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5.1: Evaluation of the evidence for infections as factors in the pathophysiology of CFS

Non-specific infections

  • Raised titres of IgG antibodies directed against common viruses (e.g., herpesviruses, enteroviruses) are common, but are of no pathophysiological or diagnostic significance (Horwitz et al. 1985; Jones et al. 1985; Straus et al. 1985; Buchwald et al. 1987a, 1987b, 1992, 1996; Calder et al. 1987; Holmes et al. 1987; Bell et al. 1988; Hellinger et al. 1988; Miller et al. 1991; Kitani et al. 1996) (Level I)

  • Common, non-specific infections (e.g., upper respiratory tract infections) are not likely to trigger CFS (Wessely et al. 1995a) (Level II)  

Epstein-Barr virus

  • Infectious mononucleosis can trigger CFS (White et al. 1995a, 1995b) (Level II)

  • Reactivation of EBV replication is not increased in prevalence (Gold et al. 1990; Sumaya 1991; Jones 1985) (Level II)  

Enteroviruses

Retroviruses

Human herpesvirus 6

Ross River virus

Non-viral infections (Q fever, Lyme disease)

  • Retrospective studies suggest CFS may follow adequately treated Q fever or Lyme disease (Bujak et al. 1993, 1996; Shadick et al. 1994; Sigal 1994; Ayres et al. 1996; Marmion et al. 1996) (Level IV)

  • The existence of Lyme disease in Australia has not been confirmed (Hudson et al. 1994) (Level III-3)

Comment: Many studies that have suggested a link between infections and CFS have relied upon the detection of antibodies against the viral or other agent as an indirect means of implicating the organism in the pathophysiology of CFS. These studies have suggested that "high" titres of IgG antibodies directed against viruses such as EBV, HHV-6 or enteroviruses reflect chronic, active, viral infection. However, case-control studies indicate that such "elevated" antibody titres are also found in healthy individuals many years after the original infection. Those studies which have sought direct evidence of chronic viral replication have not found an increased prevalence of viral isolation in people with CFS.

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