Test of Infectious Diseases HBeAg Test Card
- Known as:
- Test Infectious Diseases Hepatitis B “e” antigen Test Card
- Catalog number:
- HBeAg -242
- Product Quantity:
- 4.0 mm (strip in a card) 25cards/box price for 1000
- Category:
- -
- Supplier:
- Innoragen
- Gene target:
- Test Infectious Diseases HBeAg Card
Related genes to: Test of Infectious Diseases HBeAg Test Card
- Gene:
- MAVS NIH gene
- Name:
- mitochondrial antiviral signaling protein
- Previous symbol:
- -
- Synonyms:
- VISA, KIAA1271, IPS-1, Cardif
- Chromosome:
- 20p13
- Locus Type:
- gene with protein product
- Date approved:
- 2009-04-01
- Date modifiied:
- 2017-09-22
Related products to: Test of Infectious Diseases HBeAg Test Card
Related articles to: Test of Infectious Diseases HBeAg Test Card
- Alphaviruses, including significant human pathogens like Chikungunya (CHIKV), Venezuelan Equine Encephalitis (VEEV), and the model Sindbis virus (SINV), pose a considerable global health threat. Their ability to establish infection and cause disease is critically dependent on successfully subverting the host's innate immune defenses, particularly the Type I Interferon (IFN-I) system. This review provides a comparative analysis of the molecular strategies employed by CHIKV, VEEV, and SINV to dismantle these antiviral pathways. We first outline the conserved principles that form a core alphavirus "toolkit" for evasion, such as the formation of membrane-bound replication factories to shield viral RNA from cytosolic sensors and NSP1-mediated mRNA capping to mimic host transcripts. The review then delves into the divergent, virus-specific tactics, highlighting the central role of the non-structural protein 2 (NSP2) as a master antagonist. We contrast the aggressive strategies of pathogenic alphaviruses-such as CHIKV NSP2-mediated cleavage of MAVS and degradation of STAT2, and VEEV-induced degradation of STAT1-with the more subtle, modulatory approach of SINV, which relies more on a global shutdown of host gene expression. These distinct molecular mechanisms are directly correlated with their varying pathogenic outcomes. Furthermore, we examine the remarkable adaptability of these strategies between vertebrate hosts, where suppressing the IFN system is paramount, and invertebrate vectors, where evading the RNAi pathway is the primary challenge. A comprehensive understanding of these commonalities and divergences in immune evasion is essential for the rational design of broad-spectrum antiviral therapeutics and next-generation vaccines. - Source: PubMed
Feyzi KambizMousavi Fatemeh SadatAbbasi Samaneh - Influenza A virus (IAV) remains a significant public health threat due to its high variability and pathogenicity. Systematic identification of viral-host interfaces is critical for developing targeted therapies. In the present study, TurboID proximity labeling was applied to map interactomes of 10 H1N1 viral proteins in human alveolar epithelial cells A549. Key interactions were validated via co-immunoprecipitation (Co-IP), confocal microscopy, dual-luciferase reporter assays, and functional studies. Results showed that Hemagglutinin (HA) and polymerase acidic (PA) directly bound mitochondrial antiviral-signaling protein (MAVS), significantly suppressing interferon-beta (IFN-β) promoter activity and impairing phosphorylation of TANK-binding kinase 1 (TBK1)/signal transducer and activator of transcription (STAT) signaling proteins. HA exploited integrin alpha-2 (ITGA2) as a novel entry cofactor, with their interaction confirmed by bidirectional Co-IP and co-localization. ITGA2 silencing markedly reduced viral titers. Tripartite motif-containing protein 56 (TRIM56) restricted H1N1 replication by binding viral nucleoprotein (NP) and inducing proteasomal degradation via K48-linked ubiquitination. As a conclusion, this study delineates H1N1's coordinated tactics to hijack host pathways, identifying MAVS, ITGA2, and TRIM56 as pivotal nodes for combination therapies. TurboID-driven interactomics provides a promising framework for system-level antiviral discovery. - Source: PubMed
Wang MinWang ZhengLiu ChenyangDuan JiajiaWu TingFu QizhiSu Xin - Endogenous retroviruses (ERVs) are epigenetically silenced remnants of ancient retroviral integrations that comprise ~8% of the human genome. In cancer, DNA hypomethylation and chromatin remodeling-spontaneously or induced by epigenetic therapies-can derepress ERV loci, leading to abundant ERV-derived double-stranded RNA (dsRNA) and, in some cases, immunogenic ERV proteins. Accumulated dsRNA is primarily sensed by MDA5/RIG-I and TLR3, activating MAVS/TRIF signaling to induce IRF3/7- and NF-κB-dependent type I interferons and interferon-stimulated genes. This viral mimicry enhances antigen processing and MHC-I presentation, recruits CXCR3+ effector lymphocytes via CXCL9/10/11, promotes dendritic-cell activation, reduces immunosuppressive populations, and can convert immune-cold tumors into immune-active states while also increasing PD-L1 expression. Clinical evidence from retrospective cohorts and early prospective studies supports ERV signatures as biomarkers for immune checkpoint inhibitor (ICI) response, often independent of PD-L1 or tumor mutational burden, and enables ERV-based stratification. Therapeutic strategies that induce ERVs or target ERV antigens may sensitize tumors to ICIs, although assay standardization, prospective validation, and long-term safety remain key challenges. - Source: PubMed
Publication date: 2026/05/20
Wu FanyuanDanzeng QuezhuWu RunxiShen YiShi Guang - Respiratory syncytial virus (RSV) and human metapneumovirus (hMPV), members of the Pneumoviridae family, are major causes of acute respiratory tract infections globally. Although glycosaminoglycans (GAGs), including heparan sulfate (HS), are implicated in viral attachment, their roles beyond entry remain incompletely defined. Here, we performed a genome-wide CRISPR/Cas9 knockout screen in interferon receptor-deficient cells to identify host factors commonly required for RSV and hMPV infection. The screen identified multiple genes involved in GAG biosynthesis and sulfation, including solute carrier family 35 member B2 (SLC35B2) and β-1,3-glucuronyltransferase 3 (B3GAT3). GAG sulfation promoted viral attachment and internalization of both viruses. Beyond entry, GAG sulfation influenced post-entry RSV dynamics. Genetic disruption of GAG biosynthesis or sulfation, as well as pharmacological inhibition, reduced cell-associated RSV while increasing infectious particles released into the supernatant, indicating that sulfated GAGs are associated with RSV particle retention at the cell surface in immortalized cell-line systems. This phenotype was not observed for hMPV, supporting a virus-specific requirement for GAG sulfation during RSV infection. Furthermore, RSV infection increased cell-surface GAG-reactive signal in a mitochondrial antiviral signaling protein (MAVS)-dependent manner. Loss of MAVS abolished this increase and was associated with increased released RSV titers, suggesting that innate immune signaling may influence viral release either directly through antiviral effects or indirectly through changes in GAG-related cell-surface properties. Collectively, our findings support a dual role for sulfated GAGs in Pneumoviridae infection in immortalized cell-line systems, facilitating viral entry for both RSV and hMPV while selectively restricting RSV dissemination through modulation of viral particle retention at the cell surface. - Source: PubMed
Publication date: 2026/05/26
Yoshida KeitaroYamamoto SohOgasawara NorikoTaniguchi KiyosuNosaka TetsuyaYokota Shin-Ichi - MDA5 is a cytosolic pattern-recognition receptor (PRR) that binds to double-stranded RNA (dsRNA) and subsequently interacts with the signaling adaptor protein MAVS to initiate the antiviral interferon (IFN) response. Our group previously demonstrated that MDA5 is essential for host resistance against the fungal pathogen, . Although fungal dsRNA was sufficient to activate MDA5 signaling, the precise source of dsRNA responsible for this MDA5-stimulating function remains unknown. Here, we demonstrate that the magnitude of the IFN-dependent antifungal response is strain dependent. Unexpectedly, we found that isolates infected with dsRNA mycoviruses triggered a more robust MAVS-dependent inflammatory response within alveolar macrophages. Furthermore, dsRNA mycovirus infection increased fungal susceptibility to antifungal killing without altering other growth characteristics. Although dsRNA mycovirus infection did not alter virulence in an acute bronchopneumonia model of infection, it significantly impaired virulence and improved disease parameters in a chronic model of allergic bronchopulmonary aspergillosis (ABPA). Collectively, these findings reveal a novel role for trans-kingdom interactions in driving the host antifungal IFN response and modulating virulence in chronic aspergillosis models. - Source: PubMed
Publication date: 2026/05/18
Rapp Alexander WWang XiRoss Brandon SCaffrey-Carr Alayna KThomas Sean MResendiz-Sharpe AgustinOlive Andrew JLagrou KatrienCramer Robert AObar Joshua J