Abstract
HIV type 1 (HIV-1) is a lentivirus that causes a rapid viremia infecting roughly a billion cells per day, followed by a chronic illness characterized by progressive immunodeficiency due to the almost complete destruction of T helper cells (CD4+ cells). The replication of HIV-1 involves integration of its proviral DNA into the host genome, a process that occurs in a semirandom pattern with a few known hot spots and a generic bias for active transcription units.1 With the exception of the untargeted integration, all known viral pathogenicity factors have been eliminated from clinically used lentiviral gene vectors.
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