ABSTRACT
A recurring theme in the study of viral infections is the fact that host cells often act as unwitting
accomplices to their own demise. Viruses, as well as other pathogens, have evolved strategies referred to
here as ‘‘subcellular mimicry,’’ defined as the ability of an infectious agent to commandeer normal
cellular processes in order to accomplish infection. A multitude of observations in the literature
demonstrate that viruses cooperate with host cells at the level of subcellular structures and functions
enabling infection of host cells. Introduction of the term, subcellular mimicry, is meant to unify these
characteristics of viral infection conceptually, reflecting the underlying evolutionary strategies that are
shared by different pathogens. The term ‘‘mimicry’’ links this phenomenon to other examples of
convergent evolution including Batesian and Mullerian mimicry (insects sharing similar appearances
as a defense against predators) [1], molecular mimicry (molecules sharing structures that allow similar
function) [2], and antigenic mimicry (a special case of molecular mimicry in which antibodies raised
against one protein can recognize similar antigens in other proteins) [3]. The term ‘‘subcellular’’
underscores the fact that viruses mimic subcellular structures to enable interaction with other subcellular
structures, resulting in viral participation in intricate cellular processes. Molecular mimicry, a term
already in use in the literature, encompasses simple molecular interactions such as protein-protein
binding or recognition of carbohydrate or nucleic acid structures, but molecular mimicry simply does
not convey the coordination of multiple molecular interactions that contribute to the ability of viruses
to commandeer host cell functions.
