Proposed pathogenic model of CFS

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One etiologic model of CFS integrates genetic predisposition, immune perturbation, viral reactivation, and autonomic and immunoregulatory dysfunction to produce the symptom complex of CFS (Fig. 1). A persistent viral infection is one potential

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Fig. 1 Proposed model of chronic fatigue syndrome etiology, including the potential role of viral infection.

Fig. 1 Proposed model of chronic fatigue syndrome etiology, including the potential role of viral infection.

pathogenetic cofactor in this model. Immune activation (due to viral infection) can result in the release of cytokines and precipitate the observed changes in central nervous system (CNS) symptoms (required by the CDC criteria of CFS). Production of pro-inflammatory cytokines such as IL-1b and IL-6 has been correlated with acute sickness behavior, and many signs and symptoms of CFS, including fever, malaise, pain, and impaired concentration (Vollmer-Conna et al., 2004).

Alternatively, viruses and bacteria that have been maintained in a latent state and controlled by an intact immune system might be allowed to replicate and exacerbate symptoms of illness under circumstances of stress or co-morbid infections. It is currently not known whether the presence of HHV-6 (variant A or B) indicates a primary causative role in CFS, or simply the opportunistic exploitation of a suppressed immune system.

As early as 1994, Ablashi postulated that CFS might essentially represent an immunological disturbance, which allows reactivation of latent herpesviruses, such as HHV-6 (Ablashi, 1994). Ablashi concluded that the evidence at that time showed a much stronger association of CFS with HHV-6 than with other herpesviruses, including EBV, cytomegalovirus (CMV, or HHV-5), or herpes simplex viruses (HSV-1 and HSV-2).

Once reactivated, these viruses could directly contribute to existing morbidity and produce abnormal immune responses. Recently, Smith et al. (2005) reported evidence from an in vitro model that the immunosuppressive action of HHV-6 on CD4 lymphocytes is related to the suppression of IL-12 by dendritic cells. It has also been postulated that an infectious organism could have a ''hit and run'' effect by entering a host and triggering an abnormal immune response. The pathogen then resolves, but leaves behind self-propagating immune abnormalities that result in the symptoms of CFS.

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