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1994-10-25
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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).