The following was stated: “Since roses are not the usual host for RMV, one might expect that transmission to roses is not very efficient. When looking back it seems that there was a definite point in time when RMV type viruses began to infect roses. This coincides with the time when risky grafting procedures were employed. It has been widely suggested as mentioned above that the index case occurred when someone attempted to graft material from an infected fruit tree onto a rose. Prior to that, I am unaware of any instances where biting insects or mites were capable of transmitting RMV type viruses to roses. For that matter, I am unaware of any instance where bees or other pollinators carried infected fruit tree pollen to roses that resulted in infections, and though perhaps less likely, I have never heard of root to root transmission of RMV type viruses from fruit trees to roses. If those other modalities were possible, RMV type viruses would have long ago been established in roses.”
H.Kuska reply.
In addition to what I linked to earlier in this thread, maybe this will help convince the reader that PNRSV from roses did NOT have to only reach roses by transfer from other plants due to rose bud/other plant human experimentation as was “postulated” (apparently after the early literature was missed). Remember it even was found in wild roses.
There is evidence that the rose versions of PNRSV have measurable differences from the other plants’ PNRSV. (i.e. is not the same as PNRSV from many/most/all other plants.)
The following quote comes from the introduction of the recent paper whose link is:
http://www.up.poznan.pl/ptfit/pdf/PP40a/PP40_31-41.pdf
“Generally, received results have indicated that apricot,peach,plum and rose isolates are serologically different from cherry isolates and all fruit tree isolates significantly differ from those from rose and hop plants.”
Please note: “all fruit tree isolates significantly differ from those from rose and hop plants.”
In that paper’s Conclusion section they state (from their research): “Results presented in Table 2 indicated rather that rose isolates of PNRSV belonged to CH-9 serotype although they may have possessed less antigenic fractions than PNRSV isolates from fruit trees.”
In the following paper
http://www.springerlink.com/content/61n6chy7f3thb68a/
all of the rose PNRSV viruses (code names: Ring 13, Ring 25, and Ring 26) were grouped in classification I(pv32) (“Shown is the evaluation of the nucleotide sequences as described in the text. Horizontal distances are proportional to the number of changes.”) with only a few others close - also note there were even small differences between the 3 rose isolates.
There have been a number of papers pointing out the various differences between PNRSV of roses and other plants (including which will and which will not infect other species) which I have not included here as the first introduction statement summarized them (“Generally, received results have indicated …”).
To condense a response to the other “points” made in the last post. Roses have an immune system (of course in hybrids, one rose could have a more efficient immune system than another rose). The immune system has been shown to be temperature dependent - it works better at high temperature. PNRSV (one of the viruses that collectively are called RMV has been studied extensively both in roses and in other plants. The same temperature dependence is found. Also PNRSV and other members of the RMV group have a number of strains with different strengths. At one extreme is the death of most of the ApMV infected roses in the fourth year of the Florida spread experiment. At the other extreme is the PNRSV infected rose Anna in a French experiment that was observed to be cleaned by simply taking cuttings in a hot summer month.
Yes, there are observations of a particular infected rose doing very well in a northern climate. Was this due to a better than average immune systen or a lower than average virus strength (or combination) one cannot say without doing a scientific study. There also have been many, many experiences of virused roses only living about 4 or 5 years in northern gardens. Why did some survive and many die?
In my first virus response in this thread I stated:
" In cool climates there would appear to be about a 2 per cent chance of virus transfer through seeds. See link below. In hot climates, probably no transfer.
http://home.roadrunner.com/~kuska/rose%20virus%20and%20pollen.htm"
Please notice the “In hot climates, probably no transfer.”
Concerning damaged seedlings. Even in the hot summers Davis experiment where they reported no seed spread they stated: “In seedling transmission tests, all of 651 seedlings from seven virus infected scion varieties ELISA tested negative for PNRSV and ApMV. Ten other seedlings had distorted strap leaves, were chlorotic and/or had other foliar abnormalities; the abnormalities were not typical of RMD symptoms. Most of these 10 plants died before they could be tested. Herbaceaous host tests using cucumber on three of these plants were negative for virus. We suspect that the odd appearance of these plants was due to genetic weakness rather than a result of virus infection.”
H. Kuska comment: A Herbaceaous host test is not considered a sensitive test. Since there was not a “blank” consisting of the same type of seedlings (but virus free), one cannot say if there was something else in their makeup that resulted in these weak seedlings. Also we do not know what percentage of seedlings would be weak or not even germinate in a cool climate situation where the virus would be more active.
To further look at the subject of whether a hybridizer can expect problems when using infected mothers or infected fathers, the following paper should be useful. This paper reports that seeds of apricot exhibit something like a hypersensitive response when attacked by PNRSV. This defense (to quote from the abstract) “would inactivate PNRSV during seed formation and/or the storage period or even during seed germination. Those results can explain the decrease in seed germination and the low transmission of PNRSV by seeds in apricot trees.”.
http://www.ingentaconnect.com/content/mksg/ppl/2007/00000131/00000002/art00013