Spontaneous HIV-1 replication in a B-lymphoblastoid cell line obtained from an HIV-1-positive patient with undetectable plasma viral load

Combined antiretroviral treatment (ART) has improved the survival rate and retarded progression to AIDS in HIV-1 -infected patients by reducing active viral replication and allowing immune reconstitution. Nevertheless, the source of re-emerging virus after ART interruption is difficult to establish. Reservoirs of viral persistence include latently infected CD4 T memory cells, tissue macrophages and pockets of continuous low key HIV-1 replication in different tissues. Resting peripheral blood B lymphocytes are poor targets for HIV-1 infection under normal conditions, but an activated immunological environment could induce the expression of HIV-1 receptors CD4 and CXCR4 on B lymphocytes, increasing their susceptibility to infection.