BackgroundAccessory proteins have diverse roles in coronavirus pathobiology. One of them in SARS-CoV (the causative agent of the severe acute respiratory syndrome outbreak in 2002–2003) is encoded by the open reading frame 8 (ORF8). Among the most dramatic genomic changes observed in SARS-CoV isolated from patients during the peak of the pandemic in 2003 was the acquisition of a characteristic 29-nucleotide deletion inORF8. This deletion cause splitting ofORF8into two smallerORFs, namelyORF8aandORF8b. Functional consequences of this event are not entirely clear.ResultsHere, we performed evolutionary analyses ofORF8aandORF8bgenes and documented that in both cases the frequency of synonymous mutations was greater than that of nonsynonymous ones. These results suggest thatORF8aandORF8bare under purifying selection, thus proteins translated from theseORFs are likely to be functionally important. Comparisons with several other SARS-CoV genes revealed that another accessory gene,ORF7a, has a similar ratio of nonsynonymous to synonymous mutations suggesting that ORF8a, ORF8b, and ORF7a are under similar selection pressure.ConclusionsOur results for SARS-CoV echo the known excess of deletions in theORF7a-ORF7b-ORF8complex of accessory genes in SARS-CoV-2. A high frequency of deletions in this gene complex might reflect recurrent searches in “functional space” of various accessory protein combinations that may eventually produce more advantageous configurations of accessory proteins similar to the fixed deletion in the SARS-CoVORF8gene.Supplementary InformationThe online version contains supplementary material available at 10.1186/s12864-023-09482-3.