TEMPERATURE EFFECT ON ROSE MOSAIC VIRUS BEHAVIOR

revised 07-23-2022

by Henry Kuska

retired, Associate Professor, Department of Chemistry, University of Akron

Ph.D., Physical Chemistry

This page gives the information that I have collected from my own literature searches and from others posting on the internet. Please let me know if you feel anything is not clear or is not addressed at all as I am continually updating/modifying it as I get feedback.

Bold print in quotes does not mean that the bold print appeared in the original; the bold print was added by me (H. Kuska) for emphasis. Information in color indicates that a link is present for further information.

The question of whether rose mosaic virus (RMV) affects the growth of the rose comes up frequently on rose forums. Often some/many gardeners from hot climates insist that RMV has no or very little effect on the growth of roses.

First, before I get into the main topic, the term RMV does not refer to a specific virus but to a group of virus that can cause mosaic symptoms on rose leaves. In this article I will discuss mainly the temperature effect of two of the more common rose mosaic viruses PNRSV and ApMV..

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The cool temperature behavior of PNRSV infected roses was reported in 2007 by a group of scientists from Poland.

From the Abstract: "The effect of infection with Prunus necrotic ringspot virus (PNRSV) on growth, flower production and quality of three field-grown rose cultivars: Ingrid Bergman, Mr Lincoln, and Queen Elizabeth, was assessed in 2005 and 2006. One and two years after inoculation fresh and dry weight of flowers, diameter of flowers, diameter of shoots, length of shoots, number of shoots, number of flowers and number of flower petals decreased significantly."

H.Kuska comment: (For your convenience: The average high temperature for Warsaw, Poland is 73.4 F June, 75.2 F July, and 73.4 F August.)

H.Kuska comment: I have a copy of the full paper. Normally when someone is doing new research in an area, one is expected to review what has been done before. This is what the authors wrote in the historical introduction section:

"PNRSV infected glasshouse roses cultivar ‘Baccara’ produced fewer bloom (ca 13%) than healthy plants (Pool et al. 1970). Diseased plants of ‘Fragrant Cloud’ flowered later than healthy ones and produced fewer often more deformed flowers and were generally smaller (on a fresh or dry weight basis). The reduction in bloom production (ca 40%) was noted (Thomas 1982). In experiment described by Manners (1997) ‘Double Delight’ plants infected with PNRSV produced fewer flowers and shorter stems. Moran et al. (1988) also presented negative effect of PNRSV on growth and flowering of rose cultivars ‘Sonia’ and ‘Mercedes’. On the other hand, Wong and Horst (1988) have not observed any effect of viral infection on stem length and total number of rose cut flowers among ‘Bridal Pink’, ‘Fragrant Cloud’, ‘Grand Masterpiece’, ‘Samantha’ and ‘Simplicity’ cultivars. The plants were grown in greenhouse, and the elevated temperatures may have alleviated effect of PNRSV."

H.Kuska comment: Please note that the authors, reviewers, and the editor approved the wording: "The plants were grown in greenhouse, and the elevated temperatures may have alleviated effect of PNRSV.

H. Kuska comment: Will PNRSV affect the growth habit of a specific infected rose in your climate? Unfortunately Zone numbers may not accurately answer this question. Zone numbers are mainly useful for cold, freezing information. To find high temperature information, take the nearest city of appreciable size and do a Google search of the monthly average high temperatures.

Also, there are weaker and stronger stains of each virus and an individual rose may have a weaker or stronger immune system against that particular virus so your results for a particular infected plant may be different than for another rosarian in a similar climate.

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It is generally accepted that PNRSV virus symptoms appear mainly in the spring and late fall. How does the scientific literature explain this? The following 4 papers discuss various aspects of this question.

PAPER 1)

PNRSV infections in Peach have been reported to vary with the season (i.e. temperature). The following is the abstract of the published, refereed paper (please, keep in mind the reversal of our seasons with theirs). I have added bold print to indicate important sections. Their results are consistent with the casual observations that many have made that, in many roses, the symptoms are observable in the spring but disappear in the summer. This paper has been cited by 32 more recent papers according to Google Scholar.

Authors: Dal Zotto, A.; Nome, S. F.; Di Rienzo, J. A.; Docampo, D. M.

Author Address: Instituto de Fitopatologia y Fisiologia Vegetal INTA, 5009, Cordoba, Argentina.

Title: Fluctuations of Prunus necrotic ringspot virus (PNRSV) at various phenological stages in peach cultivars.

Published in: Plant Disease, volume 83, pages 1055-1057, (1999).

Abstract: " Fluctuations in Prunus necrotic ringspot virus (PNRSV) concentration were researched in single plants of six peach (Prunus persicae) cultivars-Kurakata, Red Haven, Nectar Red, Start Delicious, Meadowlark, and Loadel-by double antibody sandwich-enzyme-linked immunosorbent assay (DAS-ELISA) of dormant buds (May, June), flowers (September), new sprouts (November), and mature leaves (January) (Southern Hemisphere). The optimum extract dilution (sample weight per buffer volume) to detect the virus was also quantified. The average absorbance patterns of the six cultivars show a steady increase in virus concentration, ranging from A405nm 0.61 in May to A405nm 0.86 in July for dormant buds, to A405nm 1.22 in September in flowers, to 1.53 in November in new sprouts, where the highest concentration was found. Virus concentrations in mature leaves drop to values similar to those of noninfected plants in January (A405nm 0.12). The yearly average (six noninfected peach trees) ranged from A405nm 0.04 to A405nm 0.08. This drop coincides with an increase in summer temperature and attenuates foliation symptoms caused by PNRSV.

Analysis of dormant buds, flowers, or new sprouts with 5-cm-long leaves was reliable to differentiate infected from noninfected plants. Cluster analysis of absorbance profiles for single plants of cvs. Loadel and Meadowlark, however, showed a comparatively low profile, with a drop at flowering time (A405nm 0.20 in September) close to the average of healthy controls. The difference between infected and healthy plants did not become apparent in all cultivars from the analysis of plants at a given phenological stage, for example by the analysis of flower only, the material most preferred to diagnose the virus. Therefore, plants should be analyzed during flowering and sprouting or flowering and dormancy (dormant buds)."

END OF ABSTRACT

Now, the question is: does PNRSV in roses have the same temperature behavior? Fortunately paper 2 appeared the next year.

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Paper 2)

This 2000 PNRSV in Roses published research paper by Moury et. al. is available free at the following web link: http://apsjournals.apsnet.org/doi/pdfplus/10.1094/PHYTO.2000.90.5.522 This paper has been cited by 15 more recent papers according to Google Scholar"

Among other things, they studied the PNRSV Elisa readings on the hybrid tea rose Anna as a function of time of year.

On December 8, 1998. The ratio of the absorbance of the infected leaves and the absorbance of the leaves of a healthy plant were (see Table 4, page 526) - 4.7

Same test on February 3, 1999 - ratio 7.8

Same test on March 31, 1999 - ratio 3.8

Same test on May 10, 1999 - ratio 18.9

Same test on July 15, 1999 - ratio 3.7

Same test on September 1, 1999 - all samples were ELISA negative - they could not detect the virus!

Table 3, page 525 gives the percent of positive leaf samples for the same 6 times. They are: 33.3%, 50.0%, 53.3%, 65.6%, 22.7%, and 0.0 %.

The rose studies were carried out in Antibes, France. The average high temperature reported there is June 75 F, July 81 F, and August 81 F.

Thus, the amount (concentration) of PNRSV in roses decreases as the temperature increases (and in at least one case, until it can no longer be detected). The obvious next question is: why would the virus concentration decrease with temperature?

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PAPER 3)

The following study appears to be the critical study for explaining why plant virus infections have high concentration at lower temperatures but are attenuated at higher temperature. This 2003 paper has been cited by 535 more recent papers (according to Google Scholar).

The abstract contains the following: "Therefore, in cold, plants become more susceptible to viruses,.....".

The Introduction contains the following:

"Plant-virus interactions are strongly modified by environmental factors; especially by temperature. High temperature is frequently associated with attenuated symptoms ('heat masking') and with low virus content of virus-infected plants (Johnson, 1922; Hull, 2002). In contrast, rapid spread of virus diseases and the development of severe symptoms are frequently associated with cold air temperature (Hine et al., 1970; Gerik et al., 1990). Harrison (1956) has speculated that the virus content of a plant represents an equilibrium between replication and degradation and that the activity of the virus degrading system increases with temperature. However, the underlying molecular mechanisms of these effects of temperature are still missing. We hypothesized that RNA silencing might be the postulated virus degradation system and temperature modifies plant-virus interactions through the regulation of RNA silencing." (page 633 and 634))"

H. Kuska comment: In the Conclusion section (page 638), they state:

"We find that siRNA-mediated RNA silencing is temperature dependent in three dicot species, thus inefficient siRNA generation at low temperature is probably a universal feature of higher plants."

H. Kuska comments: Please note that statements in a reviewed published scientific paper have to be approved by the editor based on the comments of the manuscript provided to him/her by the reviewers (normally at least 3).

Here is a link that might be useful: Low temperature inhibits RNA silencing‐mediated defence by the control of siRNA generation | The EMBO Journal (embopress.org)

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Paper 4)

A 2014 Cornell University Ph.D. Thesis titled: "GRAPEVINE FANLEAF VIRUS: BIOLOGY, BIOTECHNOLOGY AND RESISTANCE" has some experimental data that support this temperature dependent immune system model:

"Multiple experiments that iteratively tested individual variables showed that systemic GFLV infection was correlated with lower ambient greenhouse temperatures,....."

"Higher cooling degree days (hotter temperatures) had negative effects on the frequency of agroinfection (Table 4-3). This corresponded to observations that systemic infection was difficult to achieve in the low frame greenhouse in summer when temperatures regularly approached daytime highs of 32�C. In contrast, when temperatures remained close to the set 22�C constantly, systemic infection frequencies were improved."

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Summary

Contrary to early "thinking" plants do have what is now called an immune system (natural defense). The rose's natural defense is better able to overcome the virus as the temperature increases so the concentration of the PNRSV virus is decreased (or possibly even eliminated in the above ground parts of the rose in which certain types of spread could occur - use of pruners, branches touching, pollen spread by insects, seed transfer). Thus, rose spread research done in hot climates may not apply to PNRSV spread in roses in cool climates.

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Is this temperature dependent behavior limited to PNRSV? A 2005 paper ( that cited Paper 1) studied Apple Mosaic Virus (ApMV) in hazelnuts. (ApMV is one of the viruses grouped under the term Rose Mosaic Virus when found in roses). Of particular interest is the following quote (page 157): "ApMV, the member of ilarvirus group, is a labile virus, concentration of which can be negatively affected by high temperatures (Matthews 1991, Zotto and Nome 1999), and whose disease symptoms are masked at such temperatures (Aramburu and Rovira 1998)."

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Concerning roses here are two observations consistent with a temperature dependent immune system.

Stephen Vann, Ph.D, assistant professor and extension urban plant pathologist with the University of Arkansas, Division of Agriculture, states in a 2011 article that:

"Cool temperatures tend to favor virus multiplication and disease development within the rose plant."

http://durhamcouncilofgardenclubs.blogspot.com/2011/08/rose-mosaic-and-rose-rosette-by-stephen.html

AND

The University Of Illinois web page about rose viruses: http://hyg.ipm.illinois.edu/pastpest/200113f.html

Of particular interest is the following:

"The heat of summer inhibits virus activity."

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My other rose virus sites can be reached from the following index page:

https://sites.google.com/site/rosevirusindexpage/