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• . .:~..: •.~ ~ ~ This Week’s Citation Classic a JA~85 fCalnek B W, Adidlnger H K & Kihn D E. Feather follicle e~ithelium:a source of I enveloped and infectious cell-free herpesvirus from Marek s disease. Avian Dis. 14:219-33, 1970. ~ [Depth. Avian Diseases and Microbiology, New York State Veterinary CoIL, Ithaca, NYJ Mareks disease herpesvirus, which causes lym- antigen over a period of several weeks. We phomas in chickens, is highly cell-associated. purposely included tissues from which virus Keratinized cells surrounding the feather shafts in could gain access to the environment, since the skin were found to be unique in their producone of the most puzzling questions about tion of en’~elopedvirions, which could be exMD was how it could spread so rapidly withtracted in infectious form and used cell-free to rein a flock when the agent was so highly cell. produce the disease in chickens. [The SCla indiassociated. cates that this paper has been cited in over 145 “The skin sections included embedded publications since 1970.] feather shafts, and It was the feather follicle epithelium (FFE) that took top honors in — terms of frequency of infection and amount of viral antigen. Obviously, that tissue offered a plausible location for virus shedding, B.W. Calnek since molted feathers or ordinary dander Department of Avian and would include desquamated keratinized Aquatic Animal Medicine cells from the FFE. This study was published New York State College of in the journalof the National Cancer InstiVeterinary Medicine tute in 1969, and we duly Cornell University 3 noted the possible significance of the FFE. Ithaca, NY 14853 “The next steps were easy. With the help of two graduate students (Hans Adldinger September 10, 1984 and Donald Kahn), cell-free skin extracts were shown to be highly infectious and able “Excitement in the area of avian tumor re- to induce MD in chickens. Electron microscopic examination proved the exsearch, especially that concerning Marek’s disease (MD), was running very high in the istence of enveloped herpes virions. The 1960s, and so it was only natural that I work was relatively simple and straightforshould join the throng as a young scientist ward once we had stumbled onto the possireturning ‘home’ to Cornell University. MD ble significance of the FFE. The difficulties, was by far the most serious disease of chick- instead, had to do with acceptance of its vaens (annual cost in the US of nearly 200 mil- lidity. Perhaps no one thought that the paralion dollars), and it appeared to be a good dox of a cell-associated herpesvirus that model for viral oncogenicity studies. could be easily spread should be so simply “In 1967, the etiology was determined by solved. Fortunately, colleagues abroad, who others to be a highly cell-associated her- I believe initially mistrusted the data, easily pesvirus~1.2just as I was going off to the Uni- confirmed it, as did colleagues at home, who versity of California at Berkeley for a sab- through a curious and poorly understood (by batical leave. Thus, it was not until my me) set of4 circumstances managed to prereturn in 1968 that I could take full advan- publish us. Regardless, it constituted one of tage of this finding. During my absence, J. the most thrilling periods of my scientific Lloyd Spencer, my graduate student, had de- career and probably gained me more attenveloped~animmunofluorescence test for lo- tion than anything else I had done to that calizing viral antigen in tissues. His proce- time. dures offered an opportunity to address “It is probable that frequent citation is some very intriguing questions regarding the attributable to two factors. First, the paper pathogenesis of MD. Because he had fin- offered the methodology required to obished his studies, I enlisted the help of S.B. tain cell-free MD virus. Second, the use of Hitchner, and we constructed a study in that methodology was widespread and prowhich 43 separate tissues involving all organ longed in5 6the very active field of MD systemswere examined sequentially for viral research.” . I. Churchill A E & Blgga PM. Agent of March’s disease in tissue culture. Nature 2l5:528-30. 1967. (Cited 335 times.) 2. Nazethn K, Solomon ii, WItler R L & Bunmeater a a. Studies on the etiology of Marek’s disease. 11. Finding of a herpesvirus in cell culture. P5oc. Soc. Exp. Riot. Mcd. 127:177-82. 1968 (Cited 210 limes.) 3. Celnek B W & flltebeen S B. Localization of viral antigen in chickens infected wish Marek’s disease hespcsvizus. J. Nat. Cancer Ins,. 43:935-49, 1969. (Cited 140 times.) 4. NarerI~nK & WIner R L. CeU-frec transmission and in vivo replication of March’s disease virus (MDV). I. Virology 5:388-97, 1970. (Cited 125 times.) 5. Payne L N, FrazIer 3 A £ Powell P C. Pathogenenis of Marek’a disease. tnt. Rev. Lxi,. Paihol. 16:59-154, 1976. (Cited 80 times,) 6. Calnek B W. March’s disease virus and lyniphoma. (Rapp F, ed.) Oncogeiuc herpes viruses. Boca Raton, FL: CRC Press, 1980. p. 103-43. 18 AB&ES © 1985 by ISI® CURRENT CONTENTS®