polymérases virales sont associées à des protéines de l’hôtes lors de la réplication des rétroïdes (e.g. Hepatitis B hepadnavirus HBV-Hsp90 [Hu, 2006 #3516]), des virus à ARN infectant les animaux (e.g. influenza [Naito, 2007 #3515] ainsi que pour les virus à ARN infectant les plantes (e.g. Cucumber necrosis tombusvirus [Serva, 2006 #3517].

Cui et al 2007 Plant Cell

Induced Expression of CDKC and CYCT1 Genes by CaMV Infection

Because of their roles in CaMV infection, we analyzed the expression of these CDKC and CYCT1 genes in CaMV-infected plants. Fully expanded lower leaves of 4-week-old Arabidopsis plants were mechanically inoculated with CaMV. As described above, it takes ;10 to 13 d after inoculation to first detect significant levels of CaMV viral DNA and observe symptom development in upper systemically infected leaves (Figure 1). As shown in Figure 6, the levels of transcripts for CDKC;1, CDKC;2, CYCT1;4, and CYCT1;5 were quite constant during the first 10 DAI but increased substantially at 14, 18, and 24 DAI. Neither mock inoculation nor TMV-cg or CaLCuV inoculation induced expression of the genes (Figure 6). Thus, the four genes were induced specifically by CaMV infection.

Mauck, K. E., C. M. De Moraes, et al. 2010 “Deceptive chemical signals induced by a plant virus attract insect vectors to inferior hosts.” Proceedings of the National Academy of Sciences 107(8): 3600-3605.

Previous studies have shown that vector-borne pathogens can alter the phenotypes of their hosts and vectors in ways that influence the frequency and nature of interactions between them, with significant implications for the transmission and spread of disease. For insect-borne pathogens, host odors are particularly likely targets for manipulation, because both plant- and animal-feeding insects use volatile compounds derived from their hosts as key foraging cues. Here, we document the effects of a widespread plant pathogen, Cucumber mosaic virus (CMV), on the quality and attractiveness of one of its host plants ( cv. Dixie) for two aphid vectors, and . Our results indicate that CMV greatly reduces host-plant quality—aphids performed poorly on infected plants and rapidly emigrated from them—but increases the attractiveness of infected plants to aphids by inducing elevated emissions of a plant volatile blend otherwise similar to that emitted by healthy plants. Thus, CMV appears to attract vectors deceptively to infected plants from which they then disperse rapidly, a pattern highly conducive to the nonpersistent transmission mechanism employed by CMV and very different from the pattern previously reported for persistently transmitted viruses that require sustained aphid feeding for transmission. In addition to providing a documented example of a pathogen inducing a deceptive signal of host-plant quality to vectors, our results suggest that the transmission mechanism is a major factor shaping pathogen-induced changes in host-plant phenotypes. Furthermore, our findings yield a general hypothesis that, when vector-borne plant or animal pathogens reduce host quality for vectors, pathogen-induced changes in host phenotypes that enhance vector attraction frequently will involve the exaggeration of existing host-location cues.