in 1946, discovered MR and proposed that the observed reactivation of damaged virus occurs by a recombination mechanism.(see refs.) This preceded the confirmation of DNA as the genetic material in 1952 in related virus T2 by the Hershey–Chase experiment. As remembered by Luria (1984, pg. 97) the discovery of reactivation of irradiated virus (referred to as "multiplicity reactivation") immediately started a flurry of activity in the study of repair of radiation damage within the early phage group (reviewed by Bernstein in 1981). It turned out later that the repair of damaged virus by mutual help that Luria had discovered was only one special case of DNA repair. Cells of all types, not just, bacteria and their viruses, but all organisms studied, including humans, are now known to have complex biochemical processes for repairing DNA damages (see DNA repair). DNA repair processes are also now recognized as playing critical roles in protecting against aging, cancer, and infertility. MR is usually represented by "survival curves" where survival of plaque forming ability of multiply infected cells (multicomplexes) is plotted against dose of genome damaging agent. For comparison, the survival of virus plaque forming ability of singly infected cells (monocomplexes) is also plotted against dose of genome damaging agent. The top figure shows the survival curves for virus T4 multicomplexes and monocomplexes with increasing dose of UV light. Since survival is plotted on a log scale it is clear that survival of multicomplexes exceeds that of monocomplexes by very large factors (depending on dose). The UV inactivation curve for multicomplexes has an initial shoulder. Other virus T4 DNA damaging agents with shoulders in their multicomplex survival curves are X-rays and ethyl methane sulfonate (EMS). The presence of a shoulder has been interpreted to mean that two recombinational processes are used. The first one repairs DNA with high efficiency (in the "shoulder"), but is saturated in its ability as damage increases; the second pathway functions at all levels of damage. Surviving T4 virus released from multicomplexes show no increase in mutation, indicating that MR of UV irradiated virus is an accurate process. The bottom figure shows the survival curves for inactivation of virus T4 by the DNA damaging agent mitomycin C (MMC). In this case the survival curve for multicomplexes has no initial shoulder, suggesting that only the second recombinational repair process described above is active. The efficiency of repair by this process is indicated