Virus interactions clearing the path towards symptom development in Lettuce big-vein disease

Lettuce big-vein disease (LBVD) is a globally distributed disease that severely affects lettuce quality and yield, causing vein-associated chlorosis, leaf deformation, impaired head formation, and bitterness. LBVD is consistently associated with two viruses, Lettuce big-vein associated virus (LBVaV) and Mirafiori lettuce big-vein virus (MiLBVV), yet their individual roles in symptom development, their interaction during co-infection, and their transmission via the soil-borne fungal vector Olpidium virulentus have remained poorly understood. The work presented in this dissertation investigated the mechanisms underlying LBVD, focusing on how LBVaV and MiLBVV contribute to symptom development, interact during co-infection, and facilitate cell-to-cell movement.
Disease assays combined with in planta virome analyses revealed that MiLBVV is never detected alone but always co-occurs with LBVaV. While LBVaV alone caused largely asymptomatic infections, the characteristic vein-associated chlorosis of LBVD depended on the presence of MiLBVV in the shoots. Time-resolved analyses showed that LBVaV spreads systemically from root to shoot earlier and more synchronously than MiLBVV, supporting a helper-dependent relationship in which LBVaV infection is a prerequisite for MiLBVV systemic spread and symptom expression.
In addition, a previously undescribed olpivirus was identified and genomically characterized, expanding the known viral complexity associated with LBVD. Furthermore, LBVaV ORF3 was shown to encode a functional 30K-like movement protein, providing insight into the molecular basis of viral cell-to-cell spread. Finally, proximity labeling of 30K movement proteins revealed distinct host protein interaction landscapes linked to different viral movement strategies. Together, these findings advance the understanding of LBVD as a disease driven by complex virus–virus and virus–host interactions.