At the molecular level, the only information that I am aware of is:

http://forums2.gardenweb.com/discussions/4693000/rose-rosette-effect-at-molecular-level?n=6

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I would expect that (if anywhere) there would be more advanced research on some of the other emaravirus viruses that infect food crops. I have not had time to look.

https://www.google.com/?gws_rd=ssl#newwindow=1&q=+emaravirus+&spf=1499193290514

"The virus causes genetic mutations in the rose DNA. This genomic change i...nstructs the plant not to store starch so the plant literally starves itself to death. "

https://www.facebook.com/DallasCountyMasterGardeners/videos/vb.379385282160263/1135759406522843/?type=2&theater

I did not come across a reviewed scientific paper that directly supported the above, but I did find a paper that reported a starch build up in infected plants of fig. So perhaps something is preventing the utilization of the starch.

"Electron micrographs of ultrathin sections prepared from healthy F. carica L. leaves
represented in (Figure 2, A) showed the normal cell structure before viral infection, while those prepared from FMV-infected F. carica L. leaves revealed many Cytopathological effects. Figure (3 A, B& C) showed starch grains accumulation inside the chloroplastides."

https://www.researchgate.net/publication/224831084_Molecular_Characterization_of_a_Potyvirus_Associated_with_a_Fig_Mosaic_Disease_in_Egypt

The starch/sugar is mentioned in the juried scientific paper by Epstein and Hill, Etiology of Rose Rosette Disease.
They also illustrated using an Iodine test for starch ....but when Jim Amrine and I did that test with some sick roses in his city, that test didn't hold up.

What I see in Tennessee and surrounding states is canes and stems that turn black. Other diseases of roses don't seem to have the black canes. I've also seen growth happen with vigor in the middle of winter and it dies in early spring, probably from freezing.

Other emaraviruses seem to be 'easier' to live with. The one that infects Date Palms reduces productivity, but doesn't kill. That might be tied to the different vascular make of date stems. Likewise Peaches. Pigeonpea sterility seems to be specific to the flowers- they make a lot fewer so pea production is greatly reduced...but those, IIRC, are annuals.

I'm not sure of the specifics, but here's how I see RRD affecting roses -- both to further the spread of the virus, and also to result in the eventual demise of the rose.

In the animal world, there are numerous examples of various parasite species causing changes in their hosts which facilitate the spreading of the parasite. I remember some examples of infected fish being attracted to swimming erratically near the surface, which makes them more obvious to avian predators. The parasite spends its second stage of life within the birds, so affecting the fish in this way would be an evolutionary advantage to those parasites. I think something similar is going on with RRD.

The virus seems to trigger the rose to produce exuberant soft new growth which doesn't seem to mature. This is the type of growth which is most attractive to pests which feed on sap, so symptomatic growth would actually be sought out and fed upon more readily than asymptomatic normal growth. By creating an attractive and easy source of food, the virus is capable of spreading more easily. Of course, viruses aren't capable of thinking this through, but those viruses capable of engendering such physiological changes in plants which facilitate infection of new plants would also have an evolutionary advantage.

Now, I don't know how RRD infected roses do in frost-free climates, but where Winters are real, those never-maturing soft RRD-infected growths would be decimated by the cold. Each year, an infected rose would have less and less live wood, and infected cells would be "forced" by the virus to continue producing this type of growth. Eventually, the reserves would be drained, and the rose dies.

I'm not completely sure, but what I've seen of RRD-infected roses seems to indicate to me that the infected growth isn't really capable of photosynthesis -- or, at least, not to the degree of producing more food than is consumed by producing that type of growth. Just as a plant which produced blooms in lieu of producing leaves would eventually starve to death, my thoughts are that in frost-free climates, RRD-infected roses would similarly starve to death. But without Winter-kill, this would likely take longer.

:-)

~Christopher

From the abstract:

" Contrary to previous reports, starch granules were found in chloroplasts of the infected cells."

From the full paper:

"The presence of starch granules in chloroplasts of cells containing VLPs (Figs. 2, 3, 5) is in disagreement with the observation of Epstein and Hill (1995) that chloroplasts in cells from diseased plants lack starch granules. The presence here of starch in the chloroplasts of cells containing VLPs may, however, be due to a briefer period or less severe state of infection of these cells than the cells studied by Epstein and Hill, assuming that the presence of the VLPs either prevents the formation or leads to a depletion of the starch. A much more extensive study would be required to resolve this matter and is beyond the scope of this report."

Abstract is at:

https://www.ncbi.nlm.nih.gov/pubmed/15517277

Thanks everyone for your thoughts. Very interesting. So, we can't know for sure that the RRV leads to a depletion of starch, it's just a hypothesis that seemed to backed up by one study.

From reading this study: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3499817/

it seems the starch buildup in Fig plants with FMV would be relevant to RRV given that FMV is also an emaravirus.

Whatever the eventual cause of death it seems to take a very long time. I've seen infected multiflora that lived (or are living) for at least 3-4 years with the disease here in 6b/7a.

The following was stated: "Other emaraviruses seem to be 'easier' to live with. The one that infects Date Palms reduces productivity, but doesn't kill. That might be tied to the different vascular make of date stems."

H.Kuska comment: The differences may / probably also be at least partially due to the differences of the development of the immune system and to the differences in the development of the virus' defense mechanisms against the immune defenses. Nature is complex.

i.e. how long the plant and the virus have coexisted.

Think of when the American Indian was first exposed to European viruses such as the common cold.

I decided to look for research reports concerning research in progress for commercially important emaravirus infected plants.

" Also relevant to this component of Objective 2 is work on RNA silencing. RNA silencing is the most effective antiviral adaptive defense mechanism mounted in higher plants to combat viral infection and proliferation. However, viruses have developed a variety of efficient counter-defense mechanisms by encoding suppressors of RNA silencing (SRS). Wheat mosaic virus (WMoV), the causative of High Plains disease, an economically important disease in wheat and maize, is an eriophyid-mite (Aceria tosichella Keifer) transmitted Emaravirus. The WMoV genome was screened for potential candidates with SRS activity and two were identified. This is the first finding demonstrating of a plant negative-sense RNA virus encoding suppressors of RNA silencing."

https://www.ars.usda.gov/research/programs-projects/project/?accnNo=424225&fy=2016

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It would appear that the rose rosette virus researchers may benefit from commutating with this research group.