T-cell and Retrovirus Studies

The Human T-cell Leukemia Virus capsid protein is a potential drug target

The paper identifies a ligand-binding pocket in the HTLV-1 capsid protein essential for infectivity, suggesting it as a potential drug target for anti-capsid therapy.

Co-expression of Bovine leukemia virus and Bovine foamy virus-derived miRNAs in naturally infected cattle

The paper identifies co-expressed BLV and BFV-derived miRNAs in naturally infected cattle and highlights their potential functional interactions in tumorigenesis and immune response.

Hyperactive PLCG1 drives non-canonical signaling to promote cell survival

This study identifies hyperactive PLCG1 mutations in T-cell leukemia/lymphoma that drive non-canonical signaling, enhancing cell survival and drug resistance.

JunB-HBZ nuclear translocation by TGF-β is a key driver in HTLV-1-mediated leukemogenesis

This study shows that TGF-β-induced nuclear translocation of HBZ-JunB complexes drives HTLV-1-mediated leukemogenesis.

Role of the CTCF Binding Site in Human T-Cell Leukemia Virus-1 Pathogenesis

This study shows that the CTCF binding site in HTLV-1 regulates viral pathogenesis by affecting proviral load, Tax expression, and T-cell activation in humanized mice.

Retroviral adapters hijack the RNA helicase UPF1 in a CRM1/XPO1 dependent manner and reveal proviral roles of UPF1.

This paper shows that HTLV-1 Rex hijacks CRM1 to retain UPF1 in the nucleus, inhibiting NMD and enabling UPF1 to support viral replication.

Whole-transcriptome analysis of BLV-infected cows reveals downregulation of immune response genes in high proviral loads cows.

The paper analyzes whole-transcriptome data from BLV-infected cows to identify gene expression differences between high and low proviral load groups, finding immune response genes are downregulated in high proviral load cows.

YTHDF1 and YTHDC1 m6A reader proteins regulate HTLV-1 tax and hbz activity

This study shows m6A RNA modifications and their reader proteins YTHDF1 and YTHDC1 regulate HTLV-1 gene expression by affecting Tax and Hbz transcripts.

Conserved residues of the immunosuppressive domain of MLV are essential for regulating the fusion-critical SU-TM disulfide bond

This paper identifies conserved residues in the immunosuppressive domain of MLV Env that regulate the SU-TM disulfide bond, essential for viral infectivity.

Peculiar transcriptional reprogramming with functional impairment of dendritic cells upon exposure to transformed HTLV-1-infected cells

This study shows that HTLV-1-infected T cells alter the transcriptional and functional responses of dendritic cells, leading to a tolerogenic immune environment.

Determinants in the HTLV-1 capsid major homology region that are critical for virus particle assembly

This study identifies key residues in the HTLV-1 MHR critical for Gag multimerization and particle assembly, contrasting with HIV-1's reliance on the CTD.

The viral oncoproteins Tax and HBZ reprogram the cellular mRNA splicing landscape

This study shows that Tax and HBZ, viral oncoproteins, alter mRNA splicing in T-cells by interacting with spliceosome components, leading to changes in cancer-related genes.

An insight to HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP) pathogenesis; evidence from high-throughput data integration and meta-analysis

This study identifies key genes involved in HAM/TSP pathogenesis through high-throughput data integration and meta-analysis, revealing differential expression of STAT1, TAP1, and PSMB8.