Author Correction: Inhibiting macrophage-derived lactate transport restores cGAS-STING signalling and enhances antitumour immunity in glioblastoma.
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Published Erratum↗
Biomedical subjects
Chong Liu
Publications and source records attributed to Chong Liu.
Genomic characteristics and tracing analysis of an acute gastroenteritis outbreak associated with rotavirus C in a boarding high school.
BACKGROUND: Rotaviruses are major pathogens of childhood acute gastroenteritis, dominated by rotavirus A (RVA). Outbreaks caused by human rotavirus C (RVC) are rarely reported, and relevant genomic data remain scarce. This genomic investigation of an RVC outbreak improves our understanding of viral diversity and transmission dynamics. METHODS: We performed epidemiological surveys, nucleic acid testing and whole-genome sequencing (WGS) on specimens from a 2025 RVC-associated gastroenteritis outbreak at a Chinese boarding high school. Sequence alignment, phylogenetic and molecular tracing analyses were conducted to explore RVC evolution via point mutation, segment reassortment and genomic recombination. RESULTS: This typical point-source campus outbreak was linked to an indoor student gathering matching the incubation period of RVC. Thirteen RVC FX strains were recovered from 11 rectal swabs and two vomitus samples. Their viral protein (VP) 4 and VP7 sequences shared high homology with Russian reference strains, carrying distinct amino acid variations. No segment reassortment or recombination was detected in VP4/VP7 genes. CONCLUSIONS: Dense, closed campus settings facilitate RVC clustered transmission. Limitations included absent screening of asymptomatic canteen staff. Rapid nucleic acid testing enabled timely pathogen identification for outbreak control. Greater attention should be paid to the public health risk of RVC. These whole-genome sequencing data enrich resources for studying RVC evolution and vaccine development.
Acute gastroenteritis outbreak↗
Inhibiting macrophage-derived lactate transport restores cGAS-STING signalling and enhances antitumour immunity in glioblastoma.
Glioblastoma (GBM) is a malignancy with a complex tumour microenvironment (TME) dominated by GBM stem cells (GSCs) and infiltrated by tumour-associated macrophages (TAMs) and exhibits aberrant metabolic pathways. Lactate is a critical glycolytic metabolite that promotes tumour progression; however, the mechanisms of lactate transport and lactylation in the TME of GBM remain elusive. Here we show that lactate is transported from TAMs to GSCs via MCT4-MCT1. TAMs provide lactate to GSCs, promoting GSC proliferation and inducing lactylation of the non-homologous end joining protein KU70 at lysine 317 (K317), which inhibits cGAS-STING signalling and remodels the immunosuppressive TME. Inhibition of lactate transport or targeting the lactylation of KU70, in combination with the immune checkpoint blockade, demonstrates additive therapeutic benefits in immunocompetent xenograft models. This study unveils TAM-derived lactate and lactylation as critical regulators in GSCs to enforce an immunosuppressive microenvironment, opening avenues for developing combinatorial therapy for GBM.
Glioblastoma↗