Table 1.
Potential role of viruses in the pathogenesis of systemic lupus erythematosus.
| Virus |
Evidence |
Potential mechanism |
Ref. |
|---|---|---|---|
| Herpes viruses | |||
| EBV |
Increased prevalence; Increased viral load |
Molecular mimicry; Induction of lupus by EBV peptide; Bcl2-like protein – prevention of apoptosis |
[1,16,17,33] [28,29,38–40] [5] |
| Cytomegalovirus |
Increased prevalence |
Induction of lupus |
[14,20,21] |
| Parvovirus B19 |
– |
Molecular mimicry |
[19] |
| Transfusion-transmitted virus | Increased prevalence | Molecular mimicry | [16] |
| Retroviruses | |||
| HIV-1 |
– |
Molecular mimicry |
[44] |
| HTLV-1 | – | Regulation of CD4+ expression | [4,49,52] |
| RNA viruses | |||
| Type C oncorna virus |
Enhanced viral expression |
– |
[54,55] |
| Measles virus | Increased antibodies | Molecular mimicry | [56,57] |
EBV: Epstein–Barr virus; HTLV: Human T-lymphotropic virus.