Abstrakt
Heat shock and almost all types of stresses associated with oxidative stress are accompanied by heat shock protein (HSP) expression. HSPs are involved in refolding denatured proteins and directing unrepairable proteins for degradation.
Thus, under stress conditions, HSPs help to restore cellular balance. However, in virus-infected plants, HSP70 can have both positive and negative effects because viruses usually recruit HSP70.
HSP70 can promote the replication and translation of the viral genome, the formation of viral replication complexes, and the propagation of viral particles from cell to cell and throughout the plant. HSP gene silencing in various virus-host plants systems and the comparison of susceptible and resistant species have shown that HSPs70 accelerate the development of infection.
Conversely, during the process known as thermotherapy, the temperature increase inhibits viral replication in some host and virus systems. The success of thermotherapy depends not only on the temperature and treatment period or duration but also on the plant species and viral strain.
In this review, we discuss the ambiguous role that HSPs70 play during viral infections in plants towards weighing the balance between their positive and negative functions.