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Background. The demonstration of in vitro cardiolipin reactivity with 2 human immunodeficiency virus (HIV)- specific, broadly neutralizing antibodies (2F5 and 4E10) has prompted reevaluation of autoimmune manifestations in HIV infection. Methods. We evaluated autoantibodies, particularly anticardiolipin (aCL), in 67 untreated, asymptomatic, HIVinfected individuals with slow progression of HIV disease and their correlation with 2F5-, 4E10-, b12-, and 2G12- like antibodies directed against epitopes involved in broad neutralization, as well as their correlation with immune activation and virological and clinical indicators. Fifty individuals with chronic HIV infection and standard disease progression were control patients. Results. The majority of the study patients with slow progression of HIV disease were men (78%); their median age was 37 years, their median CD4+ cell count was 672 cells/μL, and their median plasma HIV load was 6200 copies/mL. The majority of the control patients were also men (76%), and most (62%) were receiving highly active antiretroviral therapy; their median age was 43 years, their median CD4+ cell count was 202 cells/mL, and their median plasma HIV load was 2265 copies/mL. aCL immunoglobulin G was detected at similar levels in 49% of patients with slow progression of HIV disease and in 58% of control patients. Viral load was positively associated with aCL in both groups (P < .001), independent of CD4+ cell counts. In patients with slow progression of HIV disease, aCL levels were also correlated with plasma HIV load and cell-associated DNA level (r = 0.486 and r = 0.516, respectively; P < .001), with the proportion of activated CD4+ cells, human leukocyte antigen-DR+ cells (r = 0.445; P = < .001) but not activated CD8+ T cells, and with the level of B cell activation (quantified by soluble CD23; r = 0.354; P = .007). The level of aCL antibodies was associated with the level of antibodies to themembrane proximal region of gp41 (P = .003). Conclusion. aCL is frequently detected in HIV-infected patients, regardless of disease stage, and is strongly linked with the level of viral replication, the level of CD4+ T and B cell activation, and the level of antibodies to the membrane proximal external region of gp41, independent of CD4+ cell deficiency. [ABSTRACT FROM AUTHOR]

Marked polyclonal immunoglobulin (Ig)G4 hypergammaglobulinemia has exceptionally been reported. Here we report on two Algerian patients who presented a syndrome characterized by anemia, plasmacytic lymphadenopathy, renal manifestations, and a marked polyclonal IgG4 hypergammaglobulinemia leading to a hyperviscosity syndrome in one case. The IgG4-expressing cell percentage was significantly increased in the peripheral blood lymphocytes collected from the two patients upon diagnosis. Moreover, in contrast with normal sera, both patients’ sera significantly increased the percentage of IgG4-expressing cells when incubated with CD40-stimulated normal B lymphocytes. Similar effects were obtained with the culture supernatants of the patients’ activated T cells. Anti-interleukin (IL) 4 and/or anti-IL-13 antibodies were unable to antagonize the IgG4 production. IL-4 and IL-13 serum concentrations were found to be normal in the two patients. The increased IgG4 production was found to be mediated by soluble factor(s), most probably secreted by activated T cells, which did not require the signal transducer and activator of transcription 6 signaling pathway. [ABSTRACT FROM AUTHOR]

Background. Strong T cell and antibody responses to human immunodeficiency virus (HIV), low virus production, and some genetic traits have been individually associated with nonprogression of HIV infection, but the best correlate with protection against disease progression remains unknown. Methods. We prospectively followed 66 untreated long-term nonprogressors and analyzed relationships between HIV-1-specific CD4 T helper (Th) 1 and CD8 T cell responses and HIV-1-specific antibodies, HIV-1 RNA and proviral DNA loads, host genes, and CD4 Thi cell counts at entry into the study and 4 years later. Results. HIV-1 p24-specific CD4 Thi cell proliferation, interferon (IFN)-γ production, and IFN-γ-producing cell frequencies at entry significantly and negatively correlated with HIV- 1 RNA and proviral DNA loads and were independent of CD4 Thi cell counts and host genes. HIV-1 Gag-specific IFN-γ-producing CD8 T cell frequencies correlated with HIV-1 proviral DNA loads but not with RNA loads. Only high frequencies of HIV-1 p24-specific CD4 Thi cells combined with HIV-1 gp41-specific IgG2 antibodies significantly predicted persistence of high CD4 Thi cell counts. Conclusion. HIV-1-specific CD4 Thi responses combined with IgG2 antibodies and IFN-γ-producing CD4 Thi cells are better predictors of long-term nonprogression than are virus parameters, host genes, or HIV-1-specific CD4 Thi or CD8 T cell proliferation. [ABSTRACT FROM AUTHOR]

ABSTRACT- We report the case of a young woman with chronic neutropenia, in whom hepatitis, extensive herpetic eruption and herpes simplex viremia developed after genital herpetic ulceration. Although severe liver necrosis was present, the patient's death did not result from hepatic failure. No inflammatory cell infiltration was found circumscribing the multiple necrotic foci in the liver. This absence of inflammatory cell infiltration reflects the host's inability to normally restrain herpes simplex virus dissemination and, in this patient, might be the consequence of chronic neutropenia. [ABSTRACT FROM AUTHOR]

Study Objective: To determine whether zidovudine is effective in increasing the platelet count in patients with thrombocytopenic purpura related to human immunodeficiency virus (HIV) infection.Design: Nonrandomized controlled trial with two consecutive regimens.Setting: Immunopathology and hematology clinics at two general hospitals.Patients: Consecutive sample of 34 patients infected with HIV who had thrombocytopenic purpura (platelets less than 50 x 10(9)/L) without visceral bleeding. Twenty-nine patients completed the study; one patient was removed because of drug toxicity.Interventions: Zidovudine for 12 weeks, 250 mg every 6 hours orally in 10 patients; and 500 mg every 8 hours orally in 24 patients.Measurements and Main Results: Three of ten patients receiving 250 mg every 6 hours and 12 of 24 patients receiving 500 mg every 8 hours had a persistent increase in their platelet counts. In both groups the mean value of the platelet count increased significantly by week 12; from 28 x 10(9)/L +/- 12 (SD) to 57 x 10(9)/L +/- 36 in the first group and from 20 x 10(9)/L +/- 13 to 77 x 10(9)/L +/- 42 in the second group (P less than 0.05 and P less than 0.01, respectively).Conclusions: Zidovudine is effective on platelet counts in some patients with HIV-related thrombocytopenia. These results suggest that HIV itself may play a direct or indirect role in the pathogenesis of this disorder. [ABSTRACT FROM AUTHOR]

Presents information on a study which examined the antinuclear autoantibodies of several patients with chronic autoimmune disorder for lamins. Methodology of the study; Results and discussion.

A cross-sectional study was done to determine the seroprevalence of Mycoplasma penetrans in human immunodeficiency virus (HIV) type 1-seropositive and -seronegative persons recruited in France. The data were analyzed with respect to the sociodemographic, clinical, and biologic status of the patients. M. penetrans seropositivity was associated with HIV infection (18.2% of HIV-seropositive vs. 1.3% of HIV-seronegative persons were M. penetrans-seropositive; P < .001). M. penetrans infection was predominantly but not exclusively associated with homosexual practices in HIV-seropositive subjects and thus presumably sexually transmitted. M. penetrans seroprevalence increased with progression of HIV-associated disease. No association was found between M. penetrans and Kaposi's sarcoma. Thus, there is an unambiguous association between M. penetrans and HIV, particularly among homosexual persons, but its clinical significance remains to be investigated. [ABSTRACT FROM PUBLISHER]

Mutations of Fas or Fas ligand genes result in the autoimmune lymphoproliferative syndrome (ALPS) in humans. We report here a diffuse large B-cell non-Hodgkin's lymphoma occurring in a man with ALPS. Fas-mediated lymphocyte apoptosis was defective in vitro, owing to a mutation within the death domain of the Fas molecule. High-dose methotrexate and doxorubicin–based chemotherapy led to complete remission of lymphoma. [ABSTRACT FROM AUTHOR]