A genetic approach was used to understand how diverse positive-stranded RNA viruses achieve infection in Arabidopsis thaliana. The objective of this research is to determine the functional roles, if any, of plant-encoded heat shock genes in positive-stranded RNA virus infections. Several studies implicate heat shock proteins in various viral processes, including translation and protein folding. Microarray analyses have found that the expression of a variety of heat shock genes including HSP17.6A, HSP23.6, HSP70, HSP83, and HSP101 can be induced by viral infections in Arabidopsis. The kinetics of expression of specific heat shock genes is differently regulated in response to viruses. For example, it was found that several heat shock genes are induced early in infection by the tobamoviruses, oilseed rape mosaic virus (ORMV) and turnip vein clearing virus (TVCV). My observations have also demonstrated this for two heat shock genes at the protein level. In particular, HSP101 mRNA and protein expression peaked at 2 days after inoculation and declined to low detectable levels at 3 and 4 days after ORMV inoculation. In contrast, HSP17.6 mRNA declines but is still detectable, while its protein levels increase over a 4-day time course. The expression of heat shock genes during virus infection suggests that they could have a role in viral pathogenesis. To test this possibility, mutants for HSP101 and HSP17.6 were used to determine their functional roles, if any, in ORMV infection. CMV infection was also tested in HSP101 mutants. In addition an ascorbate peroxidase mutant was used that has been shown to strongly induce heat shock genes in response to light stress. Results from these studies indicate that HSP101 and HSP17.6A are not required for ORMV- or CMV-infection.