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Acquisition of Antibody to Lymphadenopathy-Associated Virus in Patients with Classic Hemophilia (Factor VIII Deficiency)

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Dr. Lederman is an recipient of a New Investigator Research Award (AM 28324) from the National Institutes of Health. Dr. Ratnoff is a Career Investigator of the American Heart Association.

▸Requests for reprints should be addressed to Michael M. Lederman, M.D.; Division of Infectious Diseases, University Hospitals of Cleveland, 2065 Adelbert Road; Cleveland, OH 44106.

Cleveland, Ohio; and Atlanta, Georgia

© 1985 American College of PhysiciansAmerican College of Physicians

Ann Intern Med. 1985;102(6):753-757. doi:10.7326/0003-4819-102-6-753
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Antibody to lymphadenopathy-associated virus (LAV) was assayed in 461 serum and plasma samples that had been obtained from 149 patients with classic hemophilia and 64 controls and stored for periods as long as 18 years. No control or patient samples obtained before 1980 contained antibody to this retrovirus. The prevalence of antibody to LAV in the patient samples rose from 15% (2 of 13) in 1980 to 62% (18 of 29) in 1984. During this time, none of 8 untreated hemophiliacs and none of 26 hemophiliacs treated solely with cryoprecipitates had antibody to LAV. In contrast, the prevalence of antibody to LAV among hemophiliacs treated with lyophilized antihemophilic factor rose from 25% (2 of 8) in 1980 to 78% (18 of 23) in 1984. These seropositive hemophiliacs had fewer OKT4 helper cells and lower proliferative responses to mitogen than similarly treated seronegative patients. Treatment with locally prepared cryoprecipitates was not associated with serologic evidence of virus exposure.





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