ABSTRACT
The term “hypovirulence” has been used liberally in the literature to describe the reduced capacity of some variants of a pathogen to either elicit or sustain the normal rate of progression of the corresponding disease in its host. In the context of the phytopathogenic fungi, however, “hypovirulence” has been used more stringently to define states of reduced virulence that are caused by cytoplasmically transmitted genetic factors. Initially, it was believed that all the hypovirulence-causing agents were viruses [1], but now it is evident that other cytoplasmically transmitted factors, namely mutant forms of mitochondrial DNA (mtDNA) and certain mitochondrial plasmids, also can dramatically reduce the pathological aggressiveness of the chestnut blight fungus Cryphonectria parasitica [2]. To distinguish the attenuated pathogenic states that are caused by viruses from those that are caused by mtDNA mutations and mitochondrial plasmids, they have been divided into two types and defined as “viral hypo virulence” and “mitochondrial hypo virulence,” respectively [2]. Though this distinction facilitates the description of the fundamentally different processes that result in phenomenologically similar phenotypes, it is hardly adequate because some of the double-stranded RNA (dsRNA) elements that appear to be causatively associated with hypovirulence have been classified as viruses but are located in the mitochondria [3,4].
