The first indication of evolution in
Sweet potato chlorotic stunt virus (SPCSV) was obtained when sweetpotato (
Ipomoea batatas
) plants of cv Kampala white from Busia district, eastern Uganda were shown to be infected with only SPCSV that induced mild symptoms in
Ipomoea setosa
. The objective of the study was to understand why the SPCSV isolate in Busia was not co-infected with SPFMV. ‘Mild’ SPCSV-infected plants were used to plant a field trial. The quantity of
Sweet potato feathery mottle virus (SPFMV) was measured, using quantitative PCR (qPCR), in plants of
I. setosa and cv Kampala white infected with SPFMV, ‘mild’ SPCSV + SPFMV or wild type SPCSV + SPFMV. The RNase3 and p22 genes of ‘mild’ SPCSV were sequenced and compared with those in the gene bank. qPCR assays were done to determine the titres of RNA1 (on to which RNase3 and p22 are found) and RNA2. ‘Mild’ SPCSV reduced yield by up to 50%. SPFMV titre was greatest in co-infections of SPFMV and wild type SPCSV; followed by co-infections of SPFMV and ‘mild’ SPCSV; and least in single SPFMV infections. The RNase3 of ‘mild’ SPCSV showed amino acid changes at position 34 (G to D) and 159 (H to Y), but p22 seemed normal. RNA1 was less expressed (though RNA2 continued to be ‘normally’ expressed) in the ‘mild’ SPCSV infection, than in the wild type SPCSV infection. This is the first example of a virus downgrading part of its genome to ensure that it alone benefits from RNA silencing suppression. The resulting improvement in its competiveness makes this strain likely to spread and become more important.
