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<journal-id journal-id-type="publisher-id">Front. Genet.</journal-id>
<journal-title>Frontiers in Genetics</journal-title>
<abbrev-journal-title abbrev-type="pubmed">Front. Genet.</abbrev-journal-title>
<issn pub-type="epub">1664-8021</issn>
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<publisher-name>Frontiers Media S.A.</publisher-name>
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<article-meta>
<article-id pub-id-type="publisher-id">1463350</article-id>
<article-id pub-id-type="doi">10.3389/fgene.2024.1463350</article-id>
<article-categories>
<subj-group subj-group-type="heading">
<subject>Genetics</subject>
<subj-group>
<subject>Editorial</subject>
</subj-group>
</subj-group>
</article-categories>
<title-group>
<article-title>Editorial: The intricate web of gastrointestinal virome, mycome and archaeome: implications for gastrointestinal diseases</article-title>
<alt-title alt-title-type="left-running-head">Ahmad et al.</alt-title>
<alt-title alt-title-type="right-running-head">
<ext-link ext-link-type="uri" xlink:href="https://doi.org/10.3389/fgene.2024.1463350">10.3389/fgene.2024.1463350</ext-link>
</alt-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname>Ahmad</surname>
<given-names>Asrar</given-names>
</name>
<xref ref-type="aff" rid="aff1">
<sup>1</sup>
</xref>
<uri xlink:href="https://loop.frontiersin.org/people/753853/overview"/>
<role content-type="https://credit.niso.org/contributor-roles/writing-original-draft/"/>
<role content-type="https://credit.niso.org/contributor-roles/Writing - review &#x26; editing/"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Ashfaq</surname>
<given-names>Mohammad</given-names>
</name>
<xref ref-type="aff" rid="aff2">
<sup>2</sup>
</xref>
<uri xlink:href="https://loop.frontiersin.org/people/2295867/overview"/>
<role content-type="https://credit.niso.org/contributor-roles/formal-analysis/"/>
<role content-type="https://credit.niso.org/contributor-roles/Writing - review &#x26; editing/"/>
</contrib>
<contrib contrib-type="author" corresp="yes">
<name>
<surname>Rashid</surname>
<given-names>Mudasir</given-names>
</name>
<xref ref-type="aff" rid="aff3">
<sup>3</sup>
</xref>
<xref ref-type="corresp" rid="c001">&#x2a;</xref>
<uri xlink:href="https://loop.frontiersin.org/people/1871241/overview"/>
<role content-type="https://credit.niso.org/contributor-roles/conceptualization/"/>
<role content-type="https://credit.niso.org/contributor-roles/Data curation/"/>
<role content-type="https://credit.niso.org/contributor-roles/Supervision/"/>
<role content-type="https://credit.niso.org/contributor-roles/writing-original-draft/"/>
<role content-type="https://credit.niso.org/contributor-roles/Writing - review &#x26; editing/"/>
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<aff id="aff1">
<sup>1</sup>
<institution>Center for Sickle Cell Disease</institution>, <institution>Howard University</institution>, <addr-line>Washington</addr-line>, <addr-line>DC</addr-line>, <country>United States</country>
</aff>
<aff id="aff2">
<sup>2</sup>
<institution>The University Centre for Research and Development (UCRD)</institution>, <institution>Chandigarh University</institution>, <addr-line>Mohali</addr-line>, <addr-line>Punjab</addr-line>, <country>India</country>
</aff>
<aff id="aff3">
<sup>3</sup>
<institution>Department of Medicine and Cancer Center</institution>, <institution>Howard University</institution>, <addr-line>Washington</addr-line>, <addr-line>DC</addr-line>, <country>United States</country>
</aff>
<author-notes>
<fn fn-type="edited-by">
<p>
<bold>Edited and reviewed by:</bold> <ext-link ext-link-type="uri" xlink:href="https://loop.frontiersin.org/people/986328/overview">Maxim B. Freidin</ext-link>, King&#x2019;s College London, United Kingdom</p>
</fn>
<corresp id="c001">&#x2a;Correspondence: Mudasir Rashid, <email>mudasir.rashid@howard.edu</email>
</corresp>
</author-notes>
<pub-date pub-type="epub">
<day>09</day>
<month>08</month>
<year>2024</year>
</pub-date>
<pub-date pub-type="collection">
<year>2024</year>
</pub-date>
<volume>15</volume>
<elocation-id>1463350</elocation-id>
<history>
<date date-type="received">
<day>11</day>
<month>07</month>
<year>2024</year>
</date>
<date date-type="accepted">
<day>30</day>
<month>07</month>
<year>2024</year>
</date>
</history>
<permissions>
<copyright-statement>Copyright &#xa9; 2024 Ahmad, Ashfaq and Rashid.</copyright-statement>
<copyright-year>2024</copyright-year>
<copyright-holder>Ahmad, Ashfaq and Rashid</copyright-holder>
<license xlink:href="http://creativecommons.org/licenses/by/4.0/">
<p>This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.</p>
</license>
</permissions>
<related-article id="RA1" related-article-type="commentary-article" journal-id="Front. Genet." xlink:href="https://www.frontiersin.org/researchtopic/57680" ext-link-type="uri">Editorial on the Research Topic <article-title>The intricate web of gastrointestinal virome, mycome and archaeome: implications for gastrointestinal diseases</article-title>
</related-article>
<kwd-group>
<kwd>virome</kwd>
<kwd>mycome</kwd>
<kwd>archaeome</kwd>
<kwd>human health and disease</kwd>
<kwd>gastroinestinal tract</kwd>
</kwd-group>
<custom-meta-wrap>
<custom-meta>
<meta-name>section-at-acceptance</meta-name>
<meta-value>Human and Medical Genomics</meta-value>
</custom-meta>
</custom-meta-wrap>
</article-meta>
</front>
<body>
<p>The gastrointestinal (GI) tract is a complex ecosystem containing bacteria, viruses (virome), fungi (mycome), and archaea (archaeome). It plays a significant role in ecological functioning, evolutionary changes, and host-microbiome interactions (<xref ref-type="bibr" rid="B26">Ogilvie and Jones, 2017</xref>; <xref ref-type="bibr" rid="B8">Daliri et al., 2020</xref>; <xref ref-type="bibr" rid="B28">Piewngam et al., 2020</xref>; <xref ref-type="bibr" rid="B34">Vemuri et al., 2020</xref>). Recent advances in sequencing technologies and metagenomic approaches have expanded our comprehension of the gastrointestinal-microbiome axis and its roles in maintaining gut homeostasis, health, and disease (<xref ref-type="bibr" rid="B19">Lepage et al., 2013</xref>; <xref ref-type="bibr" rid="B13">Gao et al., 2021</xref>; <xref ref-type="bibr" rid="B18">Lau and Yu, 2022</xref>). While bacteria have been extensively studied, the virome, mycome, and archaeome have recently gained attention. The human gut virome varies between individuals, composition and dynamics (<xref ref-type="bibr" rid="B24">Minot et al., 2011</xref>; <xref ref-type="bibr" rid="B10">Foca et al., 2015</xref>). They play a crucial role in gut regulation and contributing to disease development through interactions with the microbiota and immune cells (<xref ref-type="bibr" rid="B26">Ogilvie and Jones, 2017</xref>; <xref ref-type="bibr" rid="B30">Santiago-Rodriguez and Hollister, 2019</xref>; <xref ref-type="bibr" rid="B15">Hou et al., 2022</xref>; <xref ref-type="bibr" rid="B32">Tiamani et al., 2022</xref>). The gut mycobiome also plays a critical role in human health and disease, with potential implications for infants, obesity, inflammatory bowel disease (IBD) and neurodegenerative diseases (<xref ref-type="bibr" rid="B11">Forbes et al., 2018</xref>; <xref ref-type="bibr" rid="B16">Jain et al., 2021</xref>). The archaeome, a diverse and potentially important component of human gut host-associated microbiomes, plays an important role in gut physiology and health, in shaping the health and fitness of the animals (<xref ref-type="bibr" rid="B12">Gaci et al., 2014</xref>; <xref ref-type="bibr" rid="B22">Lurie-Weinberger and Gophna, 2015</xref>; <xref ref-type="bibr" rid="B4">Borrel et al., 2020</xref>; <xref ref-type="bibr" rid="B17">Kim et al., 2020</xref>). Studies have shown that Archaea play a key role in the pathogenesis of IBD and the risk of pediatric asthma (<xref ref-type="bibr" rid="B3">Barnett et al., 2019</xref>; <xref ref-type="bibr" rid="B31">Singh et al., 2023</xref>). However, their role in human health remains poorly understood, therefore, understanding these microbial communities offers new therapeutic approaches for GI disorders and enhances strategies for improving GI health as shown in <xref ref-type="fig" rid="F1">Figure 1</xref>.</p>
<fig id="F1" position="float">
<label>FIGURE 1</label>
<caption>
<p>Human microbiota composition with potential consequences. Permission obtained from <xref ref-type="bibr" rid="B15">Hou et al. (2022)</xref>, <xref ref-type="bibr" rid="B36">Spencer et al. (2022)</xref>.</p>
</caption>
<graphic xlink:href="fgene-15-1463350-g001.tif"/>
</fig>
<p>The aim of the editorial <italic>&#x201c;The intricate web of gastrointestinal virome, mycobiome, and archaeome: implications for gastrointestinal diseases&#x201d;</italic> is to explore the roles and interactions of the gastrointestinal microbiome in relation to gastrointestinal diseases. The objectives include reviewing current research on these microbial communities, discussing their implications for gastrointestinal health, highlighting potential therapeutic implications, and fostering a deeper understanding among healthcare professionals and researchers and suggest avenues for future research and clinical application in this evolving field. Recent studies have shown that, Postherpetic Neuralgia (PHN) is a chronic neuropathic pain syndrome caused by Herpes Zoster virus (HZV) reactivation, and it is more common in older and immunocompromised individuals, and vaccination is effective in preventing complications (<xref ref-type="bibr" rid="B27">Oxman et al., 2005</xref>; <xref ref-type="bibr" rid="B23">Mallick-Searle et al., 2016</xref>; <xref ref-type="bibr" rid="B9">Ferreira Sampaio et al., 2023</xref>). Additionally, it has been shown that HSV patients with peptic ulcer disease may be at a greater risk for developing PHN due to impaired cellular immunity and low nutritional status (<xref ref-type="bibr" rid="B7">Chen et al., 2013</xref>). <ext-link ext-link-type="uri" xlink:href="https://doi.org/10.3389/fgene.2024.1366824">Zhimin et al.</ext-link> have reported that the causal effect between HZV and PHN and the gut microbiota using bidirectional two-sample Mendelian randomization (MR) analysis. The study revealed the alterations in gut microbiota may influence susceptibility to HSV and the development of PHN. This research highlights the potential for specific gut microbiota to serve as a therapeutic target, offering new avenues for the prevention and treatment of viral infections and associated chronic conditions. This study highlights the importance of considering the gut microbiota not just in isolation but as a critical component in the overall immune response and susceptibility to viral infections. By understanding these causal relationships, new therapeutic strategies could be developed, focusing on modulating the gut microbiota to prevent or mitigate the effects of HSV associated PHN. Additionally, <ext-link ext-link-type="uri" xlink:href="https://doi.org/10.3389/fmicb.2024.1365043">Hanjing et al.</ext-link> carried out the study in China (Jinjiang, Fujian), and reported the interactions between <italic>Helicobacter pylori</italic>, chronic gastritis, and the gut microbiota. They demonstrate that how <italic>Helicobacter. pylori</italic> infection and chronic gastritis are intricately linked with changes in gut microbiota composition. These findings emphasize the need for a comprehensive approach in managing <italic>Helicobacter. pylori</italic> infections and gastritis, considering their impact on the overall gut microbiota health. Moreover, gut microbiome-associated metabolites in serum can accurately distinguish colorectal cancer and adenomas from normal samples (<xref ref-type="bibr" rid="B6">Chen et al., 2022</xref>). Also, another study profiled the serum antibody responses of 997 healthy individuals against 244,000 peptide antigens derived from gut microbiota, data indicated that the serum antibody repertoires displayed high diversity and stability against human microbiota and identified several factors influencing the serum antibody response, such as age, gender, body mass index, and geographical location. These findings shed light on the role of the immune system in maintaining homeostasis with the gut microbiota (<xref ref-type="bibr" rid="B35">Vogl et al., 2021</xref>). <ext-link ext-link-type="uri" xlink:href="https://doi.org/10.3389/fmicb.2024.1323842">Chen et al.</ext-link> present a differential analysis of serum immunology and gut microbiota in patients suffering from various gastrointestinal diseases. The study identifies distinct immunological and microbiota profiles associated with specific GI conditions, providing valuable insights into the interplay between the immune system and gut microbiota. This research highlights the potential for personalized medicine approaches in GI, tailoring treatments to the unique microbiota like recent report has shown that smart antibiotic (Lolamicin) can target a group of harmful microbes but does not disturb those that live peacefully in the gut (<xref ref-type="bibr" rid="B25">Munoz et al., 2024</xref>). Furthermore, <ext-link ext-link-type="uri" xlink:href="https://doi.org/10.3389/fmicb.2023.1256874">Xiao et al.</ext-link> examine the causal relationship between the gut microbiome and liver cirrhosis through a bi-directional two-sample Mendelian randomization analysis. The results highlight significant causal links, suggesting that specific alterations in the gut microbiome may contribute to the development of liver cirrhosis. This study points out the importance of considering gut microbiota health in the prevention and management of liver diseases. Also, other evidence has shown that gut microbiome plays a significant role in liver disorders, potentially contributing to disease process and severity. Prebiotics and probiotics may be effective treatments for complications and liver cirrhosis. Additionally, the gut-liver axis plays a crucial role in liver disease, and progressive changes in the gut microbiome accompany cirrhosis. It became more severe in the setting of decompensation, with the cirrhosis dysbiosis ratio being a useful quantitative index (<xref ref-type="bibr" rid="B2">Bajaj et al., 2014</xref>; <xref ref-type="bibr" rid="B14">Giannelli et al., 2014</xref>; <xref ref-type="bibr" rid="B29">Qin et al., 2014</xref>; <xref ref-type="bibr" rid="B33">Tilg et al., 2016</xref>; <xref ref-type="bibr" rid="B1">Albillos et al., 2020</xref>; <xref ref-type="bibr" rid="B20">Li et al., 2022</xref>). This issue opens a new avenue for preventive strategies and therapeutic interventions aimed at modulating the gut microbiome to improve health and patient quality of life.</p>
<sec sec-type="conclusion" id="s1">
<title>Conclusion</title>
<p>The intricate interplay between the gut microbiota, virome, mycome, and archaeome has profound implications for GI diseases and these studies provide a foundation for future research and potential therapeutic innovations. This editorial reveals how these microbial communities influence conditions such as HSV, chronic gastritis, liver cirrhosis and emphasize the potential of targeting gut microbiota for therapeutic interventions. Understanding the intricate web of these microorganisms opens new avenues for personalized medicine, aiming to improve GI health through advanced sequencing technologies and metagenomic analyses (<xref ref-type="bibr" rid="B5">Brim et al., 2017</xref>; <xref ref-type="bibr" rid="B21">Liang et al., 2017</xref>). We hope this issue inspires further exploration into the intricate web of the GI ecosystem and its impact on health, fostering a deeper understanding that can translate into better clinical practices and holds vast potential for unlocking new paradigms in the treatment and management of gastrointestinal diseases to improve patient outcomes.</p>
</sec>
</body>
<back>
<sec id="s2">
<title>Author contributions</title>
<p>AA: Writing&#x2013;review and editing, Writing&#x2013;original draft. MA: Formal Analysis, Writing&#x2013;review and editing. MR: Conceptualization, Data curation, Supervision, Writing&#x2013;review and editing, Writing&#x2013;original draft.</p>
</sec>
<sec sec-type="funding-information" id="s3">
<title>Funding</title>
<p>The author(s) declare that no financial support was received for the research, authorship, and/or publication of this article.</p>
</sec>
<sec sec-type="COI-statement" id="s4">
<title>Conflict of interest</title>
<p>The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.</p>
</sec>
<sec sec-type="disclaimer" id="s5">
<title>Publisher&#x2019;s note</title>
<p>All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher.</p>
</sec>
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