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, Paper.

On the Future of Research on the Virus Diseases of Plantsby

H. H. STOREY,

.East African AgriC1tU1tral Research Station, Amani, Twnganyika Territory.

For one lacking the prophetic insight of Mr. H. G. Wells; an attempt" at prophesy can be no more than. an elaboration of present knowledge. Fot'

that reason I approach with misgivings the task that has been set me. Ofnecessity my guide to the future of virus research .must be research now inprogress or completed; if I confine myself too strictly to immediate deductions':}~,from present facts, I shall risk stating the obvious and moreover I shall merely.fcover the same ground as Dr. Brandes and Dr. Matz, yet to. attempt to foretell~i;~developments for which there is no present basis would be extravagant specula- ~iltion. To those who deem what I have to say' eitlier banal or fantastic I now

offer my apologies.

The subject of virus diseases of plants is now a vast one and from it I .:~can only select certain small parts for discussion in this paper. I judge that,'~Sugar Technologists are primarily concerned with practice, but inevitably this)~discussion must be concerned with matters academical rather than practical. ,;\1What I may ter-m the directpra'ctical outlook has achieved much in the past,l~but future large advances in practice are to be expected from the more funda-,i;'mental type of research. If then the subjects I discuss are academical, I will!;itry to indicate what I think may be their effect on practice..;~

'~~

It can hardly be doubted that to-day the diseases due to viruses are of)~

greater economic importance than they have been in the past. Leaving on'~one side the question of recognition, which undoubtedly has done much to give,i~a fictitious "newness" to many diseases, we must agree that on the whole inr~:'ecent 'years virus diseases in crop plants ha~e increased both ~n inte~sity and'.i~l!III variety. In England, for example, until recently the VIrus diseases of).potatoes were alone deemed worthy of considerable investigation; to-day theil';:ffincidence in many other crops is viewed with much concern. Australia in recent~;~years has added two to the already con~iderable list of virus diseases of sugij,tJlcane. Much of this increase is susceptible to simple explanation: to the distribu-:;~tion of diseased material from country to country; to the extension of crops<i~into areas where they have hitherto never grown, or have in the past perhapsi~failed from some cause unknown and now forgotten; to the efforts of plallti~breeders, who in breeding desirable types have lost factors for resistance that~'hitherto maintained the variety in health. Are these and similar explanation~f!enough ~ /,;'c

')j

I find that there are workers who now question whether viruses may na:~~originate de novo. At first sight this idea is to me, and probably to you, entirel~repugnant. Yet, on consideration, I see that my repugnance is based on IIl~'training in biological continuity. At a later stage I shall have more to say6~i

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i6gical analogy; itis8ufficientnowtoremark thatso long as the ultimate"of the virus remains unknown, we cannot fairly say that anything isihle, The almost complete impossibility of proving an origin de novo,

tby a lucky chance, makes the argument that it has never been proved ofvalidity. It must not be forgotten that there are medical pathologists

views incline to the' acceptance of an explanation of this' kind for theof certain tumour viruses [14]. My own opinion however~, with which

will no doubt agree, is that plant pathologists have at present no reason toethis almost defeatist hypothesis.

:When, however, we consider the question of the evolution of viruses webn firmer ground. Let me state the present position: Pathologists now

ise that there are a large number of distinct viruses-virus species let11 them. Each species is ~tP to a point constant in its behaviour,producing

arm effects in one variety of plant under uniform conditions, but often¢ly different effects in other varieties and under other conditions; with ajte, and often small, range of host plants; often even more specialised in'elation with the species or races of the insects that transmit it; sometimesing properties in oiiro characteristic and constant. But as research pro­es, within a virus species we may find a number of strains or races, differingarily in their relative virulence to a range of host-plants. The recognition

irus strains is a recent development; at present it is a phenomenon that has'demonstrated in only a few virus species. I believe that research in there will show that it is of wide occurrence. To seek. for the manner of originirus species would at this stage be idle; the evolution of virus strains is, on

.eontrary, a matter of immediate practical concern. I suspect that virusesessentially unstable, and that the evolution of strains' is constantly and

idly occurring.,..'.

At present this view is supported by, little experimental evidence. On"contrary the experimentalist is usually impressed by the constancy of the,'aviour of the virus strains that he holds understudy. Yet workers with

virus of the curly-top of sugar beet have by suitable passage produced aMn of. the virus mild in its effect on beet [3] and from it produced again aulent strain [11]. Medical pathology provides many similar instances oferimental changes in virulence by passage. Heat treatment has also been

plied to the alteration of a plant virus [6]. We have thus indications ofperimental procedures by which new strains of a virus may appear and Ilieve that future advances in this field will be productive of more.

0-:;)

Let me use as an example of the conditions that may be encountered ine field the African streak disease of grasses. With McOlean [18] I was ableprove that the viruses of streak in maize and in cane are not identical, each

iug virulent for its nat~ral host a~d not for the other. The Uba cane of Natalbelieved to have originated from a single sett introduced some fifty years ago;w, as Mr. McClean will tell you, streak is still spreading in, this variety in~ite of some attempt to control it during recent, years. It is true that the

110

llresent position may have come about by a process of sifting out oj: viruses pre­existing in indigenous grasses, a grass virus chancing to be virulent to cane hasbeen perpetuated by the cane. I think it more probable that the virulence foreach host has evolved and virulence for Uba cane during the past fifty years.I suspect that there was recently in progress the evolution of a virus strain viru­lent to P.O.J,. 213. The history of this variety in Natal is as follows: Intro­dueed in 1914, it was grown in regions where inoculation with the streak virusfrom Uba must have been constantly occurring, yet no case of streak was foundin it until 1926; in the following years there was a considerable increase inincidence in the plot where the first cane was found. McClean [12] has reportedthat the P.O.J. variety may be infected experimentally if the dose of virus belarge, but usually the infection is transitory and recovery complete. Some plantsin the field remained diseased however and made no, recovery. The interpreta­tion of these results is quite uncertain: McClean in 1932 saw no reason to postu­late any change in the virus; but I would question whether the instability{If the infection that he encountered is not a phase in the evolution of a P.O.J.:strain of virus. In those cases where, a permanent' streak infection has becomeestablished, we must suppose that either the plant or the virus has changed; itis more probable in my view that it is the virus that has changed.

Perhaps the same type of phenomenon may be detected in sugar-canemosaic. I would remind you that in the Transvaal, in regions where sugarcanewas not grown, I found a mosaic virus, transmissible by Aphis maidis to maizeand sorghums, but not to cane [17]. Recent reports from Louisiana [21],show that there exist there dist~nguishable strains of virus affecting sugar cane.Already then we have strains of the mosaic virus existing in nature. At presentwe have no indication how they have arisen, but perhaps it is significant that,certain of the new P.O.J. varieties are found to show transitory infections ofmosaic. Is this the first phase in the evolution of strains of virus virulent tothese varieties? There will be arguments, I do not doubt,' based upon a fewyears' experience, against this view. But since my function to-day is toll r ophesy, I venture the prophecy that with the breeding of these immenselyvaluable new resistant varieties the story of mosaic in suga,r cane is not ended.

To what does the realisation of the diversity of plant viruses lead us?Undoubtedly it points to even greater caution in assuming without experimentalproof the identity of the' viruses' causing a similar disease in two differentvarieties or species of plants. This caution was soundedlong ago by Dr. Brandes[2] ; all of us must have been on our guard, yet I imagine that few of us havenot fallen into error at some time. Experimental procedure is arduous and'Sooner or later we must extrapolate. An error of my ,own may interest you:In the mosaic disease affecting sugar cane, with its comparatively exact(\:1' recent distribution to most cane-growing countries, the presumptive evidenceTor its causation in cane by a single virus is strong. During my time in1 found a cane variety Agaul showing typical mild mosaic-symptoms, andassumed that it was attacked by the then prevalent mosaic virus. I have recently;

111

ted· to re-investigate' this problem and I have failed .to transfer mosaicli\'aul to any variety.veithen by needle 01' by Aphismaidis.Furthermoreevidence that no dissemination from it occurs in the field in East Africa:this mosaic-pattern is a varietal character-a highly improbable conjec­

.or the Agaul virus is different from the common sugar-cane virus. This1 variety was imported to Natal from India; the literature of mosaic inshows many anomalous features-great variability of symptoms within a

e cane variety, failures of transmission experiments with Aphismaidis,ssful infection ofUba. 'These considerations led me to suggest to an

'n authority that there, might exist in India a distinct indigenous mosaic~in addition to the common virus introduced in recent years. My suggestion::with the lack of enthusiasm that its impertinence merited. I remain,

W¥ver, uneonvineed that the Agaul virus is the common cane virus, although,,lie my hypothesis requires that the vector of the Agaul virus be some insect'r than Aphis maidis, and probably not existing in Africa, I can do little to

"it. If my ideas have any truth in them sugarcane practice in the futurehave to take account not only of strains, but of species also, of mosaic

ses.

,The principle of the direct method of control of virus diseases is the'king of the plant-insect cycle through which the virus passes. Control iof

us diseases should be easy, since the virus, unlike many other plant pathogens,no saprophytic development and usually very limited survival outside

• g tissue. Doubtless the main reason why the procedure based on thisciple oftenfails is our ignorance of, or inability to deal with, alternate host­ts of the virus. As our knowledge increases, we may anticipate success

'm the selective weeding of the locality in which crops are grown,a procedureeady reported to be effective with some crops [22J. But our knowledge willd to cover not only those plants that carry the virus unchanged and those

Itt attenuate it to a relatively harmless strain-as has been demonstrated fore sugar beet curly-top virus [3J-but also those plants that carry the virusithout showing symptoms. There is before us a formidable field of detailedork in the delimiting of the host range of virus strains; and perhaps anending one if the position, as I suspect, is never static.

There is however a crumb of comfort to be gleaned-from a considerationthe multiplicity of virus strains. A number of workers, and in particular'nkel [10J, have shown that infection by a mild strain may confer upon a plant

munity from severe strains of the virus. This discovery may have a profound,ect upon practice in the future. If the principle could be applied to a~getatively propagated 'crop we should be equipped with a highly desirableeans for control, for it would be necessary to inoculate but one plant of anyesired variety with a mild virus capable of producing only insig:nificant ill­ects; all the vegetative progeny of that plant would retain the mild virus and

ereforethe immunity' resulting from its presence. , Infact, however, I doribthether such magnificent simplicity will be .often' achieved. I have myself

~ 1-'. ( - - - .

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recently attempted to apply the principle to the control of the mosaic diseaseof cassava; on the whole my experiments have failed, and yet even here Ithink something may result, but only after an arduous sorting out of strainsand' perhaps virus species.

For his experiments Kunkel (loc. cit.) employed a mild strain of virus.artifieially produced by heat treatment. Perhaps in this or some similar methodfor artificial attenuation we may find the most advantageous means for obtaining;immunising viruses. My cassava experiments were done with mild viruses foundin the field; if a method of artificial attenuation could be found more consistentresults might be obtained.

One of the most striking characters of the plant viruses is their dependenceupon insects for their natural transmission from plant to plant.'l'he tendency,evident even to-day [7J, to separate viruses into those transmitted .by insects.and those not so transmitted has, in my view, no real basis except in ignorance.I am writh those who believe that the adaptation of a virus to insect-transmissionis a necessary condition of its natural survival, although perhaps those fewviruses that are carried over in the true seed may be excluded from this generali­sation. The laboratory methods of transmission-gra.fting, needle inoculation­though. often highly effective cannot operate in nature, even though in someinstances they may be caused to operate in the field by cultural practices. Ibelieve that ignorance accounts for the list of viruses not transmitted by insects;each year reduces th.eir number and only recently the vector has been foundof such a long-known disease as peach yellows [9J and perhaps also SandalSpike [16J. At the same time it is hard to understand how the vector of such.a virus as the X-virus of potatoes can have been overlooked. Can it be thatthere is another natural method by which viruses may be transmitted ~ If soI cannot conjecture what it can be.

Recent research has made it clear that some insect-vectors act merelyas mechanical carriers of the virus [4J. With the majority however we have"biological internal transmission" of which Rand and Pierce [13J wrote longago. This process has hitherto received comparatively little study. The out-

.standing discovery of the past has been the proof of a non-infectivefollowing an insect's first exposure to a source of the virus (e.g. Severn [15]Kunkel[8J ). At present we have no certain interpretation of this phenomenon.Suggestions that have been or can be made are :-(1) that the delay is occupiedmerely by the transfer of the virus within the insect's body from the sitereception (the intestine) to the site of ejection (generally supposed to besalivary gland); (2) that part of .the delay is due to a necessary multiplication':of the virus within the insect before an infective dose can be ejected;the virus undergoes a necessary cycle of development within the insect.of these alternatives will the future prove oorrecti We can only make l2'uesseson very uncertain grounds.

..

L~t me .consider . the insect with which IGicadt~~ina mbila, a vector of .the streak virus of

. of a technique for needle inoculation of the viruscl the following points [20]: After feeding upon a ..' plant,.has some virus in its falces; the virus has therefore entered the intestine

omehas passed throughunchanged. Afteratimeequalto about half thet period, virus, may be detected in the insect's blood. After a further time,

know, the insectstarts to inoculate virus into plants on whichit may feed.rnatively we-may inoculate virus directly into the blood of an insect thatnever fed upon a diseased plant; that insect in like manner will becomehle of inoculating plants. So we must suppose that in the normal processirus passes through the insect's intestinal wall and js carried by the blood

$ome site whence it may be ejected into a plant. What is this site 7 Theyconceivable answer is the salivary gland. Yet when I attempt to detect:Us in this gland or in saliva ejected by an infective insect I find none. What.. be the explanation of this 7 Can there be some alternative vehicle of theuS inoculation 7 I can imagine none. Can it be then that my methods usedthe attempt to find virus in the saliva are faulty ¥ That I think is possible.evirus may be present in the saliva in such small quantities-in such extreme

llltion-that my methods are too insensitive to find it. Or the virus may be. a form in which my methods fail to detect it when it issues in the saliva.'t me give examples of some of the experiments I have done: A small areaa maze leaf is exposed to the feeding of many infective insects so that that

'¢ce of leaf undoubtedly receives' a great number of doses of virus .capable. establishing an infection of the plant. The piece of leaf may be crushed ands juice either inoculated into non-infective insects or fed to them through aembrane, or non-infective insects may be fed upon the undamaged leaf, eitherter the infective insects,*or simultaneously with them by adopting someevice for ensuring their subsequent recognition. By any of these methods

,tehe non-infective insects will never become infective. and yet, if I inoculate thejuice of a leaf bearing the lesions of streak into non-infective insects, or feedhat juice to them, they will become infectiv~~ Either then thevirus in the saliva

}s too dilute to take effect in my experiments or it is in a form that is incapable.of establishing itself in the insect. I cannot at present decide between. thesealternatives. If the latter prove to be correct we must admit the idea of a cycle()f dev-elopment of the virus in the insect.

I must accept the' saliva as the .vehicle. of the virus .inoculation "for I:'eansuggest no other. Yet how the saliva so functions. I cannot understand.iThe saliva of Gicadu~ina mbi~aisa viscous fluid-that is ejected by the stylets

::discontinuously---.:only when the stylets are in motion, and not while .the .insecti'js sucking. On ejection the saliva sets to agel, being penetrated and moulded. somewhat by the advancing styletsand constituting the salivary sheath so well-

* In an early paper {Ann. Appl, Biol, v, 15, p. 1)' I reported a small proportion ofsuccesses following this procedure, Beeentvexperiments have however -beenulliformly

I c.annot explain how the error (if such itbe) arose in the earlier experiments., t' ~

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. known in histological preparations. One would imagine that this material wouldbe a highly unfavourable medium for the introduction of a virus into aplant,whereas we know that virus becomes rapidly mobile and may travel a distanceof several centimetres within an hour; would not the virus particles tend to beheid in the gel ¥ Yet another difficulty arises: The insect ejects saliva primarilyduring movements of penetration, particularly during the first seconds afterpuncture and periodically .thereafter when the site of sucking is altered. Andyet with Gicadrulima there Is a threshold duration of puncture for success ininoculation; several hundred punctures of less than a certain minimum durationwill fail to cause infection, whereas one or a few punctures of longer durationmay succeed. Perhaps it may be suggested that these short-period puncturesfail to reach the phloem, for it has been shown that penetration of the phloemis necessary for infection by some viruses (e.g, Bennett [1]) and this is true ofthe streak virus. But I have found that many punctures of less duration thanthe threshold period do in fact reach the phloem. Short-period punctures often,penetrate the phloem and show large deposits of salivary material there, yetthey are never successful in in.oculation.If it were known that the insect werecapable of ejecting some second form of saliva, that failed to gel in the planttissues, an explanation of the mechanism of inoculation might be forthcoming,but of this I can find no evidence.

It seems to be generally believed that the virus multiplies in some tissueof the insect. The basis of this belief is the evidence that an insect may remaininfective over long periods without receiving further supplies of virus.Cicadalina mbila provides a typical instance of an insect that normally remainsinfective throughout its life, but recently I have found that if the original doseof virus that it receives is small it will become non-infective within a few weeks.If multiplication occurs .within this insect the multiplication is not unlimited.Can it be that the insect is extremely economical in its output of virus, thatafter all there is no multiplication, but that a prolonged feed on a source ofvirus gives the insect sufficient store ·to last its life-time ¥

A point of great interest is the extreme specificity of most viruses .toparticular insect-vectors. The specialisation may be carried even further thanthe species; I have shown that in the species Gicadnlina mbila there are tworaces,. which I have entitled active and inactive, the one able and the otherunable to transmit [19] . The two races breed true for this character; inheritancein crosses -between the two races follows simple Mendelian lines. I believe thatthe future will show that this phenomenon is of much wider occurrence than wehave-hitherto suspected. One other species of Gicadulina, now under investiga­tion, has given clear evidence of this dimorphism. Dr. Eubanks Carsner informsme that different races of EuteUix' tenell1tsmay show differences in inoculativeability. Finally I would-refer to Ruff's work [5] on bird malaria in which heshowed that the ability to .. transmit was inherited by it·· mosquito; there are inaddition records of local races of mosquitoes unable to transmit malaria thoughmorphologically indistinguishable from races known to be vectors elsewhere.

"can conceive that the study ofal outcome of some importance.

~~differing in ability to transmit, may differ also in other physiological~ters. My attempts to breed pure active lines of Cicadulina zeae underi conditions have been repeatedly frustrated by the dying out of the lines,as inactive lines are readily bred. Perhaps this may denote a difference

'matic tolerance. Th~re is thus the possibility: jhat by a change incultura,ltice a small .change may be effected in the eco-climata of a plantationi~nt to upset the balance between active and inactive races of a vector. It

,appear to you extravagant to suggest such a possibility. Yet the influencehe eco-climate upon insect populations is well known to entomologists.

'thermore I can provide you with an instance where this procedure is proving)y effective in controlling a virus disease. In East Africa by plantingundnuts at an extremely close spacing the crop can be raised almost free

rosette disease. 'I'his -proesdure was evolved by the native cultivator.ded; experiments bothin East and West Africa have confirmed its efficacy

,'ompared with wide spacing. In Uganda I found that Aphis leg1~minosCe thetitor of the rosette virus, was subject to the attacks of an Entomophthora sp.elieve that close planting slightly alters the ceo-climate in favour of the

ngus parasite and results in an, effective control of the aphid. Perhaps theture may provide us _with further opportunities for the application of thisineiple.

I have left to the end the central problem of our subject-that of theiimate nature of the virus. There are doubtless many who would be sceptical','to any -practical- outcome from a clarification of our ideas upon the naturea virus. It is true that remarkable advances in practice have been achieved

ithout direct knowledge of the causative agent, and that an hypothesis explain-,g the nature, physiology and manner of multiplication of a virus might doothing to alter our outlook upon the practical problems of disease control. Torgue against this view is perhaps to become unduly speculative.rand I cannotnjecture whither advances in knowledge of the nature of the virus might lead

,s. I can only dimly perceive possibilities, because the future may show that a.'irus is a kind of thing with which we have hitherto been unacquainted. It is:i'ue that our present knowledge of the manner of action of the virus' affords'0 particular reason for postulating something new to our experience. Wehall rarely be in error in handling our problems if we picture the virus as an

,'rganism, minute but not fundamentally different from the organisms that we~~now; exceptional, but not unique, in being an obligate parasite of living proto- ,illasm. But the biological analogy does not necessarily represent the truth. 'I'he,~ssence of the organism is its organisation; the manifestations of life are the',chain of processes occurring in the complexity of this organisation. The virusunit, if we may accept modern estimates of its size, is such that it can consist,of but a finite number of the molecules of the complex substances that go tothe makeup 'Of protoplasm. Can we conceive of cellular organisation with only,. finite number of molecules?

~: :

"I!IiiII

this question I do not attempt to. tell. Ione day we may .travel beyond the .biological

outlook may bring fundamental changes in practice.

REFERENCES.[1] Bennett, C. W. 1934. .Ioum. Agric. Res., v, 48, p. 665.

,[2] Brandes, F. W. 1923. .Iourn. Agric. Res., v, 24, p. 247.

[3] Carsner, E. 1925. Phytopath., v, 15, p. 745. _

[4] Hoggan, I. A.1933. Joum. Agric. Res., v, 47, p.689.[5] Huff, C. G. 1931. .Ioum, Prey. Med., v. 5, p. 249.

,[6] Johnson, J. 1926. Science, N.S., v-. 64, p. 210.[7] Johnson, J., and Hoggan, I. A. 1935. Phytopath., V. 25, p. 328.

[8] Kunkel, L. O. 1926.. Amer, Journ. Bot., v.13, p. 646.[9] Kunkel, L. O. 1933. Oontr, Boyce Thompson Inst., v, 5, p. 19.

[10] Kunkel, L. O. 1934. Phytopath., v, 24, p. 437.

[11] Lackey, C. F. 1932. Joum. Agrie. Res.,. V. 44, p. 755..[12] McClean, A. P. D. 1932. Fourth Congress, I.S.S.C.T., Bull. 27.

[13] Rand, F. V., and Pierce, W. D. 1920. Phytopath., v. 10, p. 189.

[14] Rivers, T. M. 1928. Filterable Viruses. Bailliere, Tindall and Cox, London.

[15] Severin, H. H. P. 1921. Phytopath., V. 14, p. 424.

[16] Sreonivasaya, JIlL 1.934. Nature, V. 133, p. 382.

[17] Storey, H. I-I. 1929. Ann. Appl. BioI., v. 16, p. 525.[18] Storey, H. H., and McClean, A. P. D. 1930: Ann. Appl. BioI., V. 17, p. 691.

[19] I Storey,H: H. 1932. Proc, RS., B., v: 112, p. 46.

[20] Storey, H. H. 1933. Proc, n.s., B., v, 113, p. 463.

[21] Summers, E.M. 1934. Phytopath., v.24, p. 1040.

[22] Wellman, F. L. 1932. Science, N.S., v, 76, p. 390.

Discussion.

In reply' to Dr. Bolle, Mr. McClean said there were no morphologicaldifferences noticeable between the active and inactive strains of Oicad1llinambila,

Dr. Brandes referred to Dr. Storey's remarks on the saliva setting toa gel. In the case of curly top of beet, they .had fed insects through a paraffinmembrane on sugar solution to which an indicator had been added.. The pHof the entire drop changed instantly indicating that the saliva was not whollya gel but contained some substance capable of rapid diffusioti.

.As regards protective inoculation, it was possible that the immunitymight be conferred by inoculating with a strain which was less serious, butno strain was so mild that he would care to recommend wholesale inoculation.This point became .complicated in the case of recovery from this mild strain,as it would then require re-inoculation. He thought it had but little practicalapplication, and the possibility of dealing with new strains had, to be con­sidered.

yet lately,'fterent andthesehad probably,91ved from

." In reply to Mr. Femberton, Mr. McOlean stated there wasno evidencet C. 1nbilapecomipgepidemicon, cane, ,maize being the common host. It')S a very efficientyectorand few hoppers were required for transmission;.' (l hope was held out ofthebiologicalcontrolofC. mbila.

lVIr. Syrezeymentioned that the vector of corn stripe 'in Hawaii waseregrinus maidis.

Mr. Bell considered the papeI' presented by Dr. Storey should be ofiarticularillteresttoentomologists; One weakness in this, class of researchas the great difficulty ill rmlisting, the interest. of the "entomologists in virusiseases; More fundamental investigations of insect physiology were .neces­'ary, and Dr. Storey's research on infective •andnon-infectiveraces of thearne insect species should be a good starting point for 'other' entomological

~investigafions. .

In Queensland there existed an interestingsituation inconllection with,II).osaicdisease. , There were three well-defined climatic areas, namely-thewet tropical, the dry tropical. and the sub-tropical.: III the two latter areasthere was a rapid spread ofm{jsaic disease, yet in the, wet. tropical areas the

"disease was practically •non-existent although Aphis ~Ulxidiswas found in.',these areas from tiITle to time,butapparently, there was littleornospread.

Dr. Brandes' said that such a plea was apparently- ·.offensive to3entomologis,ts.A project was put forward in Puerto Rico, at the last Con~,ference"with a, view to interesting entomologists in the relationship 'of insects:.to plants,but seeminglywithout success.

, Mr. Pemberton quoted the interesting work which had been carried'out in Hawaii in regard. to, the association between PseitdococciUibrevipesand pineapple wilt. Somerindividuals were capable, and others incapable,

:of passing ,on a condition known as" green spotting," and Carter had shown. that this, depended on the associated symbiollts. He thought there was

for research ofa .sitnilar nature in regard tq O.mbila.

.lVIr.Swe2;ey expressed the opinion that lack of interest in the virus,.,disease question was not the reason why-entomologists did not pay more, attention to .the subject.•Thisstudywas a, comparativelynewrealm, .and upto the present, entomologists had been eoncerned mainly with the directresult of insect attack, rather than the minute relationship of the insect withthe transmission of diseases. Furtherm,ore,entoITlologists were not, in general,equipped. wihthepainstaking .techniqul:l required,for the elucidation of, thesematters.

work,

Mr. Pemberton then presented his paper, on " The Insect Vectors ofVirus Diseases of Sugar Cane," The author wade acknowledgment of theassistance he had received from'Mr. Swezey in compiling the data relating tothe distribution of the various species of Perkinsiella: In such cases whereonly one specimen had been recorded from a country the correctness of theidentification must be considered as doubtful.

Dr. Brandes thought theentomblogist should work on supplementaryor co-ordinating features which were purely entomological. Insect ecologyand physiology lay within the field of entomology. '

Mr. McClean considere'a'that lack of co-ordination was due rather tothe organisations concerned than to the entomologists.

'Mr. Dodds stated that Dr. Storey had established the existence ofvarieties or strains of virus diseases, and it was due to his excellent workthat South Africa had been able to recover from two diseases.

Dr. Brandes also 'paid a tribute to the excellent standard of Dr. Storey's

Paper.

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•HawaiianExec'/,~tive

The Insect Vectors of Virus Diseases of Sugar Caneby

O. E. 'PEMBER'l'ON,

Entomoloqist; Experiment Station,S'/,~gar Plamiers' Association.

\ Fiji Disease.

Fiji disease is known to occur in Fiji, Australia, Papua and the Philip­pine Islands and was reported in 1930 to be present on two' Philippine canesin the newly established quarantine station at Ranoe Daroengan, J ava [1].The writer saw native canes at Kokopo, New Britain, during March 1929,which were badly infected with the disease. Mungomery and Bell [1] haveshown that the insect vector of this disease in Australia is the leafhopperPerkinsiella saccharicida Kirk.; while Ocfemia [3]' has established proof thatan allied species 'PerkinsieUa vastatr'ix (Breddin) can transmit the disease inthe Philippine Islands. As .suggested by Mungomery and Bell [Ioc. dt.r, theinsect vectors of Fiji' disease are evidently several species of leafhoppers of thegenus Perkinsiella and the species responsible for the transmission of the diseasein Fiji must be Perkinsiella 'uitiensis Kirk., since this species prevails in thecane fields of Fiji. It isi probable that where more than one species of Perkin­siella occur on cane in the same locality, several or all of the species, may actas vectors of the disease.