNAs or chemical inhibition of FASN by Cerulenin leads to reduced viral replication. Interestingly, a subset of FASN proteins localizes in the Golgi apparatus, and Cerulenin treatment retards the trafficking of virions out of the Golgi. Collectively, our findings reveal a novel mechanism by which FASN regulates viral replication: a portion of the FASN protein located in the Golgi apparatus facilitates viral trafficking out of the Golgi, which is essential for the completion of the viral replication cycle.
IMPORTANCE: Here, we found that fatty acid synthase (FASN) protein is potentially involved in virus infection both in vitro and in vivo. In terms of mechanism, a subset of FASN protein co-localizes with the viral glycoprotein gD, as revealed by confocal microscopy in both MDBK and Neuro-2A cell cultures. Interestingly, a subset of FASN protein localizes in the Golgi apparatus, and Cerulenin treatment retards the trafficking of virions out of the Golgi. Therefore, we propose that a portion of the FASN protein in the Golgi apparatus plays an important role in viral trafficking out of the Golgi, which is essential for the completion of the viral replication cycle. This represents a novel mechanism of virus infection regulation, which has not been reported in other viruses, although the FASN protein is involved in the regulation of multiple viruses through distinct mechanisms.

Keywords:  BoAHV1; FASN; viral replication

DOI:  https://doi.org/10.1128/spectrum.01388-25
Front Cell Infect Microbiol. 2025 ;15 1649724

Comparative plasma metabolomics of Delta and Omicron SARS-CoV-2 variants: insights into variant-specific pathogenesis and therapeutic implications.

Eric Pimentel, Mohammad Mehdi Banoei, Chel Hee Lee, Brent W Winston.

   Background: The emergence of SARS-CoV-2 led to a global pandemic. Delta and Omicron, classified as concerning variants, differ significantly in transmissibility, disease severity, and antibody neutralization. Delta is associated with more severe disease, whereas Omicron is linked to increased transmissibility yet milder disease. This study investigates plasma metabolomic differences between Delta and Omicron infections and their associations with disease severity and treatment response. Importantly, this work examines variant-specific treatment metabolic effects - an aspect that remains underexplored despite the ongoing evolution of SARS-CoV-2 variants - and thus begins to fill a critical gap in the literature.
Methods: A total of 109 hospitalized SARS-CoV-2 patients, confirmed by RT-PCR positivity (53 Delta, 56 Omicron), were matched by age and sex. Plasma samples collected on hospitalization days 1, 2, and 7 were analyzed using DI/LC-MS/MS-based (direct injection, liquid chromatography-tandem mass-spectrometry) targeted metabolomics. We employed univariate and multivariate statistical and pathway analyses to investigate and characterize metabolomic differences.
Results: Distinct metabolic profiles differentiated Delta and Omicron infections. Specific metabolites, including tyrosine, asparagine, leucine, and acylcarnitines (C3, C4, C5), significantly distinguished variants and severity groups. Delta infections showed higher associations with severe outcomes. Corticosteroid treatment influenced metabolic profiles, revealing associations with modulation of metabolic and clinical responses.
Conclusion: This study reveals significant plasma-based metabolic differences between Delta and Omicron SARS-CoV-2 variants, potentially reflecting their distinct clinical outcomes and severities.

Keywords:  COVID-19; Delta; Omicron; SARS-CoV-2; metabolomics; severity; treatment

DOI:  https://doi.org/10.3389/fcimb.2025.1649724
J Gen Virol. 2025 Nov;106(11):

Hepatitis B virus is a stealth virus that minimizes proteomic and secretomic changes in primary human hepatocytes.

Karolína Štaflová, Kamila Clarová, Michal Doležal, Martin Hubálek, Alena Křenková, Jan Hodek, Iva Pichová, Aleš Zábranský.

  Hepatitis B virus (HBV) is a hepatotropic DNA virus that infects over 250 million people worldwide and causes serious liver diseases. HBV infection can modulate host cellular processes, potentially inducing proteomic changes in hepatocytes. In this study, we investigated how acute HBV infection alters the proteome and secretome of primary human hepatocytes, a physiologically relevant in vitro model that retains essential liver-specific functions. Protein-level changes in cell lysates and culture supernatants were quantified 8 days post-infection using data-independent acquisition MS. We used HBV infection in the presence of the entry inhibitor bulevirtide as a control to separate the effects of productive infection from those caused by inoculum-associated components. Despite robust infection, active HBV replication induced only subtle changes in host protein levels. Orthogonal validation of MS-identified candidates confirmed reticulocalbin-2 as a novel host factor downregulated during productive HBV infection. The functional role of candidate proteins identified by MS was assessed in vitro by siRNA-mediated knockdown and measurement of viral replication markers. Knockdown had no impact on viral RNA or antigen levels, suggesting that the observed proteomic changes may reflect stress responses or broader modulation of the hepatic microenvironment. Our findings support the concept of HBV as a stealth virus and underscore the importance of carefully controlled experimental systems for studying host responses to infection in vitro.

Keywords:  bulevirtide; hepatitis B virus; host factor; proteomics; reticulocalbin-2; secretome; virus–host interaction

DOI:  https://doi.org/10.1099/jgv.0.002170
Mol Imaging Biol. 2025 Nov 05.

Validation of Lung [18F]FDG Uptake as a Quantitative PET Biomarker for Influenza-Associated Pulmonary Inflammation.

Carla Bianca Luena Victorio, Shantanu Gupta, Arun Ganasarajah, Joanne Ong, Ann-Marie Chacko.

   PURPOSE: Influenza (flu) is a respiratory illness caused by lung infection with influenza viruses. This study establishes lung [18F]FDG uptake by PET/CT as an accurate measure of lung inflammation associated with influenza A virus (IAV) H1N1 infection.
PROCEDURES: Immunocompetent BALB/c mice were infected with a highly lethal dose of influenza A virus (PR8 strain) and intravenously injected with [18F]FDG. Ex vivo tissue biodistribution was assessed by gamma counting, while in vivo tissue biodistribution was analyzed by VOI analysis of PET/CT images. Disease severity was also investigated by VOI measurements of high-resolution lung CT images. Infection and inflammation were confirmed by immunohistochemical staining; while viral replication and expression of inflammatory proteins (cytokines and chemokines) were measured in lung tissues by qRT-PCR and multiplex ELISA, respectively.
RESULTS: Ex vivo tissue biodistribution of [18F]FDG revealed that the lungs were the only relevant imaging target in influenza-infected mice. Lung [18F]FDG uptake on PET/CT images increased with disease severity and exhibited 1.53-fold increase on day 1 and up to 2.63-fold increase on day 6 post-infection compared to pre-infection levels. Lung uptake correlated with the increased production of pro-inflammatory proteins associated with influenza infection.
CONCLUSIONS: Lung [18F]FDG uptake on PET images is a non-invasive molecular biomarker of influenza-A virus-induced lung inflammation and disease, effectively distinguishing infected from non-infected lungs as early as day 1 post-infection.

Keywords:  Imaging biomarker; Influenza; Lung inflammation; Molecular imaging; Viral infection imaging; [18F]FDG-PET

DOI:  https://doi.org/10.1007/s11307-025-02051-y
Cell Mol Life Sci. 2025 Nov 05. 82(1): 382

Parechovirus-3 infection disrupts immunometabolism and leads to glutamate excitotoxicity in neural organoids.

Pamela E Capendale, Anoop T Ambikan, Inés García-Rodríguez, Renata Vieira de Sá, Dasja Pajkrt, Katja C Wolthers, Ujjwal Neogi, Adithya Sridhar.

  Parechovirus ahumpari 3 (HPeV-3) is among the main agents causing severe neonatal neurological infections such as encephalitis and meningitis. However, the underlying molecular mechanisms and changes to the host cellular landscape leading to neurological disease has been understudied. Through quantitative proteomic analysis of HPeV-3 infected neural organoids, we identified unique metabolic changes following HPeV-3 infection that indicate immunometabolic dysregulation. Protein and pathway analyses showed significant alterations in neurotransmission and potentially, neuronal excitotoxicity. Elevated levels of extracellular glutamate, lactate dehydrogenase (LDH), and neurofilament light (NfL) confirmed glutamate excitotoxicity to be a key mechanism contributing to neuronal toxicity in HPeV-3 infection and can lead to apoptosis induced by caspase signaling. These insights are pivotal in delineating the metabolic landscape following severe HPeV-3 CNS infection and may identify potential host targets for therapeutic interventions.

Keywords:  Astrocytes; Brain organoids; CNS; Central nervous system; Immunometabolism; Neurons; Quantitative proteomics; Stem cells

DOI:  https://doi.org/10.1007/s00018-025-05926-z
Cell Death Dis. 2025 Nov 07. 16(1): 805

Impaired natural killer cell migration in HIV-infected individuals is caused by TIGIT-mediated inhibition of HIF-1α-dependent glycolysis.

Xiaowen Yu, Jie Zhou, Jie Lei, Hongchi Ge, Zining Zhang, Yajing Fu, Xiaoxu Han, Qinghai Hu, Haibo Ding, Wenqing Geng, Hong Shang, Yongjun Jiang.

Natural killer (NK) cells serve as the first line of defense in the immune system and play a crucial role in fighting against HIV infection. The effective function of NK cells is closely related to their migratory capacity. However, the status of NK cell migration in HIV-infected individuals and the underlying regulatory mechanisms remain unknown. Here, we found that NK cell migration was significantly impaired in HIV-infected individuals, with even lower levels in immune non-responders (INRs) compared with immune responders (IRs), and was positively correlated with CD4+ T cell counts. Further investigation suggested that the reduced NK cell migration in HIV infection was caused by impaired glycolysis. Mechanistically, NK cell migration was regulated by the HIF-1α pathway. The inhibitory receptor TIGIT suppressed HIF-1α expression by inhibiting PI3K/AKT/mTORC1 and ERK signaling pathways, consequently weakening glycolysis in NK cells of HIV-infected individuals and ultimately leading to downregulation of migration. Collectively, we uncovered a mechanism of reduced NK cell migration during HIV infection and provided new insights for potential immunotherapeutic strategies. Schematic of the mechanism of regulating NK cell migration in HC and HIV-infected individuals: Under normal physiological conditions, NK cells express sufficient levels of the glucose transporter GLUT-1 to support glycolysis, enabling normal glucose uptake. Meanwhile, activation of PI3K/AKT/mTORC1 or ERK signaling pathways induces HIF-1α expression, which subsequently promotes intracellular glycolysis and maintains regular NK cell migration. During HIV infection, the expression of GLUT-1 on NK cells is down-regulated, resulting in impaired glucose uptake. Additionally, High TIGIT expression suppresses HIF-1α expression by inhibiting the PI3K/AKT/ mTORC1 or ERK signaling pathway, thereby impairing glycolysis and ultimately reducing NK cell migration.

DOI: https://doi.org/10.1038/s41419-025-08039-4
J Adv Res. 2025 Oct 24. pii: S2090-1232(25)00831-8. [Epub ahead of print]

Transcriptomics-driven antiviral drug screening identifies ATF6 as a homeostatic regulator of ER stress and innate immunity.

Zhenyu Yang, Jing Sun, Yan Zhao, Ruoqing Feng, Yanhong Tang, Shijun Bu, Yuan He, Qinan Hu, Jincun Zhao, Yuhui Hu.

   INTRODUCTION: SARS-CoV-2 caused a global pandemic with widespread devastation on health system and many other aspects. Traditional drug development strategies have primarily focused on single targets in either the virus or host cells. While these strategies can significantly inhibit viral replication at the cellular level, the clinical efficacy remains difficult to guarantee, and many host-targeting drugs are associated with relatively high toxicity and side effects. Therefore, to prepare for the possible future viral pandemics, there remains an urgent need for effective therapeutic strategies that are comprehensive and easy to administer.
OBJECTIVES: The main objective of this study is to identify the optimal antiviral transcriptomic response of host cells based on the "dynamic virus-host interaction", conduct large-scale drug screening, and discover pan-transcriptomic responses or pan-targets capable of inhibiting viral replication through the integrated analysis of pharmacologically active compounds.
METHODS: We used deep RNA sequencing techniques to study gene expression changes of host cells (Huh7 and Vero-E6) along with viral replication dynamics upon SARS-CoV-2 infection. The imbalanced host genes serve as the SARS-CoV-2 expression signatures for computational screening of the compounds with anti-viral potential, following the concept of Connectivity Map (cMap). Furthermore, the gene perturbation signatures of effective compounds were integrated via bioinformatics approaches, and combined with techniques such as CRISPR-Cas9 and Western Blot (WB) to elucidate the targets and mechanisms underlying viral replication inhibition.
RESULTS: This study found that acute activation of host innate immunity pathway plays an essential role to suppress SARS-CoV-2 replication, and a variety of compounds with pharmacological activity against SARS-CoV-2 were successfully identified. Further transcriptomic comparison revealed the endoplasmic reticulum (ER) stress as the key machinery underneath the efficacy difference. Mechanistically, ATF6, an ER stress regulator, promotes viral replication by tempering PERK/IRE1-driven rapid activation of NF-κB and innate immunity (e.g., IL-1α, TNF-α).
CONCLUSION: This work positions ER stress modulation, particularly ATF6 targeting, as a strategy to balance antiviral defense and inflammatory toxicity, offering a roadmap for pan-coronavirus therapeutics. With these results, we established a paradigm for transcriptomic signature-based drug screening system for future treatment development of virus pandemics.

Keywords:  ATF6; Computational screening; ER stress; Innate immunity; SARS-CoV-2; Transcriptomics

DOI:  https://doi.org/10.1016/j.jare.2025.10.036
mBio. 2025 Nov 04. e0239625

PEDV NSP8 inhibits IFN-III production induced by MAVS through downregulation of PEX13.

Jinxiu Lou, Huixin Zhu, Zhen Yang, Ping Jiang, Gongguan Liu, Xianwei Wang.

  Porcine epidemic diarrhea virus (PEDV), an enteropathogenic coronavirus that causes severe intestinal disease in piglets, employs sophisticated strategies to subvert host antiviral immunity. While type III interferons (IFN-III) play a pivotal role in mucosal defense at intestinal epithelial barriers, the mechanisms underlying PEDV evasion of IFN-III signaling remain poorly understood. Given that peroxisomes serve as critical platforms for IFN-III signaling and that their abundance influences immune activation, we investigated the role of pexophagy in PEDV-mediated immune evasion. We demonstrated that the PEDV nonstructural protein NSP8 functions as a potent inhibitor of mitochondrial antiviral-signaling protein (MAVS)-dependent IFN-III production. Functional analyses revealed that NSP8 significantly reduces peroxisomal protein levels and promotes pexophagy. Mechanistically, mass spectrometry identified a direct interaction between NSP8 and PEX13. NSP8 also induces dose-dependent degradation of PEX13 via the autophagy-lysosomal pathway. This downregulation of PEX13 triggers ubiquitination of the peroxisomal import receptor PEX5, facilitating its recognition by the autophagy receptor NBR1 and the ubiquitin ligase PEX2, thereby promoting autophagic clearance of peroxisomes. Collectively, our findings reveal a novel immune evasion strategy in which PEDV exploits NSP8 to disrupt peroxisome homeostasis by targeting PEX13, thereby dismantling MAVS-dependent IFN-III antiviral signaling through pexophagy.
IMPORTANCE: Porcine epidemic diarrhea virus (PEDV) NSP8 is a highly conserved protein that plays a crucial role in viral replication. Investigating the functional mechanisms of NSP8 contributes to a deeper understanding of PEDV pathogenesis and supports the development of antiviral strategies against coronaviruses. In this study, we elucidate how NSP8 suppresses type Ⅲ interferon (IFN-Ⅲ) production by promoting pexophagy through the downregulation of PEX13. We demonstrate that NSP8 directly interacts with PEX13 and enhances the ubiquitination of PEX5, leading to reduced peroxisome abundance and impaired mitochondrial antiviral-signaling protein (MAVS)-mediated IFN-Ⅲ signaling. These findings suggest that NSP8 hijacks the PEX13-dependent pexophagy pathway as a means of evading host antiviral defenses. This work provides critical insights into the interplay between viral proteins and host cellular machinery and highlights the NSP8-PEX13 axis as a promising target for therapeutic interventions aimed at enhancing antiviral immunity against PEDV and related coronaviruses.

Keywords:  MAVS; NSP8; PEDV; PEX13; pexophagy; type Ⅲ interferon

DOI:  https://doi.org/10.1128/mbio.02396-25
Arch Razi Inst. 2025 Apr;80(2): 383-388

Assessment of Oxidative Stress Biomarkers in Felines Infected with Calicivirus.

Kasra Faraji, Pourtaghi Hadi, Yasini Seyedeh Parastoo, Sarabandi Sajed.

  Feline calicivirus (FCV) is a pathogen that affects cats, causing respiratory and oral issues. Oxidative stress constitutes a pivotal element in the pathophysiology of FCV, arising from imbalances between reactive oxygen species (ROS) and antioxidant defenses. Given the heightened sensitivity of cats to oxidative stress, the present study aims to explore its presence in felines afflicted with FCV via serum markers. A total of 20 plasma samples were obtained from the control group and the patient group (n=10 each). The patient group was confirmed using RT-PCR. Furthermore, the presence of plasma markers, including malondialdehyde (MDA), superoxide dismutase (SOD), catalase, and glutathione peroxidase, has been observed. The present study will examine the relationship between GPx and Total Antioxidant Capacity. TAC) for oxidative stress were assessed using the ELISA kit. Finally, data analyses and visual representations were executed using Python. Distinct variations in oxidative stress markers were observed among feline cohorts. The patient's SOD and GPx levels were 39.73 u/L and 75.63 u/L, respectively, while the control group exhibited levels of 36.41 u/L and 218.48 u/L (p-values: 0.05, 0.017). The mean values of CAT and MDA in patients were 3.7 u/L and 9.85 nmol, respectively, contrasting with 11.81 u/L and 4.17 nmol in the control group (p-values: 0.002, 0.050). Meanwhile, the levels of TAC exhibited minimal differences. The study's findings indicated significant variations in oxidative markers such as SOD, GPx, and MDA when compared to healthy cats. The observed rise in SOD and decline in GPx activity indicate a heightened state of oxidative stress. Moreover, these findings underscore the possibility of oxidative disruptions in FCV-infected cats, underscoring the necessity for additional investigation and the potential development of therapeutic strategies. Furthermore, the exploration of potential therapeutic interventions, such as antioxidant supplementation, may facilitate the development of enhanced disease management strategies for affected felines.

Keywords:   ELISA; Feline Calicivirus; Malondialdehyde; Oxidative Stress; Superoxide Dismutase

DOI:  https://doi.org/10.32592/ARI.2025.80.2.383
Int J Womens Health. 2025 ;17 3995-4009

Study on Differential Metabolites Between Human Papillomavirus Infection and Cervical Cancer Based on Non-Targeted Metabolomics.

Jinmei Xu, Ming Wang, Yue Jia, Yanfen Chen, Yangjuan Duan, Mengting Ni, Yinghai Wang, Jie Wei, Jing Yu.

   Objective: To explore the difference of metabolites between human papillomavirus (HPV) infection and the occurrence and development of cervical cancer based on non-targeted metabolomics.
Methods: Between August 2022 and August 2023, 20 women of childbearing age at the Third Affiliated Hospital of Kunming Medical University, including the HPV-negative control, LSIL (HPV infection), HSIL (cervical intraepithelial neoplasia [CIN2-3]), and cervical cancer groups, were selected as research participants. Ultra-high-performance liquid chromatography and SCIEX mass spectrometry (TripleTOF 6600+, USA) were used to separate and detect the metabolites.
Results: According to the results of the differential metabolite analysis, the KEGG pathway was enriched. The most obvious enrichment pathway in the CIN2-3 group compared with the HPV-negative and HPV-positive groups was the steroid hormone pathway; the most obvious enrichment pathway in the cervical cancer group compared with the HPV-negative group was the steroid hormone pathway. Compared with HPV-negative group, the most obvious enrichment pathway in the CIN2-3 group was the glycerophosphate metabolism pathway. Compared with CIN2-3 and HPV-positive group, the most obvious enrichment pathway in the cervical cancer group was the sphingolipid metabolism pathway, followed by the steroid biosynthesis and amino sugar and nucleotide metabolism pathways. Compared with the HPV-negative group, the most obvious enrichment pathway in the cervical cancer group was the steroid biosynthesis pathway, followed by the sphingolipid metabolism pathway. 19-Hydroxytestosterone is involved in the synthesis of steroid hormones. Cerebroside B is involved in sphingolipid metabolism. Potassium acetate is involved in protein digestion and absorption. Methylarsonate is involved in chemical carcinogenesis - reactive oxygen species.
Conclusion: The expression levels of 19-Hydroxytestosterone, cerebroside B, potassium acetate and methylarsonate are downregulated with the aggravation of cervical lesions and can be used as potential tumor markers for cervical cancer.

Keywords:  HPV; cervical cancer; non-targeted metabolomics

DOI:  https://doi.org/10.2147/IJWH.S523559