HTLV-1 p12 is cleaved to p8 by the signal peptidase complex and its inhibition impairs p8-dependent transmission.

ABSTRACT: Infection with the oncogenic delta-retrovirus Human T-cell Leukemia Virus Type 1 (HTLV-1) causes aggressive CD4 + T-cell malignancy or progressive neuroinflammatory disorders after a long latency period. The HTLV-1 accessory protein p8 is cleaved from its precursor p12, and both proteins are required for viral persistence. Moreover, p8 enhances viral infectivity by inducing cell-cell contacts and cellular conduit formation. To date, host factors cleaving p12 to p8 remain unknown. Here, we report that p12 carries a signal peptide that is cleaved by the signal peptidase complex (SPC) to generate p8, and blocking of p12 cleavage correlated with a decreased cell aggregation and conduit formation, leading to impaired viral transmission of chronically HTLV-1 infected MT-2 cells. Bioinformatics i

SUBMITTER: Simon F 

PROVIDER: S-EPMC12513584 | biostudies-literature | 2025 Oct

REPOSITORIES: biostudies-literature