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DNA viruses often target cellular proteins to modulate host cell cycles and facilitate viral genome replication. However, whether proliferation of white spot syndrome virus (WSSV) requires regulation of the host cell cycle remains unclear. In the present study, we show that two WSSV paralogs, IE1 and WSV056, can interact withLitopenaeus vannamei retinoblastoma (Rb)-like protein (lv-RBL) through the conserved LxCxE motif. Further investigation revealed that IE1 and WSV056 could also bind toDrosophila retinoblastoma family protein 1 (RBF1) in a manner similar to how they bind to lv-RBL. Using theDrosophila RBF-E2F pathway as a model system, we demonstrated that both IE1 and WSV056 could sequester RBF1 fromDrosophila E2F transcription factor 1 (E2F1) and subsequently activate E2F1 to stimulate the G1 /S transition. Our findings provide the first evidence that WSSV may regulate cell cycle progression by targeting the Rb-E2F pathway.

White Spot Syndrome Virus IE1 and WSV056 Modulate the G 1 /S Transition by Binding to the Host Retinoblastoma Protein

White Spot Syndrome Virus IE1 and WSV056 Modulate the G ₁ /S Transition by Binding to the Host Retinoblastoma Protein