Document 3260 DOCN M94A3260 TI Complement activation in HIV infected patients with cryoglobulinemia. DT 9412 AU Schmit JL; Redeker S; Fuentes V; Prin L; Infectious Disease Unit, University Hospital Amiens, France. SO Int Conf AIDS. 1994 Aug 7-12;10(1):117 (abstract no. PA0088). Unique Identifier : AIDSLINE ICA10/94369315 AB The aim of the study was to investigate complement activation in HIV infected patients with cryoglobulinemia. In a previous study we have noticed that HIV infected patients with cryoglobulinemia had low activation fragments of the classical (C4d) and the common (C3d) pathway. The presence of cryoproteins in these patients suggested strongly complement cryoactivation. We performed in 5 different conditions (4 degrees C, 20 degrees C, 37 degrees C, EDTA and citrate) complement measurement in 10 HIV seropositive patients with cryoglobulinemia. Four patients were IVDU, 2 homosexual males, 3 heterosexual individuals, 1 blood recepients. Mean delay from first HIV seropositivity was 5.1 years (0.8). Five patients were seropositive for more than 4 years. Mean CD4 count was 252/mm3 (20-591). One patients has had opportunistic infection. Seven patients received anti-retroviral drugs (AZT 3, switch for DDI 4). Viral co-infection, characterized by isolation of viral sequences from HBV or HCV, HBV serological profils suggesting evolutive hepatitis or positive viremia for CMV, was present in 90% patients. All patients had low C4d levels and lowered normal C3d levels with normal hemolytic complement rate in each tested condition. These results suggest in vivo classical and common complement pathway activation. Our hypothesis is that complement pathway activation could be an early disease progression marker. Further studies are mandatory to establish the relationship between classical complement pathway activation and disease progression. The classical complement pathway has a key role in virus neutralisation. Viral infection or co-infection plays an important role in complement activation. Persistance of viral infection could be derived from inefficiency of the complement system and predispose to auto-immunity. DE Biological Markers *Complement Activation Complement Pathway, Classical Complement 3d/METABOLISM Complement 4/METABOLISM Cryoglobulinemia/*COMPLICATIONS/*IMMUNOLOGY Hepatitis B/COMPLICATIONS Hepatitis C/COMPLICATIONS Human HIV Infections/*COMPLICATIONS/*IMMUNOLOGY/MICROBIOLOGY Male Neutralization Tests Peptide Fragments/METABOLISM MEETING ABSTRACT SOURCE: National Library of Medicine. NOTICE: This material may be protected by Copyright Law (Title 17, U.S.Code).