Antiphospholipid antibodies in acute and post-treatment Lyme disease.

Abstract

Acute Lyme disease is caused by a Borrelia infection and typically responds to antibiotic treatment, but post-infectious chronic symptoms are common. The precise origin of these post-treatment symptoms is unknown; dysregulation of immune responses raised during the initial infection is likely to contribute. Antilipid antibodies are associated with several autoimmune diseases and have been shown to arise in both acute and post-treatment Lyme disease. To assess the potential contribution of antilipid antibodies to Lyme disease pathology and their possible use as biomarkers of both acute and chronic disease, we performed a survey of patient sera for antilipid antibodies during and after Borrelia burgdorferi infection. Results were similar in cross-sectional and longitudinal samples drawn from two different biobanks. Three antiphospholipid antibodies were elevated during infection, with two (antiphosphatidic acid and antiphosphatidylserine) significantly elevated even at the day of diagnosis before seroconversion on conventional tests. A subset of patients with chronic symptoms is identifiable by persistent elevation in antiphosphatidylserine; these antibodies found in post-treatment Lyme disease were not found in a panel of sera from patients with look-alike autoimmune disorders. Persistent elevation in antiphosphatidylserine may drive autoimmune-like symptoms of Lyme disease in some patients and could serve as a biomarker for chronic disease. The detection of antiphospholipid antibodies induced early in infection could also improve the diagnosis of acute infections.