Apoptotic neurodegeneration in whitefly promotes the spread of TYLCV.

Abstract

The mechanism by which plant viruses manipulate the behavior of insect vectors has largely been described as indirect manipulation through modifications of the host plant. However, little is known about the direct interaction of the plant virus on the nervous system of its insect vector, and the substantial behavioral effect on virus transmission. Using a system consisting of a <i>Tomato yellow leaf curl virus</i> (TYLCV) and its insect vector whitefly, we found that TYLCV caused caspase-dependent apoptotic neurodegeneration with severe vacuolar neuropathological lesions in the brain of viruliferous whitefly by inducing a putative inflammatory signaling cascade of innate immunity. The sensory defects caused by neurodegeneration removed the steady preference of whitefly for virus-infected plants, thereby enhancing the probability of the virus to enter uninfected hosts, and eventually benefit TYLCV spread among the plant community. These findings provide a neuromechanism for virus transmission to modify its associated insect vector behavior.