Infection with adeno-associated parvovirus leads to increased sensitivity of mammalian cells to stress.

Infection of the SV40-transformed Syrian hamster cells Elona with adeno-associated parvovirus type 5 (AAV-5) affects the cellular stress response. Stress-induced growth delay becomes permanent and this promotes cell death. AAV DNA is replicated in the absence of helper virus. Induction of an incomplete stress response by cycloheximide treatment still results in replication of viral DNA but not in virus-mediated growth arrest. Thus, the reactions that induce AAV DNA replication and that direct growth delay are different and replication of AAV DNA is not sufficient to induce growth arrest and cell death. Additional steps that lead to effects resembling inhibition of protein synthesis are required. The possibility that they may have their origin in the action of AAV rep proteins is discussed.