{"title":"APOBEC3 family proteins as drivers of virus evolution","authors":"Michael Jonathan, Terumasa Ikeda","doi":"10.3389/fviro.2023.1332010","DOIUrl":"https://doi.org/10.3389/fviro.2023.1332010","url":null,"abstract":"<p>The apolipoprotein B mRNA editing enzyme catalytic polypeptide-like (APOBEC) family consists of cytosine deaminases implicated in diverse and important biological functions. APOBEC3 (A3) proteins belong to the APOBEC/AID family, and they catalyze the deamination of cytosine to uracil in single-stranded DNA and, to a lesser extent, in RNA substrates. In humans, seven <italic>A3</italic> genes have been identified (<italic>A3A</italic>, <italic>A3B</italic>, <italic>A3C</italic>, <italic>A3D</italic>, <italic>A3F</italic>, <italic>A3G</italic>, and <italic>A3H</italic>). The introduction of lethal G-to-A or C-to-U mutations into certain viral genomes leads to virus inactivation. However, the mutagenic capability of A3 proteins could serve as a source of mutations to drive virus evolution. Therefore, recent studies have implied the role of A3 proteins in aiding the evolution of viruses, conferring them with severe manifestations such as drug resistance and/or immune evasion. In this review, we discuss in depth the interactions of A3 proteins with viruses that infect humans and our self-proteins.</p>","PeriodicalId":73114,"journal":{"name":"Frontiers in virology","volume":"12 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-12-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138716693","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Eric Asare Fenteng, Paul Poku Sampene Ossei, William Gilbert Ayibor, Tracy Narh-Bedu
{"title":"Beyond survival: unraveling the dynamics of Ebola virus resurgence in Sub-Saharan Africa and the remarkable journey of survivors","authors":"Eric Asare Fenteng, Paul Poku Sampene Ossei, William Gilbert Ayibor, Tracy Narh-Bedu","doi":"10.3389/fviro.2023.1227314","DOIUrl":"https://doi.org/10.3389/fviro.2023.1227314","url":null,"abstract":"Ebola virus disease (EVD) remains a significant public health threat, with sporadic outbreaks occurring in Sub-Saharan Africa. Survivors of EVD may experience various post-infection symptoms, collectively known as post-Ebola virus syndrome (PES), which include chronic arthralgia, uveitis, headache, and psychosocial stressors. In this review, we discuss the persistence of Ebola virus in survivors and its possible role in the reemergence of current outbreaks. We highlight that waning immunity of survivors enhances viral persistence and may lead to viral reactivation and recurrence of disease in previously affected tissues. The delicate equilibrium between diminished immune cell surveillance and limited viral replication may lead to enduring chronic inflammation. Our systematic review, based on an extensive survivor cohort, underscores the importance of continued research and preparedness efforts to combat future outbreaks through adequate surveillance and timely public health interventions. This review serves as a comprehensive guide to understanding the complexities of EVD survivorship, the challenges of PES, and the strategies to mitigate its impact.","PeriodicalId":73114,"journal":{"name":"Frontiers in virology","volume":"9 6","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-11-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"136352049","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Michael A. Zeller, Zebulun W. Arendsee, Gavin J.D. Smith, Tavis K. Anderson
{"title":"classLog: Logistic regression for the classification of genetic sequences","authors":"Michael A. Zeller, Zebulun W. Arendsee, Gavin J.D. Smith, Tavis K. Anderson","doi":"10.3389/fviro.2023.1215012","DOIUrl":"https://doi.org/10.3389/fviro.2023.1215012","url":null,"abstract":"<sec><title>Introduction</title><p>Sequencing and phylogenetic classification have become a common task in human and animal diagnostic laboratories. It is routine to sequence pathogens to identify genetic variations of diagnostic significance and to use these data in realtime genomic contact tracing and surveillance. Under this paradigm, unprecedented volumes of data are generated that require rapid analysis to provide meaningful inference. </p></sec><sec><title>Methods</title><p>We present a machine learning logistic regression pipeline that can assign classifications to genetic sequence data. The pipeline implements an intuitive and customizable approach to developing a trained prediction model that runs in linear time complexity, generating accurate output rapidly, even with incomplete data. Our approach was benchmarked against porcine respiratory and reproductive syndrome virus (PRRSv) and swine H1 influenza A virus (IAV) datasets. Trained classifiers were tested against sequences and simulated datasets that artificially degraded sequence quality at 0, 10, 20, 30, and 40%. </p></sec><sec><title>Results</title><p>When applied to a poor-quality sequence data, the classifier achieved between >85% to 95% accuracy for the PRRSv and the swine H1 IAV HA dataset and this increased to near perfect accuracy when using the full dataset. The model also identifies amino acid positions used to determine genetic clade identity through a feature selection ranking within the model. These positions can be mapped onto a maximum-likelihood phylogenetic tree, allowing for the inference of clade defining mutations. </p></sec><sec><title>Discussion</title><p>Our approach is implemented as a python package with code available at <uri xlink:href=\"https://github.com/flu-crew/classLog\" xmlns:xlink=\"http://www.w3.org/1999/xlink\">https://github.com/flu-crew/classLog</uri>.</p></sec>","PeriodicalId":73114,"journal":{"name":"Frontiers in virology","volume":"28 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-11-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138531603","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Eva G. Álvarez, Paula Otero, Bernardo Rodríguez-Martín, Ana Pequeño-Valtierra, Iago Otero, André Vidal-Capón, Jorge Rodríguez-Castro, Juan J. Pasantes, Carmen Rivas, Jose M.C. Tubío, Daniel García-Souto
{"title":"Corrigendum: Characterization of Human Herpesvirus 8 genomic integration and amplification events in a primary effusion lymphoma cell line","authors":"Eva G. Álvarez, Paula Otero, Bernardo Rodríguez-Martín, Ana Pequeño-Valtierra, Iago Otero, André Vidal-Capón, Jorge Rodríguez-Castro, Juan J. Pasantes, Carmen Rivas, Jose M.C. Tubío, Daniel García-Souto","doi":"10.3389/fviro.2023.1324885","DOIUrl":"https://doi.org/10.3389/fviro.2023.1324885","url":null,"abstract":"• please read through all the templates before choosing • pick the most relevant text template(s) from the following page and delete all others.• edit the text as necessary, ensuring that the original incorrect text is included for the record, please see the below. • please do not use any extra formatting when editing the templates, and only modify the red text unless absolutely necessary • submit to Frontiers following the instructions on this page.When the original text contained incorrect information, to preserve the scientific record, please include that text when editing the below templates. For example:There was a mistake in the Funding statement, an incorrect number was used. The correct number is \"2015C03Bd051.\". The publisher apologizes for this mistake.The original version of this article has been updated. In the published article, there was an error in the author list, and author Jose M.C. Tubío should share correspondence for this brief research report article with Daniel García-Souto. The corrected author list appears below.Eva G. Álvarez 1,2,3 † Paula Otero 1,2,3 † Bernardo Rodríguez-Martín 1 Ana Pequeño-Valtierra 1,3 Iago Otero 1,2,3 André Vidal-Capón 4 Jorge Rodríguez-Castro 1,3 Juan J. Pasantes 4 Carmen Rivas 5 Jose M.C. Tubío 1,2,3* ‡ Daniel García-Souto 1,2,3* ‡","PeriodicalId":73114,"journal":{"name":"Frontiers in virology","volume":"127 40","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-10-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135863453","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Evolution driven by a varying host environment selects for distinct HIV-1 entry phenotypes and other informative variants","authors":"Shuntai Zhou, Nathan Long, Ronald Swanstrom","doi":"10.3389/fviro.2023.1291996","DOIUrl":"https://doi.org/10.3389/fviro.2023.1291996","url":null,"abstract":"<p>HIV-1 generates remarkable intra- and inter-host viral diversity during infection. In the response to the dynamic selective pressures of the host’s environment, HIV-1 evolves distinct phenotypes—biological features that provide fitness advantages. The transmitted form of HIV-1 has been shown to require a high density of CD4 on the target cell surface (as found on CD4<sup>+</sup> T cells) and typically uses C–C chemokine receptor type 5 (CCR5) as a coreceptor during entry. This phenotype is referred to as R5T cell-tropic (or R5 T-tropic); however, HIV-1 can switch to a secondary coreceptor, C–X–C chemokine receptor type 4 (CXCR4), resulting in a X4T cell-tropic phenotype. Macrophage-tropic (or M-tropic) HIV-1 can evolve to efficiently enter cells expressing low densities of CD4 on their surface (such as macrophages/microglia). So far only CCR5-using M-tropic viruses have been found. M-tropic HIV-1 is most frequently found within the central nervous system (CNS), and infection of the CNS has been associated with neurologic impairment. It has been shown that interferon-resistant phenotypes have a selective advantage during transmission, but the underlying mechanism of this is still unclear. During untreated infection, HIV-1 evolves under selective pressure from both the humoral/antibody response and CD8<sup>+</sup> T-cell killing. Sufficiently potent antiviral therapy can suppress viral replication, but if the antiviral drugs are not powerful enough to stop replication, then the replicating virus will evolve drug resistance. HIV-1 phenotypes are highly relevant to treatment efforts, clinical outcomes, vaccine studies, and cure strategies. Therefore, it is critical to understand the dynamics of the host environment that drive these phenotypes and how they affect HIV-1 pathogenesis. This review will provide a comprehensive discussion of HIV-1 entry and transmission, and drug-resistant phenotypes. Finally, we will assess the methods used in previous and current research to characterize these phenotypes.</p>","PeriodicalId":73114,"journal":{"name":"Frontiers in virology","volume":"42 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-10-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138531597","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Gisele Cassão, Krist Helen Antunes, João Ismael Budelon Gonçalvez, Leonardo Duarte Santos, Bruno Lopes Abbadi, Cristiano Valim Bizarro, Pablo Machado, Luiz Augusto Basso, Christian Pasquali, Renato T. Stein, Ana Paula Duarte de Souza
{"title":"Brief research report: OM-85 reduces SARS-COV-2 viral RNA expression in nasopharyngeal cells from COVID-19 patients","authors":"Gisele Cassão, Krist Helen Antunes, João Ismael Budelon Gonçalvez, Leonardo Duarte Santos, Bruno Lopes Abbadi, Cristiano Valim Bizarro, Pablo Machado, Luiz Augusto Basso, Christian Pasquali, Renato T. Stein, Ana Paula Duarte de Souza","doi":"10.3389/fviro.2023.1111619","DOIUrl":"https://doi.org/10.3389/fviro.2023.1111619","url":null,"abstract":"OM-85 is a bacterial lysate from common respiratory tract pathogens, with an excellent safety profile, widely used to prevent recurrent respiratory tract infections. Several studies have been reporting the immunomodulating properties and antiviral roles of OM-85. The COVID-19 pandemic, originating in 2019, has presented a significant global public health crisis. While effective vaccines have been developed, vaccination rates vary considerably, and numerous concerning viral variants continue to emerge. The challenge persists in creating early interventions to halt the progression of the disease to its severe stages. To examine the therapeutic effect of OM-85 after SARS-CoV-2 infection and compared to recombinant human (rhINF-β) we collected nasopharyngeal cells from COVID-19 patients. The cells were treated ex-vivo with OM-85 or hrINF-β and the response was analyzed after 24h for gene expression by real-time PCR. We found that OM-85 decreased the SARS-CoV-2 N1 gene expression and increased RIG-I (DDX58) in these cells. The expression of ACE2 was undetected in these samples. These data support the antiviral effect of OM-85 against SARS-CoV-2.","PeriodicalId":73114,"journal":{"name":"Frontiers in virology","volume":"43 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-10-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"136376467","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Ashraf Elbahrawy, Hassan Atalla, Abdulla A. Mahmoud, Ahmed Eliwa, Alaa Alsawak, Mohamed Alboraie, Ali Madian, Ahmed Alashker, Sadek Mostafa, Ahmed Alwassief, Hussein H. Aly
{"title":"Prediction and surveillance of de novo HCC in patients with compensated advanced chronic liver disease after hepatitis C virus eradication with direct antiviral agents","authors":"Ashraf Elbahrawy, Hassan Atalla, Abdulla A. Mahmoud, Ahmed Eliwa, Alaa Alsawak, Mohamed Alboraie, Ali Madian, Ahmed Alashker, Sadek Mostafa, Ahmed Alwassief, Hussein H. Aly","doi":"10.3389/fviro.2023.1227317","DOIUrl":"https://doi.org/10.3389/fviro.2023.1227317","url":null,"abstract":"The risk of hepatocellular carcinoma (HCC) diminishes in patients with hepatitis C virus (HCV)-related advanced chronic liver disease after virological cure. However, despite viral clearance, HCV-induced epigenetic alterations, immune dysregulations, and hepatic parenchymal injuries remain, contributing to de novo HCC occurrence. While HCC incidence is low (0.45 – 0.5%) in patients with advanced fibrosis (F3), the presence of liver cirrhosis and clinically significant portal hypertension increases the HCC risk. The cost-effectiveness of lifelong HCC surveillance in patients with compensated advanced chronic liver disease (cACLD) has sparked debate, raising questions about the most reliable noninvasive tests and stratification models for predicting HCC in patients with sustained virological response (SVR). Furthermore, identifying cACLD patients who may not require long-term HCC surveillance after SVR remains crucial. Several HCC risk stratification scores have been suggested for patients with cACLD, and emerging evidence supports individualized care based on personalized risk assessments. This review focuses on revising the pretreatment and posttreatment predictors of HCC, as well as the indications for HCC surveillance in cACLD patients treated with direct-acting antivirals.","PeriodicalId":73114,"journal":{"name":"Frontiers in virology","volume":"2017 4","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-10-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135266251","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Edith A. Ogalo, Edwin Gudu, Thomas Andale, Daisy Korir, Samson Ndege, Tabu Simiyu, Richard Olekuyo, Henry Mwangi, Sylvester Kimaiyo, Wilson Aruasa
{"title":"Clinical spectrum of COVID-19 at a national referral hospital in western Kenya during the period 2020–2021","authors":"Edith A. Ogalo, Edwin Gudu, Thomas Andale, Daisy Korir, Samson Ndege, Tabu Simiyu, Richard Olekuyo, Henry Mwangi, Sylvester Kimaiyo, Wilson Aruasa","doi":"10.3389/fviro.2023.1202742","DOIUrl":"https://doi.org/10.3389/fviro.2023.1202742","url":null,"abstract":"Introduction We describe the clinical spectrum of COVID-19 cases in western Kenya from 6 April 2020 to 31 May 2021, providing baseline data for further studies into COVID-19 in Kenya. Methods We did a retrospective chart review of laboratory and inpatient files of patients diagnosed and managed for COVID-19 at the Moi Teaching and Referral Hospital in Kenya and analyzed the data using Stata ® version 16 (StataCorp LP, College Station, TX, USA) and calculated measures of association at 95% CI. Results The patients ( n = 1,770) had a mean age of 43 years (SD 20 years) and 55.4% were male. Close to 70% had asymptomatic disease, with the symptomatic cases largely being respiratory in nature. One-quarter had comorbidities. The case fatality rate was 13.6% ( n = 240). Male sex increased the odds of mortality by 1.69 (95% CI 1.27–2.25; p ≤ 0.001), and the presence of comorbidities increased the odds of mortality by 3.16 (95% CI 2.38–4.18; p ≤ 0.001). Those aged 59 years and above were 18 times more likely to die from COVID-19 than those below 15 years of age (95% CI 1.61–90.66; p = 0.015). Conclusion COVID-19 had a significantly high mortality rate in western Kenya. Male sex and the presence of comorbidities increased the risk of severe disease and mortality.","PeriodicalId":73114,"journal":{"name":"Frontiers in virology","volume":"21 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-10-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135968675","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Nidhi Kumari, Vivek Sharma, Priyankaben Patel, P. N. Sharma
{"title":"Pepper mild mottle virus: a formidable foe of capsicum production—a review","authors":"Nidhi Kumari, Vivek Sharma, Priyankaben Patel, P. N. Sharma","doi":"10.3389/fviro.2023.1208853","DOIUrl":"https://doi.org/10.3389/fviro.2023.1208853","url":null,"abstract":"Viruses are one of the major restraining factors in pepper cultivation globally. Among different viruses, pepper mild mottle virus (PMMoV) is one of the most detrimental plant viruses infecting Capsicum spp. belonging to the genus Tobamovirus and Virgaviridae family. It has a monopartite positive-sense single-stranded RNA genome of 6.35 kb size. On an average, PMMoV results in 15%–40% losses in capsicum fruit yield. However, the incidence of PMMoV can reach as high as 95%, leading to substantial yield losses ranging from 75% to 95%. The virus is transmitted via contact, soil, and seeds rather than via insect vectors. PMMoV, because of its seed-borne nature, now occurs worldwide. PMMoV mainly infects Capsicum spp. under natural conditions; however, it can experimentally be transmitted to other plants species belonging to the families Solanaceae, Cucurbitaceae, Labiatae, Chenopodiaceae, and Plantaginaceae. The resistance to tobamoviruses in capsicum is conferred by L locus. Mutations in the coat protein of PMMoV are responsible for the emergence of L -mediated resistance-breaking pathotypes. The highly contagious nature of the virus, seed transmission behavior, and the emergence of virulence complicate its management through a single approach. Therefore, efforts are directed towards providing a more practical and efficient integrated management solution using the RNA interference approach; exploitation of the L gene for resistance breeding; and the inhibitory potential of natural products, systemic resistance-inducing antagonistic bacteria, and chemically synthesized silver nanoparticles. Markers linked to L alleles have been observed to accelerate capsicum breeding programs through marker-assisted selection. In this study, an attempt has been made to compile the recent developments in PMMoV biology, pathogenic variability, genomic organization, and management strategies.","PeriodicalId":73114,"journal":{"name":"Frontiers in virology","volume":"128 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-10-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135968661","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Eva G. Álvarez, Paula Otero, Bernardo Rodríguez-Martín, Ana Pequeño-Valtierra, Iago Otero, André Vidal-Capón, Jorge Rodríguez-Castro, Juan J. Pasantes, Carmen Rivas, Jose M.C. Tubío, Daniel García-Souto
{"title":"Characterization of Human Herpesvirus 8 genomic integration and amplification events in a primary effusion lymphoma cell line","authors":"Eva G. Álvarez, Paula Otero, Bernardo Rodríguez-Martín, Ana Pequeño-Valtierra, Iago Otero, André Vidal-Capón, Jorge Rodríguez-Castro, Juan J. Pasantes, Carmen Rivas, Jose M.C. Tubío, Daniel García-Souto","doi":"10.3389/fviro.2023.1253416","DOIUrl":"https://doi.org/10.3389/fviro.2023.1253416","url":null,"abstract":"In this study, we investigated the integration of Human Herpesvirus 8 (HHV-8) into the human genome using the primary effusion lymphoma (PEL) cell line BC-3. Through next-generation sequencing (NGS) data from multiple independent sequencing runs, we identified two highly supported HHV-8 integrants. These integrants encompassed a region of human chromosome 12 that was amplified approximately 16-fold between the junctions. Significantly, these events could represent the first known instance of HHV-8 integration into a hybrid human-viral extrachromosomal chimeric circular DNA (eccDNA). The amplified fragment contained partial or complete copies of various human genes, including SELPLG and CORO1C. Analysis of long-read Nanopore data indicated that the CpGs at the SELPLG promoter were mostly unmethylated, suggesting that the additional copies of SELPLG within this eccDNA are likely transcriptionally active. Our findings suggest that viral insertion and eccDNA amplification could be crucial mechanisms in the development of HHV-8-related cancers. In conclusion, our study provides valuable insights into the molecular mechanisms involved in HHV-8-induced oncogenesis and emphasizes the importance of investigating viral integration and eccDNAs in cancer development. Furthermore, we highlight the necessity of employing multiple independent sequencing approaches to validate integration events and avoid false positives derived from library construction artifacts.","PeriodicalId":73114,"journal":{"name":"Frontiers in virology","volume":"240 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135895518","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}