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Papaya Necrosis Virus

Apical & Droopy (Plant Disease Pathogen)
Hosts Distribution Symptoms Biology Epidemiology Management Reference


F.W. Zettler

S.H. Wan

(In:Wayne Nishijima’s papaya compendium)


These viruses are specific to papaya.


Papaya droopy necrosis virus (PDNV) has only been reported in Florida. A similar rhabdovirus, papaya apical necrosis virus (PANV), occurs in Venezuela. Both viruses have similar particle morphologies and both can cause apical necrosis and plant death. Although neither of these rhabdoviruses were described until 1981, plants in Florida with papaya droopy necrosis symptoms were observed as early as 1947.


The initial symptoms of papaya droopy necrosis are drooping and recurvature of the leaves in the upper portions of the crown (Plate 20). Symptoms of the disease are much more severe during the winter than summer months. The leaves at the apex are pale yellow, do not expand normally, and are sharply recurved. Petioles are shorter and more stiff than normal. The crown is rounded and has a distinct bunchy appearance with very short internodes. Flowers on pistulate plants abort and fruit set ceases. Latex flows readily following wounding of PDNV-infected plants, in contrast with those infected by papaya bunchy top mycoplasma. Leaves produced during the winter eventually begin to abscise until all the leaves (except for one to three tiny ones near the tip) are gone. Shortly thereafter, the stem tip becomes necrotic, and the plant eventually dies.

Initial symptoms of papaya apical necrosis are yellowing of the affected plant followed by the rapid wilting and deterioration of the younger leaves. Apical portions of the plant then become necrotic and the entire plant usually dies.

Papaya apical necrosis was first detected in Zulia State, Venezuela, in 1979 and spread very rapidly, nearly eliminating papaya production there. Incidence of papaya droopy necrosis in Florida is low relative to that of papaya ringspot. Papaya droopy necrosis was detected in 18 of 43 Florida papaya plantings in 1981 with incidence in a given field ranging from 0.4 to 22.2%. Between 1977 and 1979, however, the disease eliminated all of the experimental fields maintained by the University of Florida Agricultural Experiment Station at Homestead, where old and new plantings overlapped.


The particle sizes and dimensions of PDNV and PANV resemble those of rhabdoviruses (87-98 x 180-254 nm and 80-84 x 210-230 nm, respectively). Papaya droopy necrosis virus and PANV virus particle aggregates were detected in the nuclei of parenchyma cells in vascular tissues. Virions were also found occasionally in the cytoplasm of these cells.


Neither PDNV nor PANV is mechanically transmissible. No natural vector for PDNV has been identified. Eight of 10 papaya seedlings exposed to Empoasca papayae leafhoppers that had fed on PANV-infected plants developed symptoms; however, no rhabdovirus particles were detected in these plants.



PDNV incidence in south Florida has been reduced considerably by avoiding an overlapping between successive crops and by promptly rouging infected plants.


Lastra, R., and Quintero, E. 1981. Papaya apical necrosis, a new disease associated with a rhabdovirus. Plant Dis. 65:439-440.

Wan, S. H., and Conover, R. A. 1981. A rhabdovirus associated with a new disease of Florida papayas. Proc. Fla. State Hort. Soc. 94:318-321.

Wan, S. H., and Conover, R. A. 1983. Incidence and distribution of papaya viruses in southern Florida. Plant Dis. 67:353-356.






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