|Agent(s)||Pertinent rationale or refutation for involvement in Behcet's disease|
|Hepatitis A, B, C, E viruses||
- Serological evidence of previous HAV, HCV and HEV infections not significantly different in patients with Behcet's disease as compared to controls.|
- Previous HBV infection, however, seen in a significantly lower number of patients with Behcet's disease as compared with healthy controls.
|Herpes simplex virus (HSV)||
Anti-HSV-1 antibodies observed more commonly in patients with Behcet's disease than controls.|
-DNA of HSV detectable in genital and intestinal ulcers but not in oral aphthous ulcers.
|Parovirus B19||Parvovirus B19 IgG antibodies reported more in patients with Behcet's disease as compared to controls.|
|Helicobacter pylori||Almost equal proportion of patients with Behcet's disease and controls had H. pylori infection following eradication therapy.|
- IgG seropositivity for C. pneumoniae between cases and controls not significantly different.|
- However, proportion of seropositive cases with higher IgG titres was greater.
|Streptococcus sanguis, Streptococcus mitis and Streptococcus salivarius||
- Attenuation of skin and arthritic involvement in Behcet's disease after antibiotic administration.|
- Hypersensitivity to cutaneous streptococcal antigens reported.
- Aggravation of symptoms after dental manipulations.
- Treatment of chronic oral infections impacts long term prognosis of disease positively.
|Saccharomyces cerevisiae||Unclear role, distribution and pathogenetic relationship of ASCA antibodies in patients with Behcet's disease.|
|Heat shock proteins||
- Role for heat shock proteins of mycobacteria and streptococci suggested in Behcet's disease.|
- Model of molecular mimicry thought to be responsible for manifestations of Behcet's disease.