rAAV-2 infection in CHO K1 (wild type), CHO mutant pgsD-677 (no surface HSPG) and CHO mutant pgsA-745 (deficient in all surface proteoglycans). CHO cell lines were infected with AAV2-CMV-EGFP at increasing MOIs. Cells were harvested at 48 hours and analyzed for percentage of cells expressing GFP by flow cytometry, with results compared between wild type CHO-K1 cells known to have high levels of surface HSPG and mutant CHO cell lines. Surface HSPG-deficient pgsD-677 transduction was reduced only 33% compared to wildtype CHO-K1 cells (pgsD % transduction at MOI 1000: 23.1 ± 6.8% vs. wildtype 34.6. ± 4.6%, p = 0.1, n = 4). In contrast, the pgsA-745 mutant cell line deficient for all surface GAG demonstrated a dramatic decrease in susceptibility to rAAV-2 infection (pgsA-745 % transduction at MOI 1000: 5.4 ± 2.7%, p = 0.0001 vs. wildtype and p = 0.01 vs. pgsD-677, n = 4).