Human immunodeficiency virus type 1 (HIV-1) has tropism for helper T lymphocytes and cells of the monocyte/ macrophage lineages. HIV-1 can also infect other cell types, including B cells. We show here that 10% of fresh circulating B cells from HIV-1-seronegative donors (i) express the CD4 receptor and CCR5 and CXCR4, two recently described coreceptors for HIV-1 and (ii) are permissive to HIV-1 with de novo proviral DNA integration following ex vivo infection by either SI (syncytium-inducing) or NSI (non-syncytium-inducing) isolates. To get further information on the interaction between HIV and B cells, the susceptibility of several EBV-positive or -negative B cell lines to infection by SI and NSI isolates was checked. Following infection of an EBV- CD4+ CXCR4+ CCR5- B cell line (DG75) by an SI HIV-1 isolate, we obtained a cell line which chronically produced low-level infectious HIV-1 for 2 years (HIV-DG75). Immunocytochemical data, combined with in situ PCR data, established that HIV-DG75 cells consist of at least three populations uninfected cells, infected virus-producing cells, and infected but nonproducing cells. Moreover, HIV-DG75 cells which express p24 antigen do not go into apoptosis, contrary to T lymphocytes. We infer from these results that B cells could constitute a reservoir of infectious virus in infected patients.

SummaryIn HIV-1 infection, an increased prevalence of anticardiolipin autoantibodies (aCL) and lupus anticoagulant (LA) has been described. In order to see if these antibodies are isolated or, like in autoimmune diseases, associated with hematological disorders and with antibodies to other phospholipids and to proteins of coagulation, we investigated 3 groups of patients: 1. 342 HIV-1 infected patients, 2. 145 control patients including 61 systemic lupus erythematosus (SLE) patients, 58 patients with a connective tissue disease, 15 patients with stroke, 11 patients with syphilis and 3.100 blood donors. In HIV-1 infection antiprothrombin (aPrT) antibodies were present in 25% of patients, the prevalence of antiphosphatidylcholine antibodies (aPC) (50%) was almost as high as aCL (64%), and 39% had both antibodies. Absorption on liposomes of the latter revealed an heterogeneous mixture of aCL and aPC or cross-reacting antibodies. In contrast with SLE, anti-β2-glycoprotein I (4%), LA (1%), biological false positive test for syphilis (0.3%), thrombosis (p <0.001) were uncommon. In HIV-1 infection, antiphospholipid antibodies do not associate with features linked to them in SLE or syphilis.

OBJECTIVES:Anticardiolipin antibodies belong to the group of antiphospholid antibodies, and may be seen in association with endothelial damage and recurrent vascular thrombosis. The aim of our study was to determine in patients with Crohn's disease the frequency of anticardiolipin antibodies, and to correlate their presence with clinical activity and treatment of the disease.METHODS:One hundred and thirty-eight sera from patients with Crohn's disease and 118 from age-matched controls were tested for IgG anticardiolipin antibodies. In the Crohn's disease group, we determined whether the patients had a past history of vascular thrombosis, a clinically active intestinal disease, or a current immunosuppressive therapy (steroids or azathioprine).RESULTS:Anticardiolipin antibodies were found significantly more often in patients with Crohn's disease than in controls: 11.0% versus 2.5%, P < 0.02. Three patients with Crohn's disease had a past history of vascular thrombosis, but none of them had anticardiolipin antibodies. The presence of anticardiolipin antibodies was not correlated with the fact that patients had a clinically active disease (P = 0.77), or a current immunosuppressive therapy at the time of the serological test (P = 0.95).CONCLUSIONS:There is a significantly high prevalence of patients with anticardiolipin antibodies during Crohn's disease. The positivity of the test does not seem to be correlated to the existence of a past history of vascular thrombosis, nor to the clinical activity of the disease.

Prevalences of anticardiolipin (aCLA), anti-beta(2)-glycoprotein I (anti-beta(2)-GPI) and anti-prothrombin IgG antibodies were determined by ELISA in 2174 patients and 107 blood donors. Among patients, 137 had systemic lupus erythematosus (SLE), while 683 displayed at least one clinical or biological feature suggestive of antiphospholipid syndrome: 497 patients had thrombosis, 51 patients had experienced at least 3 miscarriages or a foetal death at more than 12 weeks of gestation, 67 had thrombocytopenia, 50 had lupus anticoagulants (LA), 13 had thrombosis and LA, 3 had thrombocytopenia and LA and 2 had a history of foetal lass and LA. Connective tissue or related disorders were present in 595 patients, 759 others were suffering from miscellaneous diseases and cases of HIV infection were excluded from the study. Prevalences of aCLA and anti-beta(2)-GPI antibodies were increased in patients with SLE and/or LA in comparaison to all other groups (p < 0.001). In these patients, anti-beta(2)-GPI antibodies were often associated with aCLA, 34 (77%) of 44 patients with anti-beta(2)-GPI antibodies also having aCLA (p < 0.001). In other patients the reverse was true, anti-p,GPI antibodies being infrequent and when present rarely associated with aCLA (p < 0.001). The prevalence of sera with anti-beta(2)-GPI antibodies but no aCLA was similar in all patient groups and in blood donors. These results suggest that at least two types of antiphospholipid containing sera exist, those containing only one kind of antibody (aCLA or anti-beta(2)-GPI antibodies, type 1) which are poorly specific and those associating aCLA and anti-beta(2)-GPI antibodies (type 2), highly specific for SLE and/or LA. The prevalence of anti-prothrombin antibodies was increased in patients with SLE and/or LA (p < 0.01) and in those with an unexplained prolongation of APTT (p < 0.01). In the latter case, since these antibodies were not associated with LA, aCLA or anti-beta(2)-GPI antibodies, this indicates that anti-prothrombin antibodies may interfere in the APTT test and should therefore be screened in patients presenting an unexplained prolongation of APTT.

Vascular abnormalities are frequent in connective tissue disease. In this kind of patients a lot of autoantibodies are observed. To screen them a strategy must be selected according to the connective tissue disease that is suspected. When the diagnosis is unknown the tests must screen a great number of autoantibodies and this is the case for indirect immunofluorescence assays, at the opposite when the diagnosis is known antibodies specific for the disease should be screened. Some antibodies are specific for a disease this is the case for antibodies directed against double stranded DNA, centromere, extractable nuclear antigens Sm, RNP, Scl-70, Pm-Scl, Jo1, neutrophil cytoplasmic antigen proteinase 3, and beta 2-glycoprotein I the cofactor of anti-cardiolipin antibodies. Anti-SS-A(Ro) antibodies are very frequent in autoimmune diseases and they are not specific for anyone of them. Some autoantibodies are frequent in autoimmune and also in non autoimmune diseases and this is the case for antibodies directed against phospholipids, single stranded DNA, histones, rheumatoid factor. The detection of antibodies depends on the assays used for screening, that is why results should mention the assay used for their detection. The standardization of the detection of the autoantibodies especially when quantitative results are requested, is not yet performed enough. So to obtain reproducible results when monitoring a patient the screening must be done by the same assay in the same laboratory.

Vascular abnormalities are frequent in connective tissue disease. In this kind of patients a lot of autoantibodies are observed. To screen them a strategy must be selected according to the connective tissue disease that is suspected. When the diagnosis is unknown the tests must screen a great number of autoantibodies and this is the case for indirect immunofluorescence assays, at the opposit when the diagnosis is known antibodies specific for the disease should be screened. Some antibodies are specific for a disease this is the case for antibodies directed against double stranded DNA, centromere, extractable nuclear antigens Sm, RNP, Scl-70, Pm-Scl, Jo1, neutrophil cytoplasmic antigen proteinase 3, and beta2-glycoprotein I the cofactor of anti-cardiolipin antibodies. Anti-SS-A(Ro) antibodies are very frequent in autoimmune diseases and they are not specific for anyone of them. Some autoantibodies are frequent in autoimmune and also in non autoimmune diseases and this is the case for antibodies directed against phospholipides, single stranded DNA, histones, rheumatoid factor. The detection of antibodies depends on the assays used for screening, that is why results should mention the assay used for their detection. The standardization of the detection of the autoantibodies especially when quantitative results are requested, is not yet performed enough. So to obtain reproductible results when monitoring a patient the screening must be done by the same assay in the same laboratory.