Synergistic Interactions of a Potyvirus and a Phloem-Limited Crinivirus in Sweet Potato Plants

Abstract

When infecting alone, Sweet potato feathery mottle virus (SPFMV, genus Potyvirus) and Sweet potato chlorotic stunt virus (SPCSV, genus Crinivirus) cause no or only mild symptoms (slight stunting and purpling), respectively, in the sweet potato (Ipomoea batatas L. ). In the SPFMV-resistant cv. Tanzania, SPFMV is also present at extremely low titers, though plants are systemically infected. However, infection with both viruses results in the development of sweet potato virus disease (SPVD) characterized by severe symptoms in leaves and stunting of the plants. Data from this study showed that SPCSV remains confined to phloem and at a similar or slightly lower titer in the SPVD-affected plants, whereas the amounts of SPFMV RNA and CP antigen increase 600-fold. SPFMV was not confined to phloem, and the movement from the inoculated leaf to the upper leaves occurred at a similar rate, regardless of whether or not the plants were infected with SPCSV. Hence, resistance to SPFMV in cv. Tanzania was not based on restricted virus movement, neither did SPCSV significantly enhance the phloem loading or unloading of SPFMV. It is also noteworthy that SPVD is an unusual synergistic interaction in that the potyvirus component is not the cause of synergism but is the beneficiary. It is hypothesized that SPCSV is able to enhance the multiplication of SPFMV in tissues other than where it occurs itself, perhaps by interfering with systemic phloem-dependent signaling required in a resistance mechanism directed against SPFMV.

Prevalence and implications of sweetpotato recovery from sweet potato virus disease in Uganda

“…Further, they showed a gradual decline contrary to higher titers (600 fold increase at 5 weeks after inoculation) which should be found in dual and synergistic interactions (Karyeija et al, 2000). This clearly suggests that the synergism was somehow halted in resistant plants since SPCSV was found in lower leaves as expected in single or multiple infections whereas SPFMV was found in all leaf positions but in reduced titers .…”

“…Shukla et al (1994) observed the same in single infections and argued that serology has low detection limits, at least 1-10 ng of virus per kilogramme of infected tissue. Karyeija et al (2000) and Mukasa et al (2006) also reported that plants that tested negative from ELISA could test positive using sensitive methods like grafting on Ipomoea setosa plants. Reversion was not observed in sweetpotato unlike in cassava as reported by Storey and Nichols (1938) with respect to African cassava mosaic virus disease.…”

“…Failure to recover from SPVD and the subsequent death of some cultivars is not surprising. For instance, it was reported that during dual infection and synergistic interactions, resistance to single infections is compromised (Kreuze et al, 2005) leading to elevated titer levels of SPFMV (Karyeija et al, 2000), thus causing SPVD (Gibson et al, 1998).…”

Detection and elimination of sweetpotato viruses

“…Secondly, the perpetuation of these single viruses from one crop to the next means that there is always available inoculum from which dual and synergistic interactions could be reconstituted. Co-infection of SPCSV with SPFMV results in the severe SPVD and during this synergistic interaction the titres of SPFMV are elevated by over 600 folds while the titres of SPCSV remain unchanged (Karyeija et al, 2000a;Mukasa et al, 2006).This implies that, the farmers' practice of selecting healthy-looking vines as the source of planting material would to minimise keep SPFMV inoculums low since farmers would select against SPVD affected vines that harbor high tires of SPFMV. Among the sampled health looking vines only 8.3% were infected by SPVD.…”

Analysis of gene content in sweet potato chlorotic stunt virus RNA1 reveals the presence of the p22 RNA silencing suppressor in only a few isolates: implications for viral evolution and synergism

“…Sweet potato chlorotic stunt virus (SPCSV; genus Crinivirus, family Closteroviridae) is a phloem-limited, whitefly-transmitted, bipartite virus that acts synergistically with several unrelated viruses also infecting sweetpotato (Ipomoea batatas L.) (Gibson et al, 1998;Karyeija et al, 2000;Kokkinos & Clark, 2006;Mukasa et al, 2006;Untiveros et al, 2007). Among the synergistic interactions, co-infection of SPCSV with sweet potato feathery mottle virus (SPFMV; genus Potyvirus, family Potyviridae) causes the severe sweet potato virus disease (SPVD), economically the most devastating disease affecting sweetpotatoes (Milgram et al, 1996; The GenBank/EMBL/DDBJ accession numbers for the sequences of the 39-proximal region of RNA1 are EU124491 (isolate Is), EU124490 (m2-47), EU124493 (Mis1), EU124494 (Tug2) and EU124492 (Unj2), and for Hsp70h sequences are EU124487 (Is), EU124488 (m2-47) and EU124489 (Tug2).…”