Infections can act as environmental triggers inducing or promoting
autoimmune disease in genetically predisposed individuals. Identification of microbial
peptides similar to self-tissues may by molecular mimicry, provide the inducing mechanism for an immune response. The aim of this study was to identify
autoantibodies (autoAbs) in nonautoimmune individuals during acute bacterial, viral, or
parasitic infections. Specific Abs or specific
infections with an increased autoAb load may shed insight into the mechanisms of
autoimmune disease. Sera from 88 patients with acute
infections (41 bacterial, 23 viral, 17 parasitic, and 7 rickettsial) were tested by the ELISA method for
antinuclear antibodies (ANA) 8 Pro, and Abs to
thyroid peroxidase (TPO),
thyroglobulin,
phospholipids,
annexin-V,
laminin, anti-Saccharomyces cervisiae (ASCA), and
prothrombin, along with 80 normal controls. Elevated titers of Abs to
annexin-V and
prothrombin were the most prevalent in viral, parasitic, and rickettsial
infections and to
laminin in viral and
parasitic infections. Elevated titers of ASCA and ANA were found in viral and
bacterial infections. Antiphospholipid Abs were found in parasitic and
Q-fever infections. Thirty-four individuals harbored elevated titers of at least two Abs. An autoAb burden was detected in individuals with
hepatitis A,
hepatitis B, toxoplasma or
Q-fever infections. In nonautoimmune individuals with various (bacterial, viral, parasitic, and rickettsial)
infections, elevated titers of Abs to
annexin-V,
prothrombin,
laminin, ASCA, ANA, and
phospholipids were most frequently detected.