Rheumatoid factors and circulating immune complexes in HIV-infected individuals

Procaccia, S; Blasio, R; Villa, Paola; Lazzarin, Adriano; Bonacina, Carlo; Novati, Roberto; Bini, Teresa; Memoli, Massimo; Imondi, Nadia; Zanussi, C

doi:10.1097/00002030-199112000-00005

Cited by 16 publications

(10 citation statements)

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“…Moreover, these antibodies are not found in HIV negative drug users, suggesting that they are not related to lifestyle and are more likely to be a sequel of HIV infection itself. This is in keeping with reports of other autoimmune disorders in HIV infection, including idiopathic thrombocytopenic purpura,12 13 Sjögren’s syndrome,43 and bullous skin disease 44. In addition, increased concentrations of circulating immune complexes and various non-organ specific autoantibodies are well described in HIV positive patients 14…”

Section: Discussionsupporting

confidence: 87%

Cardiac autoimmunity in HIV related heart muscle disease

Currie

Goldman

Caforio

et al. 1998

Heart

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Objective-To assess the frequency of circulating cardiac specific autoantibodies in HIV positive patients with and without echocardiographic evidence of left ventricular dysfunction. Subjects-74 HIV positive patients including 28 with echocardiographic evidence of heart muscle disease, 52 HIV negative people at low risk of HIV infection, and 14 HIV negative drug users who had all undergone non-invasive cardiac assessment were studied along with a group of 200 healthy blood donors. Results-Cardiac autoantibodies detected by indirect immunofluorescence (serum dilution 1/10) were more common in the HIV positive patients (15%), particularly the HIV heart muscle disease group (21%), than in HIV negative controls (3.5%) (both p < 0.001). By ELISA (dilution 1/320), abnormal anti-myosin autoantibody concentrations were found more often in HIV patients with heart muscle disease (43%) than in HIV positive patients with normal hearts (19%) or in HIV negative controls (3%) (p < 0.05 and p < 0.001, respectively). Anti-myosin autoantibody concentrations were greater in HIV positive patients than in HIV negative controls, regardless of cardiac status ((mean SD) 0.253 (0.155) v 0.170 (0.076); p = 0.003). In particular the mean antibody concentration was higher in the HIV heart muscle disease patients (0.291 (0.160) v 0.170 (0.076); p = 0.001) than in HIV negative controls. On follow up, six subjects with normal echocardiograms but raised autoantibody concentrations had died after a median of 298 days, three with left ventricular abnormalities at necropsy. This compared with a median survival of 536 days for 21 HIV positive patients with normal cardiological and immunological results. Conclusions-There is an increased frequency of circulating cardiac specific autoantibodies in HIV positive individuals, particularly those with heart muscle disease. The data support a role for cardiac autoimmunity in the pathogenesis of HIV related heart muscle disease, and suggest that cardiac autoantibodies may be markers of the development of left ventricular dysfunction in HIV positive patients with normal hearts. (Heart 1998;79:599-604)

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Section: Discussionsupporting

confidence: 87%

Cardiac autoimmunity in HIV related heart muscle disease

Currie

Goldman

Caforio

et al. 1998

Heart

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“…As these antibodies are able to cross-react with Clq, they are possibly responsible for the significantly low Clq concentration in HIV-1-positive sera [46]. Clq is known to be one of the factors responsible for the clearance of insoluble immune complexes [47], and its absence might contribute to their significantly high concentrations in individuals infected with HIV [48].…”

Section: Discussionmentioning

confidence: 99%

The envelope glycoprotein of HIV‐1 gp120 and human complement protein C1q bind to the same peptides derived from three different regions of gp41, the transmembrane glycoprotein of HIV‐1, and share antigenic homology

et al. 1994

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gp41, the transmembrane glycoprotein of HIV-1, has been shown to be non-covalently associated with gp120. We have shown that it also binds human C1q. To analyze the interaction site(s) of gp41 with these two molecules, we established an enzyme-linked immunosorbent assay (ELISA) system using recombinant soluble gp41 [amino acids (aa) 539-684] and peptides thereof. In the cell-external part of gp41 three sites (aa 526-538, aa 590-613 and aa 625-655) were found to bind both gp120 and C1q. That gp120 and C1q use the same sites was evidenced by the fact that these proteins competed with each other for the same sites in recombinant soluble gp41 and gp41 peptides. It could be demonstrated by ELISA, that rabbit antibodies against human C1q recognized gp120, and rabbit antibodies against gp120 cross-reacted with C1q. Rabbit anti-gp120, HIV-1-positive human sera and anti-gp120 obtained from such sera agglutinated sensitized sheep erythrocytes with human C1q (EAC1q). These data suggest that in addition to functional homology between C1q and gp120 structural homology between these two molecules exists. This molecular mimicry might become the basis for immunologically relevant autoimmune phenomena.

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“…FCGR3A Fc fragment of IgG, low affinity IIIa, receptor (CD16a): IgA rheumatoid factor is the Fc portion of Immunoglobulin G (Procaccia et al, 1991) Removes antibody complexes from the circulation, and controls antibody-dependent responses. Expressed on natural killer cells (RefSeq)…”

Section: Autoantigens and Reference Functionmentioning

confidence: 99%

Extensive viral mimicry of 22 AIDS-related autoantigens by HIV-1 proteins and pathway analysis of 561 viral/human homologues suggest an initial treatable autoimmune component of AIDS

Carter

2011

FEMS Immunol Med Microbiol

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HIV-1 viral proteins, particularly the env protein, are homologous to 22 AIDS autoantigens, suggesting their creation by antiviral antibodies subsequently targeting human homologues. They include antibodies to T-cell receptors, CD4 and CD95, complement components, IgG, TNF and other immune-related proteins. Autoantibodies may compromise the immune system via knockdown of these key proteins, and autoimmune attack on the immune system itself, as supported by immune activation in early stages of infection and during the transition to AIDS. Over 500 human proteins contain pentapeptides or longer consensi, identical to viral peptides. Such homology explains the extensive viral/human interactome, likely related to the ability of viral homologues to compete with human counterparts as binding partners. Pathway analysis of these homologous proteins revealed their involvement in immune-related networks (e.g. natural killer cell toxicity/toll, T-cell/B-cell receptor signalling/antigen processing) and viral and bacterial entry and defence pathways (phagosome/lysosome pathways, DNA sensing/NOD/RIG-1 pathways) relevant to AIDS pathogenesis. At its inception, AIDS may have an autoimmune component selectively targeting the immune system. Immunosuppressive therapy or antibody removal, which has already achieved some success, might be therapeutically beneficial, particularly if targeted at removal of the culpable antibodies, via affinity dialysis.

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Rheumatoid factors and circulating immune complexes in HIV-infected individuals

Cited by 16 publications

References 0 publications

Cardiac autoimmunity in HIV related heart muscle disease

Cardiac autoimmunity in HIV related heart muscle disease

The envelope glycoprotein of HIV‐1 gp120 and human complement protein C1q bind to the same peptides derived from three different regions of gp41, the transmembrane glycoprotein of HIV‐1, and share antigenic homology

Extensive viral mimicry of 22 AIDS-related autoantigens by HIV-1 proteins and pathway analysis of 561 viral/human homologues suggest an initial treatable autoimmune component of AIDS

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