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Oaks' Defenses Help Gypsy Moth Caterpillar Fend Off Virus

Albuquerque, N.M. -- The relationship between gypsy moth caterpillars, the virus that kills them and the oak leaves they feast on is more complicated than expected, and leaf enzymes as well as tannins play an important role, according to a Penn State entomologist.

"We know that the tannins in oak leaves inhibit gypsy moth growth, but that they also provide protection against the nuclear polyhedrosis virus," says Dr. Heidi Appel, research associate in entomology in the College of Agricultural Sciences.

Oak trees make more tannins when gypsy moths chew on them and the tannins slow caterpillar growth, reduce the number of eggs and lead to less successful young. The trees' response should be inhibiting the caterpillar, but it takes much more virus to kill the caterpillars when they are eating tannins. The oak trees' defense -- tannin -- actually lets the gypsy moth caterpillar survive.

Nuclear Polyhedrosis virus, LdNPV, is commonly called wilt disease because the caterpillar turns into a sack of virus and slumps over. This naturally occurring virus is acquired when caterpillars eat the dormant virus left on leaves by previous victims. When the caterpillar eats the virus, together with the oak leaf and its tannin, the virus becomes activated.

"We thought the tannin acted by itself, that it did something to the viral proteins," Appel told attendees at the Ecological Society of American Conference, today (Aug. 14) in Albuquerque. "It turns out that enzymes in the leaves may be the important factor."

Appel looked at two enzymes; polyphynol oxidase (PPO), which helps tannin work better and peroxidase (POD), which inhibits the action of tannin. Both naturally occur in oak leaves.

"Peroxidase just chews up everything it comes in contact with," says Appel. "It probably inactivates the tannin. PPO, on the other hand, probably oxidizes the tannin into the products that actually inhibit the virus."


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Contact: A'ndrea Elyse Messer
aem1@psu.edu
814-867-9481
Penn State
14-Aug-1997


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