Rapid HAV IgM Test Card Infectious diseases
- Known as:
- Rapid hepatitis A virus Immunoglobulin M Test Card Infectious diseases
- Catalog number:
- 1H15C2
- Product Quantity:
- 25 tests/kit
- Category:
- -
- Supplier:
- Boson
- Gene target:
- Rapid HAV IgM Test Card Infectious diseases
Related genes to: Rapid HAV IgM Test Card Infectious diseases
- 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: Rapid HAV IgM Test Card Infectious diseases
Related articles to: Rapid HAV IgM Test Card Infectious diseases
- The persistent HIV-1 reservoir includes a subset of cells harboring transcriptionally repressed latent HIV-1 that contributes to rebound upon antiretroviral treatment (ART) interruption. However, the majority of the reservoir consists of defective proviral genomes with mutations that prevent production of HIV -1 virions. People with HIV (PWH), even with suppression of viremia, demonstrate comorbidities of the central nervous system, heart, gut, and general aging-associated inflammation. Previously, we identified a transcriptionally active element within the envelope gene ( ) of HIV-1 which mediates the expression of aberrant HIV-1 RNAs. We hypothesize that spurious expression of defective proviruses contributes to the general inflammation that drives these comorbidities. We observed correlations between levels of pro-inflammatory cytokines in serum of PWH and levels of HIV-1 transcripts from this intragenic promoter. To investigate the impact of defective proviruses, we employed CRISPR-Cas9 to render the 5' Long Terminal Repeat (LTR), which acts as the enhancer and promoter for proviral transcription, non-functional. HIV-1 infected cells harboring this deletion produce significantly higher levels of IP-10 in both monocytic cell lines and primary monocyte-derived macrophages. Transcripts generated from the promoter, include a 5' cap and polyA tail and the induction of IP-10 expression was dependent on the cytosolic innate immune sensing pathway components MDA5 and MAVS. We propose that defective HIV proviruses contribute to chronic inflammation in PWH via an MDA5-dependent induction of type I interferon pathways. - Source: PubMed
Publication date: 2026/04/07
Kilroy JonathanDeokar AparnaPatalano SamanthaBass Juan FuxmanSagar ManishGummuluru SuryaramHenderson Andrew J - Ubiquitination is a critical post-translational modification that regulates protein stability, signalling pathways, and cellular homoeostasis. Increasing evidence shows that oncogenic viruses exploit the host ubiquitin system to promote viral persistence, immune evasion, and malignant transformation. Among the various host factors targeted, deubiquitinating enzymes (DUBs) play a pivotal role because they reverse ubiquitination, thereby regulating the stability, localization, and activity of key signalling proteins. Ubiquitin-specific peptidase 10 (USP10) has emerged as a particularly critical DUB in the context of viral tumourigenesis, functioning as a molecular rheostat that balances tumour suppression and oncogenic progression. The dysregulation of USP10 by viral oncoproteins facilitates a dual assault on the host: the subversion of innate immune sensors, specifically the RIG-I, MAVS, and cGAS-STING pathways, and the evasion of adaptive immune surveillance through the stabilisation of immune checkpoints, such as PD-L1, and the disruption of MHC-I antigen presentation. This comprehensive analysis explores the biochemical architecture of USP10, its paradoxical roles in cancer, and the specific mechanisms through which oncogenic viruses exploit this enzyme to drive malignancy and immune escape. - Source: PubMed
Li ZikeZhang DongjingChen SiqiZhang XinWang ZhihongHuang ChangshengWu QiLiu AnyiLi KangdiWei ZiranHu Junbo - Takayasu arteritis (TAK) is a refractory chronic vasculitis of the aorta and its major branches, characterized by unsatisfactory treatment responses and high relapse rates. This review synthesizes current evidence to propose and elaborate a novel pathogenic paradigm: a self-reinforcing "metabolism-epigenetics-inflammation" feedback loop that sustains chronic vascular inflammation in TAK. We detail how immunometabolic reprogramming in immune and vascular wall cells not only meets bioenergetic demands but also generates metabolites (e.g., acetyl-CoA, lactate) that serve as substrates or cofactors for epigenetic modifications. These modifications, in turn, lock in a persistent pro-inflammatory gene expression profile. A central focus is the dissection of the ANK2-MAVS-IL-8 axis, a critical link connecting genetic susceptibility (via ANK2 variants) through mitochondrial dysfunction to sustained, IL-8-driven vascular injury. Building on this mechanistic framework, the review explores the translational potential of emerging biomarker candidates (e.g., IL-8, specific methylation marks) and proposes stratified therapeutic strategies that target distinct nodes within this interactive network, including metabolic drivers, epigenetic stabilizers, and inflammatory effectors. Ultimately, this work provides an integrated conceptual and translational roadmap for advancing precision medicine in TAK. - Source: PubMed
Publication date: 2026/04/03
Xie TianjianZhang LeyuLi ShurongXu BenmoZhang XinyuWang YajunShang ZixiangXi HongxuanShi HanNi XinLi PingLi Hengxi - Human cytomegalovirus (HCMV) encodes the viral mitochondria-localized inhibitor of apoptosis (vMIA) protein which blocks host cell apoptosis. vMIA also inhibits innate immune signaling through the DNA sensing cGAS-STING pathway and the RNA sensing RLR pathway which interacts with the mitochondrial adapter protein MAVS. We demonstrate stable expression and mitochondrial localization of vMIA in a human Mueller cell line (MIO-M1). In a real time apoptosis assay, vMIA significantly reduced staurosporine (STS)-induced apoptosis in MIO-M1 cells. In addition, immunoblots indicated that vMIA blocked apoptotic cleavage of the nuclear enzyme PARP1. vMIA also reduced STS mediated necrosis at later time points in MIO-M1 cells. The steady state level of cGAS protein was increased in vMIA expressing MIO-M1 cells. In contrast, vMIA decreased the amount STING protein in MIO-M1 cells. A decrease in the percentage of aggregated mitochondrial antiviral-signaling protein (MAVS), and alteration of the classic mitochondrial localization of MAVS, in the presence of vMIA suggested that vMIA induced changes in mitochondrial morphology in MIO-M1 cells. Activation of NF-κB by stimulators including LPS, poly I:C, hrTNFα, and zymosan was significantly reduced in MIO-M1 cells expressing vMIA. The transduction efficiency of a lentiviral gene delivery vector was not reduced in the presence of vMIA. These results represent the first demonstration of the anti-apoptotic and anti-innate immune signaling capabilities of vMIA in a human retinal cell line. The dual functions of vMIA could provide an effective strategy to treat multiple neurodegenerative diseases and also reduce gene therapy induced ocular inflammation. - Source: PubMed
Publication date: 2026/04/10
Sauter Monica MNoel Hongyu RBrandt Curtis R - The DNA sensing signaling pathway mediated by cGAS-STING has achieved significant progress in cancer therapy. However, the role of the RNA sensing signaling pathway mediated by RLRs-MAVS in cancer has been relatively underexplored. In this review, we first elaborate on the structural basis, activation, and regulatory mechanisms of MAVS, and examine its functional interplay with other innate immune pathways. We then comprehensively review its functions in cancer. Finally, we summarize its potential clinical applications, existing challenges, and proposed solutions. Moreover, we compare MAVS with STING across these three dimensions and find that they exhibit similarities in signaling pathways, perform analogous functions in cancer, and share comparable potential for clinical applications. Therefore, we propose that MAVS could emerge as the next STING in cancer therapy. - Source: PubMed
Publication date: 2026/04/08
Li SiyingBai JunqiangWang XinmiaoGuo ShutianGuo XiaomengShang ZhengjunShao Zhe