The cryptic interplay between systemic lupus erythematosus and infections.

The underlying trigger for systemic lupus erythematosus (SLE) has remained elusive, and multiple interacting environmental and genetic factors likely contribute to the onset and perpetuation of the disease. Among environmental influences, infectious agents have been suggested to play a pivotal role in driving autoimmunity pathogenesis via structural or functional molecular mimicry, the expression of proteins that induce cross-reactive responses against self-antigens, and the aberrant activation or apoptosis of different immune system cells in the context of a peculiar genetic background. The increased viral load and changing subsets of lytic or latent viral proteins observed in selected populations with SLE have indicated that common viruses, such as Epstein-Barr virus, parvovirus B19, cytomegalovirus, retroviruses and transfusion-transmitted viruses, might be triggers for this disease. Alternatively, some infectious agents might exert a protective effect from autoimmunity. Existing achievements have not been fully investigated and clarified. Thus, the aim of this review is to analyze the medical literature within the last 15years regarding the role of infectious agents in the pathogenesis of SLE.