Apoptosis induction by the 5′ NCR of infectious Bursal disease virus.

Abstract

Virus invasion and replication can induce apoptosis and play an important role in the life cycle of viruses. To illustrate the relationship between apoptosis induction and the non-coding region (NCR) of infectious bursal disease virus (IBDV), the 5� NCR of Harbin-1 (a very virulent IBDV) segment A was sequentially deleted using PCR and exchanged with the corresponding region of the mild virulent strain Cj801. IBDV mutants were recovered using a reverse genetics system and named H� 35, H� 74, H� 94, and HCA. Apoptosis in chicken embryo bursal cells was then determined by flow cytometry. The results revealed that the IBDV mutants could induce apoptosis, but with varying capability. As the length of the deleted sequence increased, the capacity to induce apoptosis decreased. However, there was no marked difference in apoptosis induction between H� 35 and H� 74. The above results indicate that the NCR may increase the ability to induce apoptosis. Quantitative nested real-time PCR was performed to illustrate the relationship between replication and apoptosis. The result showed an obvious positive correlation for H� 35 and HCA but an independent process for H� 74 and H� 94.