LETTERS TO THE EDITOR Hemophilia treatment and the AIDS tragedy: closing the circle Dubin and Francis1 present an account of the AIDS crisis in the blood supply. Their account is, understandably, emotive. The eminence of the authors and the importance of the issue require additional consideration of some aspects. The treatment of hemophilia is acknowledged by the authors as having been revolutionized over the 1970s by the increasing availability of coagulation factor concentrate. Fractionation chemistry for the main product Factor (F)VIII was, and still is, bedeviled by the extraordinary instability of this protein, which has limited yields of product from plasma to not more than 25%. This unquestionably influenced and impeded research in viral inactivation techniques in the pre-AIDS era, but the authors’ implied message of industry complacency and neglect was not confirmed by the Institute of Medicine process which they describe (page 82 of Leveton et al.2). The risk of hepatitis transmission was not ignored and drove the development of the first virally inactivated FVIII product in 1979 (reported in Heimburger et al.3), through a process that resulted in a yield of factor of 8% over plasma. Hence, universal immediate adoption of this approach would have restricted access to a small minority of patients; nevertheless, the technology was rapidly adopted in Germany for treating newly born diagnosed patients. The search for appropriate technology continued, before and after the AIDS era, culminating in the current generation of products that have protected patients from established and emerging agents for the past 25 years. The difficulties of grappling with novel pathologies such as AIDS, and the doubts on the level of morbidity associated with, for example, HCV by respected leaders of the treater community,4 also deserve mention. The authors’ assertion that plasma from high-risk donors was systematically included in the plasma pool for hemophilia products is puzzling and is unsupported by citation. Donors with high-risk behavioral profiles, assessable through the then-current epidemiologic knowledge, were excluded from the plasma pool for all derivatives. The plasma industry voluntarily excluded groups at high risk of AIDS before such measures were mandated by regulators or the mainstream blood sector (page 109 in Leveton et al.2). The inclusion of anti-hepatitis and other protective antibodies was necessary to protect all patients, as is demonstrated by the breakthrough of hitherto unknown infections when such antibodies were depleted.5

In summary, the infection of people with hemophilia was a tragedy in which progression of technology was unable to prevent the transmission of a totally novel pathology. As in all human affairs, errors were made. These should not obscure the scientific achievements that have transformed a quasi-uniformly lethal disease to a condition that allows normal and productive life expectancy. These achievements and developments in governance have positioned the therapeutic environment so that the prospect of a repeat of the errors of the past has been minimized. This has happened as a result of the efforts of many more players than acknowledged by Dubin and Francis. A complete understanding of events, as well as a rejection of complacency, is the best memorial to those who bore the consequences of the era described by Dubin and Francis.

CONFLICT OF INTEREST The author reports no conflicts of interest or funding sources.

Albert Farrugia, PhD1,2 e-mail: [email protected] 1 Department of Surgery University of Western Australia Crawley, WA, Australia 2 Global Access Plasma Protein Therapeutics Association Annapolis, MD

REFERENCES 1. Dubin C, Francis D. Closing the circle: a thirty-year retrospective on the AIDS/blood epidemic. Transfusion 2013; 53(10 Pt 2):2359-64. 2. Leveton LB, Sox HC, Stoto MA. HIV and the blood supply—an analysis of crisis decisionmaking. Washington DC: National Academy Press; 1995. 3. Heimburger N, Schwinn H, Gratz P, et al. Factor VIII concentrate, highly purified and heated in solution [author’s transl]. Arzneimittelforschung 1981;31:619-22. 4. Mannucci PM, Colombo M, Rizzetto M. Nonprogressive course of non-A, non-B chronic hepatitis in multitransfused hemophiliacs. Blood 1982;60:655-8. 5. Peerlinck K, Goubau P, Coppens G, et al. Is the apparent outbreak of hepatitis A in Belgian hemophiliacs due to a loss of previous passive immunity? Vox Sang 1994;67(Suppl 1):14-6, discussion 17.

© 2014 AABB Volume 54, April 2014

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