INACTIVATION OF THE HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 (HIV-1) BY ULTRAVIOLET AND X-IRRADIATION

Here we report the kinetics of inactivation of HIV-1 by ultraviolet (UV) or X irradiation. Inactivation of HIV-1 by UV irradiation followed quasi first-order, i.e., single-hit, kinetics. The LD37 for inactivation of syncytia formation in SupT1 cells by limiting dilutions was approximately 780 J/m2. The LD37 for inactivation of HIV-1-induced syncytia by UV irradiation was nearly identical when measured in UV repair-proficient and deficient lymphoblastoid cell lines (LCLs), demonstrating that immediate host cell reactivation (repair) of UV damage in the HIV-1 genome does not occur. The ability of HIV-1 to induce the accumulation of reverse transcriptase activity showed similar dose-dependent inhibition by UV irradiation (LD37, 845 J/m2). Inactivation of HIV-1-induced syncytia formation by X rays also approached first-order kinetics. The LD37 for syncytia formation as measured by limiting dilutions was approximately 3 x 103 Gy. HIV-1-induced accumulation of reverse transcriptase activity was slightly more resistant to inactivation by X rays, with an LD37 of approximately 4.5 x 103 Gy. Syncytia-forming ability was still present in HIV-1 preparations X-irradiated with 1.6 x 104 Gy. For the first time, we utilized the polymerase chain reaction (PCR) to measure the effects of radiation on virus replication. A decrease in the presence of the HIV-1 DNA could be detected by PCR in PBL cultures infected with UV- and X-irradiated virus. It required 12.96 J/m2 to eliminate the signal specific for HIV-1 DNA completely. The ability of HIV-1 to establish long-term infection in LCLs was also resistant to UV and X irradiation. Only linear and circular forms of HIV-1 DNA could be detected in LCLs established from PBL cultures infected with UV-irradiated virus. The significance of the relative resistance of HIV-1 to inactivation by UV and X irradiation is discussed.