Understanding the role of virus-host interactions in tissue tropism of plant viruses

To establish productive infection, plant viruses need to be able to efficiently invade and spread within a plant. Most viruses are introduced into a plant via the epidermal or mesophyll cells where they undergo disassembly, replication, translation of their proteins, and assemble new virions. Viruses then move to the adjacent cells until they reach the phloem, which serves as the highway by which viruses spread throughout their hosts. It was shown that the phloem has evolved additional protection against these molecular intruders. Virus entry into, translocation through, and exit from the phloem involve additional viral factors and complex virus-host interactions. Although the majority of plant viruses are capable of infecting most types of cells within their hosts, there are several groups of plant viruses whose tissue tropism is limited to the phloem. These viruses are typically introduced directly into the phloem by vectoring phloem-feeding insects. Interestingly, the movement systems of such viruses are complex and involve multiple viral proteins. The factors and processes that control phloem restriction of these viruses are not well understood. We are working with Citrus tristeza virus (CTV), the largest non-segmented positive-sense RNA virus of plants, which belongs to the family Closteroviridae. In our recent study, we showed that the p33 protein of CTV is a viral effector, which affects viral pathogenicity by modulating a host immune response. Upon CTV infection, p33 triggers the accumulation of reactive oxygen species (ROS) and plant cell death. Deletion of the p33 gene from the CTV genome resulted in a significant decrease in the ROS production during virus invasion of the host plants and an increase in the virus accumulation and spread.  Remarkably, the p33 deletion mutant was able to spread beyond the phloem and enter the immature xylem cells where it perturbed the vascular tissue differentiation leading to the enhancement of the stem pitting syndrome. We hypothesize that the plant recognizes p33 and activates the host immune response to restrict CTV into the phloem tissue and minimize the disease.

Learning Objectives:

1. Learn how plant viruses move cell-to-cell and long-distance in their hosts

2. Understand how plant viruses modulate phloem to their advantage

3. Get familiar with mechanisms plants have developed to perceive and defeat viruses

4. Learn what factors mediate phloem restriction of certain plant viruses.