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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