Ask about this productRelated genes to: PVRL1 antibody
- Gene:
- NECTIN1 NIH gene
- Name:
- nectin cell adhesion molecule 1
- Previous symbol:
- HVEC, ED4, PVRL1
- Synonyms:
- PRR, PRR1, PVRR1, SK-12, HIgR, CLPED1, CD111, OFC7
- Chromosome:
- 11q23.3
- Locus Type:
- gene with protein product
- Date approved:
- 1999-11-15
- Date modifiied:
- 2016-02-12
Related products to: PVRL1 antibody
Related articles to: PVRL1 antibody
- Herpes B virus (BV; ) is a zoonotic alphaherpesvirus endemic in macaques that can cause severe, often fatal encephalomyelitis in humans. However, genomic data from wild macaque populations remain limited. Here, we report the isolation and genomic characterization of a BV strain from a wild long-tailed macaque () in Thailand and assess its zoonotic potential. Among 138 macaques screened across six populations, BV shedding was detected in a single oral swab (0.72%). The virus (BV/Thailand/Ranong_TPK5/2024) was successfully isolated and propagated in Vero and LLC-MK2 cells, with higher replication efficiency observed in Vero cells. The TPK5 isolate exhibited a high infectious titre (8 × 10⁷ PFU/mL), and transmission electron microscopy confirmed typical herpesvirus morphology. Whole-genome sequencing achieved deep coverage (∼20,974×) and revealed 98.4% identity to a reference strain (E90-136) from captive long-tailed macaques. Phylogenetic analyses of 12 envelope glycoproteins demonstrated host-associated clustering, with the TPK5 isolate grouping within the long-tailed macaque lineage. Key entry glycoproteins (gB, gD, gH, and gL) were highly conserved among macaques but diverged from human herpes simplex viruses. In contrast, host receptors nectin-1 and nectin-2 were highly conserved between macaques and humans (≥95% identity), suggesting preserved receptor compatibility. Despite the low prevalence of shedding, the isolation of an infectious BV strain from an asymptomatic macaque highlights an ongoing zoonotic risk. Conservation of viral entry mechanisms and host receptors supports the potential for cross-species transmission in high human-macaque interface settings. - Source: PubMed
Publication date: 2026/07/20
Paungpin WeenaChaiwattanarungruengpaisan SomjitThongdee MetaweeSariya LadawanSapkanarak KrittigaKemthong TaratornDangsagul WorawatSuwanpakdee SarinWiriyarat WitthawatMalaivijitnond Suchinda - The alphaherpesvirus (PRV), which causes Aujeszky's disease (AD), primarily infects swine but has zoonotic potential and can infect multiple species, including humans. Upon infection, interferons (IFNs) trigger the expression of hundreds of interferon-stimulated genes (ISGs), thereby establishing a robust cellular antiviral state. However, ISGs exhibiting anti-alphaherpesvirus activity have not yet been fully characterized. Here, we perform an unbiased screen of 268 ISGs and identify Nectin4, also known as PVRL4, as a potent antiviral ISG against alphaherpesvirus, including herpes simplex virus (HSV). Mechanistically, Nectin4 inhibits viral internalization into host cells, in which the IgV domain plays a critical role. Specifically, Nectin4 interacts with the viral gD protein through this domain, thereby inhibiting the interaction between gD and viral receptor, Nectin1, and blocking gD-mediated viral entry. Together, our data identify a previously unrecognized function of Nectin4 in host anti-alphaherpesvirus immunity and highlight a novel cellular barrier that restricts alphaherpesvirus infection. - Source: PubMed
Publication date: 2026/07/20
Wang YiBo ZongyiZhao SenhongFazlani Tanveer AliYang FayuFeng ZhengshanCao TianxingZhang ZhonghuiXue WenchaoChen ShuaiQiao YupanZhu ZixiangCheng GenhongWang YipingZheng HaixueZhang Shilei - Glioblastoma (GBM) remains one of the most aggressive and lethal malignancies, with clinical outcomes under the standard-of-care Stupp protocol remaining suboptimal. While oncolytic virus (OV) therapy has emerged as a mechanistically distinct and promising approach, its clinical success is frequently hindered by profound intratumoral heterogeneity and emerging resistance. This critical review proposes that the efficacy of virotherapy may be meaningfully enhanced by integrating circadian biology into treatment schedules; a paradigm termed "Oncolytic Chronovirotherapy." Recent evidence demonstrates that the infection cycle of neurotropic viruses, which serve as the scaffold for many OVs, is not a static process but is inherently regulated by the host's circadian clock. Fundamental studies reveal that the expression of essential viral entry receptors, such as Nectin-1 (for HSV-1) and p75NTR, exhibits robust circadian oscillations directly coordinated by the core molecular clock, specifically the BMAL1/CLOCK complex. Furthermore, the tumor immune microenvironment and cellular vulnerability to adjuvant chemotherapy (temozolomide) show synchronized peaks of activity, typically concentrated during the morning window, which often coincides with the nadir of DNA repair enzymes like MGMT. We argue that synchronizing OV administration with these windows of maximal receptor density and robust immune surveillance may maximize tumor lysis and facilitate the conversion of "cold" tumors into "hot," immune-responsive environments. The utilization of personalized circadian biomarkers and mathematical modeling to guide therapy delivery will be essential for the next generation of precision neuro-oncology. - Source: PubMed
Publication date: 2026/07/06
Guterres Alexandro - Oncolytic virotherapy represents a promising yet under-explored approach for precision cancer treatment, particularly when tailored to tumor-specific molecular profiles. Patients with high-grade isocitrate dehydrogenase (IDH) mutant astrocytomas have limited treatment options and poor prognoses. Here, we investigate the therapeutic efficacy of rQNestin34.5 v.2 (CAN-3110), an engineered oncolytic herpes simplex virus 1 (oHSV-1), in IDH1-R132H-mutant diffuse gliomas. We demonstrate that the IDH1-R132H mutation enhances glioma susceptibility to viral infection through upregulation of Nectin-1, the main HSV-1 entry receptor. Concurrently, IDH1-R132H-driven DNA hypermethylation suppresses interferon (IFN) signaling, creating a permissive microenvironment that facilitates viral replication and tumor cell apoptosis. In immunocompetent murine glioma models, intratumoral administration of rQNestin34.5 v.2 induces robust antitumor immune activation, including increased immune infiltration and systemic IFN-γ release. However, elevated expression of poliovirus receptor (PVR) and the immune checkpoint T-cell immunoreceptor with immunoglobulin and ITIM domain (TIGIT) on tumor-infiltrating leukocytes suggests a potential resistance mechanism to virotherapy. Combining rQNestin34.5 v.2 with TIGIT blockade enhances therapeutic efficacy compared to monotherapy, identifying IDH1-R132H as a potential predictive biomarker for oncolytic virotherapy response. - Source: PubMed
Publication date: 2026/06/17
Panagioti EleniKelley Hunter JLing Alexander LSejour LeinalSaini ShikhaGoins William FRoberts DanielSotiriou SotirisBryan Iorgulescu JDixon Karen OYaffe Michael BVlachos Ioannis SCastro Maria GLawler Sean EFreeman Gordon JKuchroo Vijay KAntonio Chiocca ECook Charles H - The continuous evolution and cross-species transmission risk of pseudorabies virus (PRV) poses a substantial threat to the swine industry and public health. Nectin-1, an essential host receptor for PRV entry, represents a promising antiviral target; however, direct gene knockout (KO) raises biosafety concerns, and conventional genome-editing approaches remain inefficient for precise multiplex modification of critical functional residues. - Source: PubMed
Publication date: 2026/05/29
Xie TangyuanOuyang HanxiWang YanZhang ShuhuiYang ShuaikangKong JingHuang TianCao Gengsheng