Until recently (Almazan et al., 2000; Thiel et al., 2001) , infectious cDNA clones were lacking for coronaviruses. Consequently, most studies on coronavirus sg RNA synthesis were carried out using defective interfering (DI) RNAs. These replicons carried body TRSs from which moderate levels of sg mRNAs could be produced in the presence of helper virus. Using this system, Joo and Makino (1992) and van der Most et al. (1994) performed body TRS mutagenesis studies for the murine coronavirus (MHV). Joo and Makino systematically mutagenized the core of the MHV body TRS. In contrast to our results, they found that in only two of 21 body TRS mutants was sg RNA synthesis from the DI RNA genome abolished, whereas all others supported normal levels of sg RNA production. Thus, it is possible that the MHV TRS which was used in that study is more tolerant to single-nucleotide mismatches than the EAV sg RNA7 TRS.