Murine norovirus (MNV) undergoes large conformational changes in response to the environment. The T=3 icosahedral capsid is composed of 180 copies of ~58 kDa VP1 that has N-terminal (N), shell (S) and C-terminal protruding (P) domains. In phosphate buffered saline, the P domains are loosely tethered to the shell and float ~15Å above the surface. At conditions found in the gut (i.e. low pH with high metal ion and bile salt concentrations) the P domain rotates and drops onto the shell with intra P domain changes that enhance receptor interactions while blocking antibody binding. Two of our monoclonal antibodies (2D3 and 4F9) have broad strain recognition and the only escape mutants, V339I and D348E, are located on the C D loop and ~20 Å from the epitope. Here we determined the cryo-EM structures of V339I and D348E at neutral pH +/- metal ions and bile salts. These allosteric escape mutants are constitutively in the activated state without the addition of metal ions or bile salts, thus explaining how they escape neutralization. Dynamic simulations of the P domain further suggest that movement of the C D loop may be the rate limiting step in the conformational change and that V339I increases the motion of the A B /E F loops compared to wt, making it easier for the virus to transition to the activated state. These findings have important implications for norovirus vaccine design since they uncover a form of the viral capsid that should lend superior immune protection against subsequent challenge by wild type virus.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11838585 | PMC |
http://dx.doi.org/10.1101/2025.02.04.636510 | DOI Listing |
J Virol
March 2025
Department of Biological Science, Florida State University, Tallahassee, Florida, USA.
Zika virus (ZIKV) is spread by mosquito bites and is unique among known flaviviruses for being able to cause microcephaly. Entry factors for ZIKV are incompletely understood, but phosphatidylserine (PS) receptors, including the TAM (Tyro3, AXL, and Mer) and TIM (T-cell Ig mucin) families, can serve as cofactors for flavivirus entry in a cell type-specific manner. We identify AXL as the top hit in a CRISPR/Cas9 genome-wide screen in human glioblastoma cells and establish a definitive role of AXL, but not TYRO3 or MerTK, for ZIKV infection.
View Article and Find Full Text PDFNat Commun
March 2025
Department of Pharmacology and Chemical Biology, Emory University School of Medicine, Atlanta, GA, USA.
Harnessing the power of immune system to treat cancer has become a core clinical approach. However, rewiring of intrinsic circuitry by genomic alterations enables tumor cells to escape immune surveillance, leading to therapeutic failure. Uncovering the molecular basis of how tumor mutations induce therapeutic resistance may guide the development of intervention approaches to advance precision immunotherapy.
View Article and Find Full Text PDFCell Death Dis
March 2025
Department of Gastroenterology, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China.
Aberrant expression of programmed death ligand-1 (PD-L1) facilitates tumor immune evasion. Protein arginine methyltransferase 3 (PRMT3), a member of type I PRMT family, mediates asymmetric dimethylarginine (ADMA) modification of various substrate proteins. This study investigates the role of PRMT3 in PD-L1-associated tumor immunosuppression in hepatocellular carcinoma (HCC).
View Article and Find Full Text PDFElife
March 2025
AIDS Research Center, National Institute of Infectious Diseases, Tokyo, Japan.
HIV and simian immunodeficiency virus (SIV) infections are known for impaired neutralizing antibody (NAb) responses. While sequential virus-host B cell interaction appears to be basally required for NAb induction, driver molecular signatures predisposing to NAb induction still remain largely unknown. Here we describe SIV-specific NAb induction following a virus-host interplay decreasing aberrant viral drive of phosphoinositide 3-kinase (PI3K).
View Article and Find Full Text PDFCancer Sci
March 2025
Cancer Molecular Diagnostics Core, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center of Caner, Key Laboratory of Cancer Immunology and Biotherapy, Tianjin's Clinical Research Center for Cancer, Tianjin, China.
Not all ovarian cancer patients with homologous recombination deficiency, especially those with germline BRCA mutations, can benefit from platinum-based and targeted therapy. Our study aimed to determine the value of nonsense-mediated mRNA decay, which targeted these mutations. The retrospective analysis of 797 ovarian cancer patients was performed using two public cohorts and one in-house cohort.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!
© LitMetric 2025. All rights reserved.