The chestnut blight fungus, Cryphonectria parasitica, and its hypovirus are a useful model system in the study of the mechanisms of hypoviral infection and its consequences, such as a biological control of fungal pathogens. Strains containing the double-stranded (ds) RNA viruses Cryphonectria hypovirus 1 show characteristic symptoms of hypovirulence and display hypovirulence-associated changes, such as reduced pigmentation, sporulation, laccase production, and oxalate accumulation. Interestingly, symptoms caused by hypoviral infection appear to be the result of aberrant expression of a number of specific genes in the hypovirulent strain. Several viral regulated fungal genes are identified as cutinase gene, Lac1, which encodes an extracellular laccase, Crp, which encodes an abundant tissue-specific cell-surface hydrophobin that mediates physical strength, and Mf2/1 and Mf2/2, which encode pheromone genes involved in poor sporulation in the presence of hypovirus. Since the phenotypic changes in the fungal host are pleiotropic, although coordinated and specific, it has been suggested that the hypovirus disturbs one or several regulatory pathways (Nuss, 1996). Accordingly, several studies have shown the implementation of a signal transduction pathway during viral symptom development. Although further studies are required, hypovirulence and its associated symptom development due to the hypoviral regulation of a fungal heterotrimeric G-protein have been suggested. In addition, recent studies have shown the presence of a novel protein kinase gene cppk1 and its transcriptional upregulation by hypovirus. In this review, the presence of important components in signal transduction pathway, their putative biological function, and viral-specific regulation will be addressed.