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Conference Paper: The gut virome in non-alcoholic fatty liver disease: distinct changes in Phapecoctavirus composition in a human microbiota associated animal model
Title | The gut virome in non-alcoholic fatty liver disease: distinct changes in Phapecoctavirus composition in a human microbiota associated animal model |
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Authors | |
Issue Date | 2022 |
Publisher | Elsevier Inc.. |
Citation | International Liver Congress, European Association for the Study of the Liver (EASL), London & Online, 22-26 June 2022. In Journal of Hepatology. Volume 77. Supplement 1, Abstracts of The International Liver Congress: London, United Kingdom, 22-26 June 2022, p. S177-S178 How to Cite? |
Abstract | Background and aims: There is increasing knowledge on the role of the gut microbiome in the development of non-alcoholic fatty liver disease (NAFLD), but the role of the gut viral community in disease development remains poorly understood. We aimed to discover gut virome related to NAFLD development via a human-microbiotaassociated (HMA) rodent model of NAFLD. Method: Human fecal donors were recruited and classified into obese NAFLD, non-obese NAFLD and non-obese healthy controls. Liver steatosis was assessed by vibration-controlled transient elastography (Fibroscan, Echosens, Paris). The HMA-NAFLD rodent modelwasestablishedbyhigh-fatdiet andtransplantationofhuman fecal microbiota (FMT) for 12 weeks. The profile of the gut virome of both human donors and rodents was assessed by shotgun metagenomic sequencing (Illumina NovaSeq 6000, US). Results: Human donors with NAFLD had a significantly higher controlled attenuation parameter measurement when compared to healthy controls (median 324 [IQR 305.5–355.75] vs. 182.5 [179.25199.25] dB/m, p <0.001). Based on Bray-Curtis distance and PERMANOVA testing, human NAFLD donors had a distinct gut DNA viromecomparedwithhealthycontrols(p=0.04). Analysis via linear discriminate analysis (LDA) effect size method identified the Phapecoctavirus genus as a potential biomarker (LDA score 3.80), indicating a lower median relative abundance of Phapecoctavirus in NAFLDdonors whencomparedtohealthy donors (3.54% [IQR 2.93%3.98%] vs. 4.15% [3.94%-4.94%], p=0.038). As a putative host for Phapecoctavirus, the abundance of Escherichia coli was negatively associated with Phapecoctavirus (rho= −0.51, p=0.012). In the animal model, mice receiving FMT from obese NAFLD (FMT-ON) displayed a more severe NAFLD phenotype than those receiving FMT from healthycontrol (FMT-HC) (liver triglyceride: median 65.35 [IQR 62.32–73.33] vs. 48.7 [38.61–54.44] mg/g liver tissue, p=0.015; blood triglyceride: 207.89 [187.87–216.94] vs.110.05 [102.16–120.76] mg/dL,p<0.001). Phapecoctavirus genus was similarly identifiedas a potential fecal biomarker when comparingFMT-ONvs.FMT-HC(LDA score 3.19). It wasthe only viral genusthat distinguished NAFLD from control in both human donors and mouse recipients. FMT-ON mice with more severe NAFLD had a significantly lower level of fecal PhapecoctavirusthanFMT-HCmice(median2.47%[IQR2.39%-2.75%] vs. 2.82% [2.6%-3.14%], p =0.038). Conclusion: We reported the association of reduced fecal Phapecoctavirus with NAFLD in both human donors and HMA-mice recipients. Further interventional studies in animal and human are warrantedtodetermineitspotentialcausalityandfunctioninNAFLD. |
Description | Poster Presentations: Thursday 23 June, THU154 |
Persistent Identifier | http://hdl.handle.net/10722/314757 |
DC Field | Value | Language |
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dc.contributor.author | Chau, HT | - |
dc.contributor.author | Tun, HM | - |
dc.contributor.author | Zhang, S | - |
dc.contributor.author | Zhang, D | - |
dc.contributor.author | Huang, FY | - |
dc.contributor.author | Mak, LY | - |
dc.contributor.author | Yuen, RMF | - |
dc.contributor.author | Seto, WKW | - |
dc.date.accessioned | 2022-08-05T09:34:02Z | - |
dc.date.available | 2022-08-05T09:34:02Z | - |
dc.date.issued | 2022 | - |
dc.identifier.citation | International Liver Congress, European Association for the Study of the Liver (EASL), London & Online, 22-26 June 2022. In Journal of Hepatology. Volume 77. Supplement 1, Abstracts of The International Liver Congress: London, United Kingdom, 22-26 June 2022, p. S177-S178 | - |
dc.identifier.uri | http://hdl.handle.net/10722/314757 | - |
dc.description | Poster Presentations: Thursday 23 June, THU154 | - |
dc.description.abstract | Background and aims: There is increasing knowledge on the role of the gut microbiome in the development of non-alcoholic fatty liver disease (NAFLD), but the role of the gut viral community in disease development remains poorly understood. We aimed to discover gut virome related to NAFLD development via a human-microbiotaassociated (HMA) rodent model of NAFLD. Method: Human fecal donors were recruited and classified into obese NAFLD, non-obese NAFLD and non-obese healthy controls. Liver steatosis was assessed by vibration-controlled transient elastography (Fibroscan, Echosens, Paris). The HMA-NAFLD rodent modelwasestablishedbyhigh-fatdiet andtransplantationofhuman fecal microbiota (FMT) for 12 weeks. The profile of the gut virome of both human donors and rodents was assessed by shotgun metagenomic sequencing (Illumina NovaSeq 6000, US). Results: Human donors with NAFLD had a significantly higher controlled attenuation parameter measurement when compared to healthy controls (median 324 [IQR 305.5–355.75] vs. 182.5 [179.25199.25] dB/m, p <0.001). Based on Bray-Curtis distance and PERMANOVA testing, human NAFLD donors had a distinct gut DNA viromecomparedwithhealthycontrols(p=0.04). Analysis via linear discriminate analysis (LDA) effect size method identified the Phapecoctavirus genus as a potential biomarker (LDA score 3.80), indicating a lower median relative abundance of Phapecoctavirus in NAFLDdonors whencomparedtohealthy donors (3.54% [IQR 2.93%3.98%] vs. 4.15% [3.94%-4.94%], p=0.038). As a putative host for Phapecoctavirus, the abundance of Escherichia coli was negatively associated with Phapecoctavirus (rho= −0.51, p=0.012). In the animal model, mice receiving FMT from obese NAFLD (FMT-ON) displayed a more severe NAFLD phenotype than those receiving FMT from healthycontrol (FMT-HC) (liver triglyceride: median 65.35 [IQR 62.32–73.33] vs. 48.7 [38.61–54.44] mg/g liver tissue, p=0.015; blood triglyceride: 207.89 [187.87–216.94] vs.110.05 [102.16–120.76] mg/dL,p<0.001). Phapecoctavirus genus was similarly identifiedas a potential fecal biomarker when comparingFMT-ONvs.FMT-HC(LDA score 3.19). It wasthe only viral genusthat distinguished NAFLD from control in both human donors and mouse recipients. FMT-ON mice with more severe NAFLD had a significantly lower level of fecal PhapecoctavirusthanFMT-HCmice(median2.47%[IQR2.39%-2.75%] vs. 2.82% [2.6%-3.14%], p =0.038). Conclusion: We reported the association of reduced fecal Phapecoctavirus with NAFLD in both human donors and HMA-mice recipients. Further interventional studies in animal and human are warrantedtodetermineitspotentialcausalityandfunctioninNAFLD. | - |
dc.language | eng | - |
dc.publisher | Elsevier Inc.. | - |
dc.relation.ispartof | Journal of Hepatology. Volume 77. Supplement 1, Abstracts of The International Liver Congress: London, United Kingdom, 22-26 June 2022 | - |
dc.title | The gut virome in non-alcoholic fatty liver disease: distinct changes in Phapecoctavirus composition in a human microbiota associated animal model | - |
dc.type | Conference_Paper | - |
dc.identifier.email | Tun, HM: heinmtun@hku.hk | - |
dc.identifier.email | Zhang, S: saisaicc@hku.hk | - |
dc.identifier.email | Huang, FY: fungyu@hkucc.hku.hk | - |
dc.identifier.email | Mak, LY: lungyi@hku.hk | - |
dc.identifier.email | Yuen, RMF: mfyuen@hku.hk | - |
dc.identifier.email | Seto, WKW: wkseto@hku.hk | - |
dc.identifier.authority | Tun, HM=rp02389 | - |
dc.identifier.authority | Mak, LY=rp02668 | - |
dc.identifier.authority | Yuen, RMF=rp00479 | - |
dc.identifier.authority | Seto, WKW=rp01659 | - |
dc.identifier.doi | 10.1016/S0168-8278(22)00728-0 | - |
dc.identifier.hkuros | 334949 | - |
dc.identifier.spage | S177 | - |
dc.identifier.epage | S178 | - |