Viral infections and antiphospholipid antibodies*,**
Section snippets
Methods
We reviewed the medical literature from 1968 to 2000 using MEDLINE and the key words virus, infection, aPL, and aCL. The relevant publications for the following viral infections were evaluated and described in chronological order: hepatitis C virus (HCV), HIV, cytomegalovirus (CMV), varicella zoster, Epstein-Barr virus (EBV), adenovirus, and parvovirus B. Clinical features of APS associated with aCL antibodies in the different viral infections are summarized in Table 1.
Hepatitis C virus
Investigators have frequently reported aPL antibodies in patients with chronic HCV infection. In 1994, in the earliest report on this association, al-Saeed et al (16) tested the sera of 52 hemophiliacs and demonstrated that HCV infection is strongly associated with raised serum levels of aPL antibodies even in the absence of HIV infection. In a later study by Biron et al (17), 33% of 124 patients with chronic HCV infection had aPL antibodies. Prieto et al (18) studied aCL antibodies in the sera
Discussion
These observations may suggest that certain infections in genetically predisposed individuals may induce autoimmunity. This hypothesis is further supported by some recent experiments; we induced aPL and anti-β2-GPI antibodies with properties similar to autoimmune aPL antibodies in mice by immunization with PL-binding synthetic peptides derived from adenovirus, CMV, and bacillus subtilis (54). Some of these aPL antibodies induced by CMV peptides were shown to be pathogenic. They activated the
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2022, Best Practice and Research: Clinical HaematologyCitation Excerpt :In this study, a high prevalence of non-Sapporo criteria antibodies was also observed (aCL IgA, 20% to more than 90% of patients; aβ2GPI IgA, 0–86%; aPS/PT, 0–24%; anti-annexin V antibodies, 3–19%) [21]. While most studies of aPL in COVID-19 have focused on hospitalized patients, one retrospective multicenter study examining both hospitalized and ambulatory COVID-19 patients found no significant difference in prevalence of aPL between these two populations (50% versus 43.3%, respectively) [49–51,63–65]. A few mechanisms have been proposed to explain the development of aPL in COVID-19: molecular mimicry, neoepitope formation, and phosphatidylserine exposure [31,66].
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Imad W. Uthman, MD, MPH: Associate Professor, Department of Internal Medicine, Faculty of Medicine, American University of Beirut, Beirut, Lebanon; Azzudin E. Gharavi, MD: Professor of Medicine, Morehouse School of Medicine, Atlanta, GA.
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Address reprints to Imad W. Uthman, MD, MPH, American University of Beirut Medical Center, PO Box 113-6044, Beirut, Lebanon. E-mail: [email protected]