The following recent paper reported zero transmission of PNRSV and/or ApMV to 651 seedlings from infected plants:
The seedlings were ELISA tested in the spring after their first season of growth.
My (H. Kuska) observations:
Apparently open pollination was used. If so, virused pollen from the infected mother plant would have been in competition with healthy pollen from virus free neighboring plants (the experimental details did not mention bagging or other methods to restrict contact with healthy pollen). Why should such a detail be important? The following apricot virus study reported that PNRSV infected pollen is at a disadvantage relative to healthy pollen (PNRSV infected apricot pollen had a germination rate of 27% while healthy pollen had a germination rate of 64%).
Thus, the interpretation of the results of this study are complicated by not knowing the extent that the results are influenced by the relative ability of virused pollen and healthy pollen to compete with each other. As a hybridizer, I would like to know if it is safe to raise seeds from crosses where one has placed pollen from an infected rose on another rose. The experiment reported here does not provide an unambigious answer to this question. It could of provided information concerning whether it would be safe to use infected mothers in hybridizations if one other precaution was taken in the experimental setup. This precaution is “temperature control”.
Apparently, there was no attempt to control the temperature of the plants during the hip ripening process. Temperature sensitive ilarviruses such as PNRSV and ApMV are inactivated at high temperatures. Temperature data for Davis, California indicate that the average daily high temperature is above 90 deg F (30 deg C) for 2 months each year. The internal temperature of hips exposed to full sunlight should/could be considerably higher than the air temperature (dependent on air flow-wind). The following link reports that PNRSV can be eliminated by “Alternating heat treatment regimes (39 deg C 16 hrs; 28 deg C 8 hrs dark for 18-20 days”. Please note that 39 degrees C is 100 deg F and 28 deg C is 82 deg F.
Thus, the ripening hips/seeds could of had their virus concentration reduced considerably during the hot days of a California summer.
I suggest that a controlled climate greenhouse be utilized in order to have a definitive seed virus transfer experiment at this location.
Another potential limitation in this seed transfer experiment is that the ELISA testing was only done once and only when the seedlings were 1 year old. As discussed in the following link seeds 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”.
http://www.ingentaconnect.com/content/mksg/ppl/2007/00000131/00000002/art00013
The following paper reports that the viral defences are more effective at higher temperatures:
http://www.plantphysiol.org/cgi/content/abstract/138/4/1828
(The full paper can be downloaded from the above site.)
The following quote is from the full paper (page 1829): “It has long been recognized that environmental factors such as temperature greatly influence plant-virus interactions. In virus-infected plants, high temperature is frequently associated with attenuated symptons (heat masking and with low virus content (Johnson, 1922). By contrast, low temperature is often associated with rapid spread of virus diseases and the development of severe symptoms (Hine and others, 1970; Gerik and others, 1990). Thermotherapy has been a method of choice to free vegetative material from infected viruses (Manganaris et al., 2003). Half a century ago, Harrison(1956) speculated that the virus content of a plant represents an equilibrium between r e p l i c a t i o n and d e g r a d a t i o n of the virus by the host system and that the activity of the virus - degrading system increases with temperature.”
The above suggests to me (H. Kuska) that both the relatively high temperatures during seed formation (at this location) and the seeds defense mechanisms could result in a very low concentration of live virus in the seedlings (below the detection limits of an ELISA test). If this low level equilibrium does exist in the new seedling, one may want to consider that it is possible that the virus level may not build up to detectable levels until the seedling is older than the 1 year used for the test in the U. C. Davis paper and/or has undergone some type of stress that weakens its virus defense mechanisms.
The following link provides background information about the possibility that a negative ELISA test does not guarantee that a virus is absent.
http://home.neo.rr.com/kuska/discussion_of_whether_virus_have.htm