Induction of antiphospholipid autoantibody during cytomegalovirus infection.

2. Mastroianni A, Coronado O, Nanetti A, Manfredi R, Chiodo F. Staphylococwho described an association between cytomegalovirus (CMV) cus cohnii: an unusual cause of primary septic arthritis in a patient with infection and antiphospholipid syndrome. We have looked at the AIDS. Clin Infect Dis 1996;23:1312–3. production and possible mechanisms of induction of antiphospho3. Mastroianni A, Coronado O, Nanetti A, Manfredi R, Chiodo F. Communitylipid autoantibodies during viral infections, including those caused acquired pneumonia due to Staphylococcus cohnii in an HIV-infected by hepatitis and dengue viruses [2]. We suggest potential pathways patient: case report and review. Eur J Clin Microbiol Infect Dis 1995; that may account for the increased serum concentration of these 14:904–8. antibodies in patients with CMV infection. 4. Mastroianni A, Coronado O, Nanetti A, Manfredi R, Chiodo F. Infectious First, it has been reported that autoantibodies to specific antigens diseases due to Staphylococcus cohnii in AIDS [abstract]. In: Program can be generated when viral proteins combine with antigens. Preand abstracts of the 8th International Symposium on Staphylococci and sumably, the viral-host complexes become immunogenic; these Staphylococcal Infections (Aix-Les-Bains, France). 1996. virally induced specific antibodies have been shown for DNA as well as phospholipids [3, 4] Reprints or correspondence: Dr. Antonio Mastroianni, Dipartimento di MediSecond, there is evidence that phospholipid-binding proteins cina Clinica Specialistica e Sperimentale, Istituto Malattie Infettive, Policlinico such as B2-glycoprotein I annexins are involved in the attachment Sant’Orsola-Malpighi, Università di Bologna, Via Massarenti 11, 40138 Bologna, Italy. of viruses, including CMV and hepatitis B, to their cellular targets by complexing with viral phospholipids [2, 5]. During this process Clinical Infectious Diseases 1997;25:1492–3 q 1997 by The University of Chicago. All rights reserved. the induction of antiphospholipid autoantibodies (the immunogen 1058–4838/97/2506–0050$03.00 expressed as viral phospholipid-host protein) may be seen as an event secondary to the cellular binding and entry of viruses. Third, the accelerated cell death, or apoptosis, associated with a viral infection will be accompanied by the externalization of Herpes Simplex Virus Hepatitis anionic phospholipids, particularly phosphatidylserine, in the apoptotic cell membrane [6]. The activation of antiphospholipid autoSIR—I read with interest the recent report by Kaufman et al. antibody synthesis in this situation could be involved in the immuconcerning herpes simplex virus hepatitis [1]. Although I apprecinoclearance of the dead cells [6, 7]. ate being reminded of this clinical entity, I wondered how the Investigators recently demonstrated that CMV infection of authors performed their literature review. They cited a number of smooth muscle cells increases the uptake of oxidized low-density reports that included 52 patients; however, their literature review lipoprotein and may thus play a role in the development of artherdid not appear to be complete. For example, my files (which are oma [8]. The findings that elevated antiphospholipid autoantibody not that extensive) contain two reports about herpes simplex virus levels are also linked with a greater frequency of myocardial inhepatitis (one on patients with solid-organ transplants [2] and one farctions and that antiphospholipid autoantibodies also cross-react on patients with marrow transplants [3]), neither of which was with oxidized low-density lipoprotein [9] imply a link and overlapincluded in their literature review. ping mechanisms between CMV infection and antiphospholipid antibody induction. However, whether CMV-activated antiphospholipid autoantibodies are definitely pathogenic or merely an imRobert M. Rakita munologic result of the viral infection remains to be established Department of Internal Medicine, Division of Infectious Diseases, [2, 10]. University of Texas, Houston, Houston, Texas