Work

CD4 T cells from patients with chronic myeloid leukemia are resistant to HIV-1 proviral integration and transcription after prolonged withdrawal of treatment with tyrosine kinase inhibitors

Year: 2019

Type: article

Abstract: Supplement 3): 1-58 53 stimulation for 24h or 72h.The viral inhibition assay was performed with cells from patients on antiretroviral treatment (ART) using R5 HIV (ratio CD4:CD81:1).Nevirapine was added at the same time than LRAs and stimulation lasted for 6 days.Results: In CCL19-treated rCD4 T cells, MVC reactivated X4 HIV with a potency similar to other LRAs (Fig. A).These combinations did not affect viability neither proliferation (Fig. 1B).We did not detect an additive or synergistic effect of the combinations on viral reactivation.The combination of MVC with panobinostat or disulfiram maintained the effect of both drugs.These Results: were confirmed using R5 HIV and IL-7-model.Finally, MVC did not alter the viability of CD8 T cells from patients on ART after 16 days (Fig. 1C), although it was reduced after stimulation with disulfiram or panobinostat from 2 days onwards.The ability of CD8 T cells to block HIV replication was not changed in CD4 T cells treated with MVC alone or combined with panobinostat or disulfiram (Fig. 1D).Conclusions: MVC is a LRA as potent as disulfiram, romidepsin or panobinostat.In contrast to these LRAs, MVC did not affect viability of CD8 T cells from ART-treated patients.PP 6.8.

Source: Journal of Virus Eradication

DOI: 10.1016/s2055-6640(20)30214-4