Viral Interactions with the Plant host mediate subsequent vector transmission – VIP

We study the transmission of CaMV and other plant viruses by microscopy and transmission tests, where aphids are allowed to acquire virus from isolated cells or from intact plants under different experimental conditions. This allows to correlate changes observed in cells visited by aphids with transmission efficiency and to deduce its mechanisms.

We have shown how virus factories (reservoirs for virus particles) participate in CaMV transmission. We have preliminary evidence that CaMV recognizes aphid presence by chitin, a natural compound that aphids leave behind during their feeding activity.
We have shown that TuMV react also on the presence of aphids on infected plants to trigger its transmission. However, the mechanisms for TuMV transmission diverge from CaMV transmission after an initial step in common.

We will continue research on the mechanisms of CaMV transmission on the molecular and cellular level.
We will continue to study TuMV transmission and characterize common and divergent steps in the transmission of these viruses.

We published a study on the role of virus factories in CaMV transmission (Bak et al. 2013, J Virol). We published several revues, two of them in high impact journals, The Annual Review In Phtyopathology and Current Opinion In Virology.

Transmission is a crucial step of every virus life cycle and knowledge of transmission mechanisms will certainly help fight epidemics. In the most common vector-transmission of viruses, research has focused mainly on viral and vector determinants of transmission, but the role of the host has been amply neglected. This project addresses precisely this, the role of the host, in the transmission of Cauliflower mosaic virus (CaMV) by its vector (aphids in this case, a very important virus vector). Like many plant viruses, CaMV is a non-circulative virus, meaning that transmitted virus particles are “simply” retained at and released from the extreme tip of the aphid vector's stylets (needle-like exterior mouth parts forming a “pumping” tube). Binding to the stylets is mediated by the viral helper component protein P2 that binds with one domain to a stylet receptor and with another to the virus particle, thus forming a molecular bridge between the two. We have previously shown that CaMV induces formation of a single large inclusion body in each infected plant cell, that contains all P2 and is specialised in the control of vector-transmission; hence referred to as the Transmission Body (TB).
Our unpublished results (partially contained in a submitted manuscript) show that the TB is a dynamic structure that “reacts” on the presence of the vector in order to optimise transmission efficiency: Stressing infected cells mechanically, or chemically with NaN3 or CO2, induces rapid (within seconds) and massive influx of tubulin into TBs, followed by – depending on the treatment – disintegration of the TB and immediate redistribution of P2 and virus particles on cortical microtubules throughout the cell. These morphological changes correlate strongly with increased transmission rates (+200-300%). We have also shown that aphid feeding activity itself triggers this TB response. This would mean that CaMV “senses”, via the perception mechanisms of the host plant, the presence of its vector and induces an immediate and coordinated response of the TB, resulting in facilitated accessibility and acquisition of CaMV to the vector, and thus in optimal transmission. That a virus is able to perceive its environment, beyond the cell and in quasi-real-time, and to immediately and appropriately react to it, is an extremely original and novel concept not only in plant virology, but of great interest also for general virology and cell biology.
Having established that at least the TB of CaMV reacts on the vector's presence in order to optimise transmission, this project now aims to: I) decorticate the perception/signalling pathways in TB activation in order to better understand CaMV acquisition but also to use this response as a reporter system to elucidate the very early aphid-plant interactions (another great unknown), II) describe the cellular mechanisms behind this phenomenon, and III) to test whether also other viruses have developed similar strategies to increase transmission efficiency. The latter point, if confirmed, would be a major breakthrough in vector-transmission research. But even further, similar concepts or phenomena (viruses “sensing” stimuli from the outside of the cell and immediately translating them into adapted response) could be searched for in any virus and any host, for any stage of the infection cycle.