HIV-1 mutants expressing B cell clonogenic matrix protein p17 variants are increasing their prevalence worldwide. Sanger analysis of HIV-1 matrix protein p17

We have demonstrated that amino acid insertions at the HIV matrix protein p17 (p17) COOH-terminal region cause protein destabilization leading to conformational changes. Differently from wild-type p17, misfolded vp17s strongly impact on clonogenic B-cell growth properties that may contribute to B-cell lymphomagenesis. Aim of this study was to expand our previous observations by assessing the prevalence of vp17s in large retrospective cohorts of patients with lymphoma and without lymphoma.