The emergence of human immunodeficiency virus (HIV) in the 1980s heightened our awareness that immunodeficiency could be acquired through viral infection. Historically, measles and hepatitis B and C viruses were implicated as immuno-suppressive viruses; however, there is growing evidence that a number of the her-pesviruses have properties similar to HIV with serious clinical sequelae. This chapter is devoted to a discussion of the impact of human herpesvirus-6 (HHV-6) infection on the immune system, focusing on the cell-mediated immune response. It is unclear whether preexisting immunodeficiency is a prerequisite for infection with HHV-6 or whether these viruses use stealth strategies for initial entry, establish latency and then exert their immunosuppressive effects. Given the complexity of the immune system, the mechanism(s) by which this virus family exerts its effect is not well understood. This chapter will review the range of evidence of immune system involvement from in vitro studies, clinical complications, and the number of immune-mediated disease associations that continue to mount as well as identify the need for the tools that will be required to research this highly prevalent, commensal organism. Even when causality cannot be clearly established and the coexistence of viruses in the same individual presents enormous scientific and epidemiological challenges to proving the etiological agent, there is a growing body of data that HHV-6 is an emerging pathogen with serious consequences ranging from its first clinical manifestation as exanthem subitum in infants to more debilitating fibromyalgia, chronic fatigue syndrome (CFS), and potentially multiple sclerosis. As molecular, serological, and cellular methodologies for HHV-6's detection improve, insight into causality will provide avenues for developing prophylactic and treatment strategies for this ubiquitous virus that affects millions of individuals.

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