We have previously shown that cauliflower mosaic virus (CaMV) isolate H30, a chimeric virus in which most of gene VI and the large intergenic region are derived from the mild CaMV strain CM1841 and genes I-V are derived from the severe strain W260, was significantly more severe and attained higher virion antigen concentrations than either W260 or CM1841 (E. J. Anderson, S. G. Qiu, and J. E. Schoelz, Virology 181:647-655, 1991). We have now determined that sequences within the 5' half of CM1841 gene VI, rather than the 35S promoter or translational regulatory sequences present in the large intergenic region, were responsible for the increases in virion antigen concentration and symptom severity. The levels of H30 DNA and RNA in infected turnip leaves were also higher than either CM1841 or W260. Although CM1841 inclusions were less stable than W260 inclusions, gene VI did not determine the difference in inclusion stability, demonstrating that the enhanced severity of H30 was not attributed to the role of gene VI in inclusion body structure. Instead, the increased concentration and severity of H30 may be related to the function of the gene VI product in post-transcriptional transactivation. Additionally, the purification and stability characteristics of wild type and chimeric viruses indicated that purified CM1841 virions were less stable than purified W260 virions. CM1841 virions were recovered from infected tissue at a much lower level than W260 virions, were less infectious than W260 virions in a local lesion assay, and were more heterogenous in CsCl gradients.