Knowledge mapping of severe fever with thrombocytopenia syndrome: a bibliometric analysis

BackgroundSevere fever with thrombocytopenia syndrome (SFTS), caused by the Dabie bandavirus (DBV), formerly known as the SFTS virus (SFTSV), is characterized by rapid progression, high morbidity, and mortality. This study aims to analyze the current research status, hotspots, and trends of SFTS since 2009 through bibliometrics, focusing on original research and providing valuable references and inspirations for future basic research, prevention and control of SFTS.MethodsThe Web of Science Core Collection (WOSCC) was used to extract global papers on SFTS from 2009 to 2024. VOSviewer and CiteSpace software were also used to process and visualize results.ResultsA total of 760 publications relevant to SFTS were reviewed. Among these publications, the most active country, author, and publication type included China, Liu Wei, and original articles, respectively. Among the institutions, the National Institute of Infectious Diseases emerged as the top publisher. The most frequently used keywords were “China,” “Bunyavirus,” and “person-to-person transmission.” The bibliometric analysis reviewed and summarized the research results in the field of SFTS and demonstrated the research trends in the field. In addition, the study revealed the current research hotspots and predicted the future research frontiers and potential challenges in the field of SFTS, which will provide references for further exploring and investigating the SFTS-related mechanisms and inspire new therapeutic strategies.ConclusionBibliometric visualization provides an overview of research advances, hotspots, and trends regarding SFTS and consolidates existing knowledge. SFTS research is in a phase of rapid development, and the number of annual publications in the field is growing steadily and rapidly. This is laying the groundwork for further research and providing new ideas for clinicians engaged in SFTS-related therapies and researchers working to improve public health. Currently, researchers are focused on elucidating the biology of SFTS, exploring antibodies, delving into pathogenesis, and investigating specific therapies

Research trends on alphavirus receptors: a bibliometric analysis

BackgroundAlphaviruses are a diverse group of pathogens that have garnered considerable attention due to their impact on human health. By investigating alphavirus receptors, researchers can elucidate viral entry mechanisms and gain important clues for the prevention and treatment of viral diseases. This study presents an in-depth analysis of the research progress made in the field of alphavirus receptors through bibliometric analysis.MethodsThis study encompasses various aspects, including historical development, annual publication trends, author and cited-author analysis, institutional affiliations, global distribution of research contributions, reference analysis with strongest citation bursts, keyword analysis, and a detailed exploration of recent discoveries in alphavirus receptor research.ResultsThe results of this bibliometric analysis highlight key milestones in alphavirus receptor research, demonstrating the progression of knowledge in this field over time. Additionally, the analysis reveals current research hotspots and identifies emerging frontiers, which can guide future investigations and inspire novel therapeutic strategies.ConclusionThis study provides an overview of the state of the art in alphavirus receptor research, consolidating the existing knowledge and paving the way for further advancements. By shedding light on the significant developments and emerging areas of interest, this study serves as a valuable resource for researchers, clinicians, and policymakers engaged in combating alphavirus infections and improving public health

The emerging role of E3 ubiquitin ligase RNF213 as an antimicrobial host determinant

Ring finger protein 213 (RNF213) is a large E3 ubiquitin ligase with a molecular weight of 591 kDa that is associated with moyamoya disease, a rare cerebrovascular disease. It is located in the cytosol and perinuclear space. Missense mutations in this gene have been found to be more prevalent in patients with moyamoya disease compared with that in healthy individuals. Understanding the molecular function of RNF213 could provide insights into moyamoya disease. RNF213 contains a C3HC4-type RING finger domain with an E3 ubiquitin ligase domain and six AAA+ adenosine triphosphatase (ATPase) domains. It is the only known protein with both AAA+ ATPase and ubiquitin ligase activities. Recent studies have highlighted the role of RNF213 in fighting against microbial infections, including viruses, parasites, bacteria, and chlamydiae. This review aims to summarize the recent research progress on the mechanisms of RNF213 in pathogenic infections, which will aid researchers in understanding the antimicrobial role of RNF213

A role for tunneling nanotubes in virus spread

Tunneling nanotubes (TNTs) are actin-rich intercellular conduits that mediate distant cell-to-cell communication and enable the transfer of various cargos, including proteins, organelles, and virions. They play vital roles in both physiological and pathological processes. In this review, we focus on TNTs in different types of viruses, including retroviruses such as HIV, HTLV, influenza A, herpesvirus, paramyxovirus, alphavirus and SARS-CoV-2. We summarize the viral proteins responsible for inducing TNT formation and explore how these virus-induced TNTs facilitate intercellular communication, thereby promoting viral spread. Furthermore, we highlight other virus infections that can induce TNT-like structures, facilitating the dissemination of viruses. Moreover, TNTs promote intercellular spread of certain viruses even in the presence of neutralizing antibodies and antiviral drugs, posing significant challenges in combating viral infections. Understanding the mechanisms underlying viral spread via TNTs provides valuable insights into potential drug targets and contributes to the development of effective therapies for viral infections

Elucidating the Host Interactome of EV-A71 2C Reveals Viral Dependency Factors

Viral protein 2C plays a critical role in EV-A71 replication. The discovery of 2C binding proteins will likely provide potential targets to treat EV-A71 infection. Here, we provide a global proteomic analysis of the human proteins that interact with the EV-A71 2C protein. TRIM4, exportin2, and ARFGAP1 were validated as 2C binding partners. Further functional studies revealed that TRIM4, exportin2, and ARFGAP1 were novel host dependency factors for EV-A71. Moreover, enteroviruses’ 2C family proteins interacted with exportin2 and ARFGAP1. In conclusion, our study provides a cellular interactome of the EV-A71 2C and identifies the proviral roles of TRIM4, exportin2, and ARFGAP1 in EV-A71 infection

ARF1 and GBF1 Generate a PI4P-Enriched Environment Supportive of Hepatitis C Virus Replication

Cellular levels of phosphatidylinositol 4-phosphate (PI4P) have been shown to be upregulated during RNA replication of several viruses, including the HCV replicon model. However, whether PI4P is required in an infectious HCV model remains unknown. Moreover, it is not established whether the host transport machinery is sequestered by the generation of PI4P during HCV infection. Here we found that PI4P was enriched in HCV replication complexes when Huh7.5.1 cells were infected with JFH1. HCV replication was inhibited upon overexpression of the PI4P phosphatase Sac1. The PI4P kinase PI4KIII$\beta$ was also found to be required for HCV replication. Moreover, the vesicular transport proteins ARF1 and GBF1 colocalized with PI4KIIIβ and were both required for HCV replication. During authentic HCV infection, PI4P plays an integral role in virus replication

Meta-analysis of the association between toll-like receptor gene polymorphisms and hepatitis C virus infection

ObjectiveThe objective of this study is to investigate the association between toll-like receptor (TLR) 3/7 gene polymorphisms and the infection by hepatitis C virus (HCV).MethodsPubMed, Embase, Web of Science, Scopus, CNKI, Wanfang Data, and SinoMed were searched to identify studies focusing on the association between the TLR3 rs3775290 or the TLR7 rs179008 single nucleotide polymorphisms (SNPs) and the HCV infection. All the related articles were collected from the inception of each database to 15 January 2023. Our meta-analysis was conducted using the allelic model, the dominant model, and the recessive model. Outcomes were presented by odds ratio (ORs) and 95% confidence interval (95%CI). The heterogeneity across studies was assessed by the I2 test. A subgroup analysis was performed to explore the source of heterogeneity. Funnel plots were drawn to assess the risk of publication bias. Review Manager 5.4 was used for statistical analysis.ResultsTen articles were finally included, among which six studies were analyzed for rs3775290 and five studies were analyzed for rs179008. Studies relating to rs3775290 included 801 patients and 1,045 controls, whereas studies relating to rs179008 included 924 patients and 784 controls. The results of the meta-analysis showed that there is no significant association between rs3775290 gene polymorphism and HCV infection (T vs. C: OR = 1.12, 95%CI 0.97–1.30; TT+CT vs. CC: OR = 1.20, 95%CI 0.73–1.96; TT vs. CT+CC: OR = 1.13, 95%CI 0.68–1.89). The recessive model showed that rs179008-T allele homozygotes had an 89% increased risk of infection by HCV compared with rs179008-A allele carriers (TT vs. AT+AA: OR = 1.89, 95%CI 1.13–3.16). The results of the subgroup analysis demonstrated that the characteristics of the control population may serve as an important source of heterogeneity. In the African populations, individuals with homozygous rs179008-T alleles had a higher risk of infection by HCV than rs179008-A allele carriers (OR = 2.14, 95%CI 1.18–3.87). We did not find that this difference existed in the European populations (OR = 1.24, 95%CI 0.43–3.56).ConclusionThere is no significant association between rs3775290 single nucleotide polymorphism and the infection by HCV. Individuals with homozygous rs179008-T alleles have a higher risk of an infection by HCV than rs179008-A allele carriers, which is statistically significant in the African populations

Picornavirus 2C proteins: structure-function relationships and interactions with host factors

Picornaviruses, which are positive-stranded, non-enveloped RNA viruses, are known to infect people and animals with a broad spectrum of diseases. Among the nonstructural proteins in picornaviruses, 2C proteins are highly conserved and exhibit multiple structural domains, including amphipathic α-helices, an ATPase structural domain, and a zinc finger structural domain. This review offers a comprehensive overview of the functional structures of picornaviruses’ 2C protein. We summarize the mechanisms by which the 2C protein enhances viral replication. 2C protein interacts with various host factors to form the replication complex, ultimately promoting viral replication. We review the mechanisms through which picornaviruses’ 2C proteins interact with the NF-κB, RIG-I, MDA5, NOD2, and IFN pathways, contributing to the evasion of the antiviral innate immune response. Additionally, we provide an overview of broad-spectrum antiviral drugs for treating various enterovirus infections, such as guanidine hydrochloride, fluoxetine, and dibucaine derivatives. These drugs may exert their inhibitory effects on viral infections by targeting interactions with 2C proteins. The review underscores the need for further research to elucidate the precise mechanisms of action of 2C proteins and to identify additional host factors for potential therapeutic intervention. Overall, this review contributes to a deeper understanding of picornaviruses and offers insights into the antiviral strategies against these significant viral pathogens

Inhibition of Macrophage Activation by the Myxoma Virus M141 Protein (vCD200)▿

The M141 protein of myxoma virus (MYXV) is a viral CD200 homolog (also called vOX-2) that inhibits macrophage activation in infected rabbits. Here, we show that murine myeloid RAW 264.7 cells became activated when infected with MYXV in which the M141 gene was deleted (vMyx-M141KO) but not with the parental wild-type MYXV. Moreover, transcript and protein levels of tumor necrosis factor and granulocyte colony-stimulating factor were rapidly upregulated in an NF-κB-dependent fashion in the RAW 264.7 cells infected with vMyx-M141KO. M141 protein is present in the virion and counteracts this NF-κB activation pathway upon infection with the wild-type MYXV. Our data suggest that upregulation of these classic macrophage-related proinflammatory cytokine markers following infection of myeloid cells with the M141-knockout MYXV is mediated via the rapid activation of the cellular NF-κB pathway