PEBP balances apoptosis and autophagy in whitefly upon arbovirus infection

Apoptosis and autophagy are two common forms of programmed cell death (PCD) used by host organisms to fight against virus infection. PCD in arthropod vectors can be manipulated by arboviruses, leading to arbovirus-vector coexistence, although the underlying mechanism is largely unknown. In this study, we find that coat protein (CP) of an insect-borne plant virus TYLCV directly interacts with a phosphatidylethanolamine-binding protein (PEBP) in its vector whitefly to downregulate MAPK signaling cascade. As a result, apoptosis is activated in the whitefly increasing viral load. Simultaneously, the PEBP4-CP interaction releases ATG8, a hallmark of autophagy initiation, which reduces arbovirus levels. Furthermore, apoptosis-promoted virus amplification is prevented by agonist-induced autophagy, whereas the autophagy-suppressed virus load is unaffected by manipulating apoptosis, suggesting that the viral load is predominantly determined by autophagy rather than by apoptosis. Our results demonstrate that a mild intracellular immune response including balanced apoptosis and autophagy might facilitate arbovirus preservation within its whitefly insect vector. Arbovirus has co-evolved with its insect vector, enabling efficient and persistent transmission by vectors. Here, the authors reveal an immune homeostatic mechanism shaped by apoptosis and autophagy that facilitates arbovirus preservation within its whitefly vector.

Automated summary

Apoptosis and autophagy are two common forms of programmed cell death used by host organisms to fight against virus infection. In this study, researchers found that the coat protein (CP) of an insect-borne plant virus TYLCV interacts with a phosphatidylethanolamine-binding protein (PEBP) in its vector whitefly, leading to the activation of apoptosis and autophagy in the whitefly, affecting viral load. The results suggest that the viral load is predominantly determined by autophagy rather than apoptosis.