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C Parravicini

Publications and source records attributed to C Parravicini.

At least 55 records · Page 3Linked to original sources
PubMed1992

Spindle cell ploidy and proliferation in endemic and epidemic African Kaposi's sarcoma.

Comparative studies of ploidy and proliferative activity of spindle cells in sections of 20 (skin, 17; lymph node, 3) biopsy specimens from African patients, 10 with endemic Kaposi's sarcoma (EKS) and 10 with AIDS-associated Kaposi's sarcoma (AKS) were performed by histopathology, feulgen-based DNA measurement and proliferating cell nuclear antigen (PCNA)/cyclin immunohistochemistry, respectively. All specimens were classified as nodular lesions with basically the same histology. In 17 cases immunostained for cyclin/PCNA, the percentage of proliferating spindle cells range between 2-18, with a higher mean rate in AKS although this was not statistically significant. In situ measurement of DNA showed no significant values greater than the diploid level of control cells indicating that spindle cells in both EKS and AKS have euploid DNA content. Our findings indicate that both EKS and AKS represent the same type of euploid low rate cell proliferations. This corroborates previous suggestions that KS could represent a reactive process to yet undefined stimulus rather than a clonal proliferation, of transformed malignant cells.

Adult↗
PubMed1992

Macrophage association of polyomavirus in progressive multifocal leukoencephalopathy: an immunohistochemical and ultrastructural study. Case report.

Progressive multifocal leukoencephalopathy (PML) in a patient following autologous bone marrow transplantation for a non-Hodgkin's centroblastic lymphoma was studied by immunohistochemistry and transmission electron microscopy. Our observations indicate that a large amount of polyomavirus, most probably JC virus, is taken up and segregated within vacuoles of macrophages by phagocytosis. A relevant role of macrophages in the pathogenesis of PML is emphasized.

Brain↗
PubMed1992

Hypophyseal pathology in AIDS.

One hundred and eleven pituitary glands of patients (93 males, 18 females; mean age 32 years, 5 months) who died of fully developed AIDS or ARC were examined under light microscopy with the aid of immunohistochemistry. On post mortem (p.m.) examination a wide series of multiorgan alterations was noticed. Microscopically various lesions in both adeno- and neurohypophysis were seen. These ranged from vessel damage to secondaries to systemic infections, neoplasms and functional derangements. Necrotic lumps due to recent infarction could appear in both parts of the gland, while old fibrous scars sustained a previously overcome necrosis. Different pathogens (mainly fungi) could be seen either within the gland or arising from its meningeal surroundings. Examples of tumour pathology were provided by microadenomas, gliosis/gliomas; the frequency of adenomas (11.7%) was similar to that typical of senility. The functional impairment was mainly connected with ACTH cell hyperplasia, which seems in keeping with corticoadrenal or ACTH-receptor damage.

AIDS-Related Complex↗
PubMed1991

A6--a new 45RO monoclonal antibody for immunostaining of paraffin-embedded tissues.

The authors report on the extensive characterization, on normal and pathologic tissues, of the T-cell-specific monoclonal antibody (MoAb) A6, which the authors previously found to identify a fixation- and paraffin-embedding-resistant epitope. A6 reacted with most T lymphocytes, macrophages, and Langerhans' cells of normal tissues and with peripheral T-cell lymphomas (31 of 34), Ki-1+ lymphomas (12 of 18), and T-cell leukemias (1 of 5). All cases of X and non-X histiocytosis examined and monocytic leukemias with mature phenotype only were A6 positive. Three of 47 cases of B-cell lymphoma and leukemia were labeled. Hairy cell leukemias, multiple myelomas, and Hodgkin's and Reed-Sternberg cells were negative. The A6 reactivity was preserved with different fixatives (formalin, Bouin's fluid, Carnoy's fixative, and B5) and decalcification procedures and was slightly enhanced by trypsin digestion. The pattern of reactivity of A6 was similar to that obtained with MoAb UCHL-1, recognizing the CD45RO determinant of leukocyte common antigen; however, in pathologic tissues, A6 labeled a higher percentage of cells than UCHL-1. Cross-blocking and enzyme digestion studies (Pronase E [Sigma Chemical, St. Louis, MO] and neuraminidase [Sigma Chemical]) indicated that the two MoAbs may identify close epitopes on the same molecule. In conclusion, the authors' study indicates that A6 is an excellent reagent for detection of the CD45RO molecule on paraffin-embedded normal and pathologic tissues.

Antibodies, Monoclonal↗
PubMed1991

Phenotype of intramyocardial leukocytic infiltrates in acquired immunodeficiency syndrome (AIDS): a postmortem immunohistochemical study in 34 consecutive cases.

In 34 hearts, obtained at autopsy in consecutive AIDS cases, leukocytic phenotype and presence of viral antigens were investigated in paraffin-embedded (34 cases) and frozen myocardial sections (10 cases) by different monoclonal antibodies. The total frequency of focal lymphocytic infiltrates with and without myocell necrosis was 26.4 and 32.3%, respectively. In six control cases (HIV-negative i.v. drug abusers dying from acute fulminating hepatitis), these infiltrates were absent. In AIDS patients, the number of infiltrative foci per section, their wall distribution (subendocardial, middle layer, subepicardial), number of leukocytes per focus, and cell phenotype (prevalence of CD8+ suppressor/cytotoxic T-lymphocytes with CD4/CD8 ratio of 0.6 +/- 0.09 SE, absence of B-cells and granulocytes) were similar in cases with and without myocell necrosis. Significant differences were not observed between homosexual and i.v. drug abuser patients. In inflammatory foci associated with myocell necrosis CD45+/CD68+ monocytes prevailed, as a possible manifestation of nonspecific reparative process. In addition, in both AIDS patients and HIV-negative drug abusers, a population of CD68+ dendritic monocytes (histiocytes) characterized by a restricted CD45 expression (PanLeu-/9.4+) was found dispersed in the interstitium, with a significant higher frequency in the subendocardial layer. Histologic evidences of myocardial virus infections were not observed. Cytomegalovirus (CMV) antigens, however, were found in frozen sections of five of the six cases with lymphocytic infiltrates, supporting the view that this virus can be one of the possible causes of myocarditis in AIDS. Moreover, in two of these CMV-positive cases, a concomitant expression of HIV1 antigens in isolated intramyocardial leukocytes was also observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Acquired Immunodeficiency Syndrome↗
PubMed1990

Absence of HIV antigens in renal tissue from patients with HIV-associated nephropathy.

HIV-associated nephropathy (HIV-N) is considered a distinctive disease, the pathogenesis of which is still undefined. Direct virus-induced renal cell damage has been postulated. The numerous cytolytic ultrastructural changes and a few studies by immunoperoxidase support this hypothesis, but there has been no demonstration of virus by electron-microscopy (EM) or by tissue culture. In seven out of 12 cases with histological characteristics of HIV nephropathy, with proteinuria (five cases) or with nephrotic syndrome (two cases), we tested renal tissue for HIV antigens: core p18 and p25; envelope gp45 and gp110, by means of immunoperoxidase avidin-biotin complex monoclonal antibodies (MoAbs). Light-microscopy (LM) showed in five patients a focal and segmental glomerular sclerosis, and in two a mesangial hyperplasia with vacuolisation of visceral epithelium and protein inclusions. Electron-microscopy, performed in five of seven patients, showed several protein inclusions in podocyte cytoplasm, tubuloreticular inclusions in endothelial cell cytoplasm in all cases, nuclear degranulation of tubular cells in four cases and nuclear bodies in two. HIV antigens by MoAbs on renal tissue were negative in all cases, in both glomeruli and tubules. These results do not confirm the presence of HIV proteins in renal tissue of patients with HIV nephropathy. A possible explanation, apart from no direct HIV in the disease, may be the low viral load in tissues, because of the early phases of renal damage in most cases.

AIDS-Associated Nephropathy↗
PubMed1990

Expression of integrins in human bone marrow.

Expression of integrins, a superfamily of glycoprotein alpha/beta heterodimers which integrate the cytoskeleton with the extracellular matrix and/or mediate cell-cell adhesive interactions, was examined on normal and leukaemic bone marrow cells by immunohistochemistry and immunotransmission electron microscopy (immuno-TEM). Among the beta 1/VLA molecules studied, VLA-2 and 6 were expressed on megakaryocytes and platelets, while VLA-4 was present on 40% of haemopoietic cells, including monocytes, erythroblasts and immature cells; this molecule was typically localized at sites of intercellular contact, as seen by immuno-TEM, suggesting it may be involved in interactions among haemopoietic cells during differentiation. In human long-term bone marrow cultures (LTBMC), VLA-1 and 3 were present respectively on 35% and 40% of the adherent cells which included fibroblasts and endothelial cells, as shown by double-labelling experiments; VLA-2 was expressed only on a subpopulation of fibroblasts. beta 2/LeuCAM molecules were absent from platelets, megakaryocytes and HLA-DR+/myeloperoxidase- early myeloid precursors, and appeared progressively during maturation in both lymphoid and myeloid cells. Expression of beta 3/cytoadhesin molecules was restricted to megakaryocytes and platelets and, in the adherent layer of LTBMC, to endothelial cells. The regulated expression and specific localization of integrins in the bone marrow suggest that these molecules may have a role in normal haemopoiesis.

Bone Marrow↗
PubMed1990

Malignant lymphomas in cynomolgus monkeys infected with simian immunodeficiency virus.

Malignant lymphomas were observed in 38% (9 of 24) of simian immunodeficiency virus (SIV)-infected cynomolgus monkeys (Macaca fascicularis) 5 to 15 months after inoculation with SIV strain SMM3. Lymphomagenesis in the SIV-infected monkeys was not related directly to the SIV-infectious dose given. All SIV-infected animals developed severe immunodeficiency. No significant difference in immunodeficiency was observed between tumor-bearing and non-tumor-bearing animals. In contrast, no lymphomas were observed in a comparable group of HIV-2-infected monkeys, which did not develop immunodeficiency; nor did the noninfected control monkeys. All 9 SIV-related tumors were high-grade B-cell lymphoblastic or pleomorphic lymphomas with extranodal, disseminated growth. Most tumors showed marked infiltration by monocytes and CD8+ T lymphocytes. Occasional tumor infiltrating cells showed immunohistochemical reaction for SIV. The cells of two tumors were established in vitro and shown to be of B-cell phenotype. The tumor cell cultures showed no reverse transcriptase activity and no evidence of virus infection by electron microscopy. Our observations indicate that SIV-induced immunodeficiency in cynomolgus monkeys also mimics HIV infection and AIDS in humans with regard to increased lymphomagenesis and type of lymphomas.

Animals↗
PubMed1989

Terminal deoxynucleotidyl transferase-positive B cell precursors in fetal lymph nodes and extrahemopoietic tissues.

Terminal deoxynucleotidyl transferase (TdT)-positive B cell precursors populate fetal lymph nodes (LN) of mid-term (16th-22th week) fetuses. These cells have a B cell phenotype (HLA-DR, CD45R, CD22, mu) and lack mature differentiation antigens (CD1c, CD20, L26). TdT+ cells are also present in the extranodal mesenteric mesenchyme, pancreas and LN primordia. Extranodal TdT+ cells are found among proliferating (i.e. Ki-67+) B cells and lack leukocyte function-associated antigen (LFA-1) and HLA-DQ; these latter molecules are acquired by nodal TdT+ elements. Adult LN, adult and fetal spleen contain less TdT+ cells than fetal LN. The fetal LN contains the full range of the B cell differentiation compartment, from the TdT+ precursor cell to the mature B lymphocyte.

Antigens, Surface↗
PubMed1989

Cell association of HIV in AIDS-related encephalopathy and dementia.

The presence of HIV gag and env proteins (HIV Ag) and virus replicating cells was studied by immunohistochemistry and in situ hybridization, respectively, in brain specimens from five HIV infected patients. HIV antigens were detected in 3 of 5 brains in micronodular areas characterized by increased cellularity and the presence of multinuclear giant cells. By double immunostaining, HIV Ag positive cells were shown to express markers common to macrophages and microglia i.e. Leu M5+, My4+, HLA-Dr+, RCA-1+, and to a lesser extent CD4+ (Leu3+). Another macrophage specific marker, KiM6, was found only on HIV+ cells in HIV infected specimens and not in uninfected, control brains. Medium-sized, virus replicating cells were found exclusively in micronodular areas, but in much smaller quantities than HIV Ag+ cells. Our observations provide further evidence to support the hypothesis that macrophages play an important role in CNS infection by HIV and additionally support the concept that reactive microglial originate from activated macrophages infiltrating the brain. Both direct effects of viral components and cell mediated reactions can be implicated from our findings as mechanisms involved in the pathogenesis of the CNS lesions.

Acquired Immunodeficiency Syndrome↗
PubMed1989

[Primary retroperitoneal tumors].

The Authors report 7 cases of primary retroperitoneal tumors observed in a five-year period. On the basis of the literature data, they examine the diagnostic, therapeutic and prognostic features, emphasizing the need for a surgical treatment supported, only when useful, by radio- and chemotherapy. The importance of an early diagnosis, thanks to modern technologic progress, is also stressed, echography in particular.

Adult↗
PubMed1989

HIV infection of monocytic cells: rôle of antibody-mediated virus binding to Fc-gamma receptors.

We investigated whether human immunoglobulin G (IgG) directed to gp110 may serve as an attachment system to Fc-gamma receptors (Fc-gamma R), allowing eventual infection of cells of the macrophage lineage. An anti-HIV IgG preparation that prevented viral particles and soluble recombinant radiolabelled envelope precursor gp160 from binding to CD4 on CEM lymphoid cells, and that strongly inhibited infection of these cells by HIV, was selected. In contrast, anti-HIV IgG, whether or not previously complexed to viral particles, bound to monocytic U937 cells that express both high Fc-gamma RI and low affinity Fc-gamma RII receptors. Precoating these cells with anti-HIV IgG or complexing the antibodies with soluble 125I-gp160 resulted in increased fixation of gp160 to the cells, which was inhibited by aggregated human normal IgG. These data indicate that anti-HIV IgG-dependent attachment of gp160 to monocytic cells occurs through both types of Fc-gamma R. In addition, this method of attachment resulted in productive infection of U937 cells that, since it was blocked in the presence of Leu3a, still appeared to involve gp110-CD4 interaction. Only slight enhancement of infectivity, such as described for other enveloped viruses, was noted, even when antibody concentration was titrated down. This mechanism may be one of the explanations why the humoral response to HIV is not usually protective.

Acquired Immunodeficiency Syndrome↗
PubMed1989

Morphogenesis, evolution and prognostic significance of lymphatic tissue lesions in HIV infection.

Morphological changes in lymph node biopsies of HIV-infected patients can be classified in four stages, based upon the degree of damage to follicular structures: (1) follicular hyperplasia, (2) follicular lysis, (3) follicular atrophy and (4) follicular and lymphocytic depletion. To define the relative usefulness of morphological, clinical and immunological findings for prognostic purposes, we followed the clinical evolution of 86 biopsied HIV+ patients for a period ranging from 1 to 56 months. A relatively good correlation between histological and clinical findings, at the time of biopsy, was observed. Statistical analysis confirmed the prognostic value of the histological features for clinical deterioration, progression to AIDS and survival. Moreover, histological findings gave more reliable prognostic information than clinical values. Our data suggest that lymph node biopsy can be utilized for prognostic purposes in the evaluation of the progression of the disease and effectiveness of antiviral therapeutic trials.

Acquired Immunodeficiency Syndrome↗
PubMed1988

A molecular mechanism of inhibition of HIV-1 binding to CD4+ cells by monoclonal antibodies to gp110.

We have investigated the possible involvement in the interaction between HIV gp110 and its CD4 receptor of epitopes different from the currently known binding site(s) of the molecule. Four monoclonal antibodies (MAbs) to gp110 were used (Genetic Systems Corporation, Seattle, Washington, USA): one (110-1) recognized a peptide corresponding to the C-terminal part of gp110 (494-517); the other three (110-3, 110-4, 110-5) recognized the same peptide located at position 308-328. HIV or purified gp110 obtained from a vaccinia recombinant (Transgene S.A., Strasbourg, France) were pre-incubated with the MAb prior to addition to CD4+ cells. Specific binding of viral particles or of the soluble molecule was then determined by flow cytometer analysis, compared with that of control preparations where the MAb was added after HIV or gp 110 had been allowed to bind CD4+ cells. Significant inhibition of HIV binding was noted with the three MAbs to peptide (308-328), but not with 110-1. At the molecular level, these same MAbs decreased the affinity of interaction between CD4 and soluble gp110, although they could still label the latter molecule after it had bound to CD4+ cells. Therefore, steric hindrance may account for neutralization of HIV binding by antibodies that are actually directed to epitopes topographically distinct from the site of binding of gp110 to CD4.

Antibodies, Monoclonal↗
PubMed1987

HIV env glycoprotein shares a cross-reacting epitope with a surface protein present on activated human monocytes and involved in antigen presentation.

A serological cross-reactivity between env gp120 glycoprotein of the human immunodeficiency virus (HIV) and a human cellular surface protein has been defined by a monoclonal antibody (M38) raised against HIV. The cellular antigen is a protein of ca. 80 kDa expressed on a small fraction of mononuclear cells in peripheral blood and in lymph nodes. The protein behaves as an activation antigen of the monocytic lineage since it is expressed by monocytes in plastic-adherent culture conditions and by interferon-gamma-treated monocytes and pro-monocytic U937 cells. The protein is involved in antigen presentation since the antibody efficiently inhibits the proliferation of responsive lymphocytes in autologous tetanus toxoid presentation assays. In the T lymphoblastoid line H9, the protein is present in very small amounts, is not induced by interferon-gamma and increases after HIV infection. Sera from lymphoadenopathy syndrome and acquired immunodeficiency syndrome (AIDS) patients fail to detect the cellular protein, although containing antibodies reacting with gp120. We propose that both viral and cellular structures recognized by the monoclonal antibody (mAb) are involved in interactions with CD4 molecules of T helper lymphocytes and that such molecular mimicry might be relevant in the pathology of HIV infection. This view is supported by the finding that BL/10T4, a CD4-specific mAb, binds to M38 neutralizing its interactions with HIV and with monocytes. mAb M38 thus behaves as the internal image of CD4. This single property would explain all its diverse binding characteristics.

Antibodies, Monoclonal↗
PubMed1987

Brain pathology induced by infection with the human immunodeficiency virus (HIV). A histological, immunocytochemical, and electron microscopical study of 100 autopsy cases.

Neuropathological examination of brain tissue of 100 patients with infection by the human immunodeficiency virus (HIV), including 98 with clinically manifest acquired immune deficiency syndrome (AIDS), revealed distinct multifocal-disseminated and diffuse brain tissue lesions, which can be regarded as HIV-induced brain lesions: multifocal giant cell encephalitis (MGCE; 4) and progressive diffuse leukoencephalopathy (PDL; 25). These lesions were found in 38 brains, and in 17 in absence of infectious, necrotizing or inflammatory changes of other types. In 13 brains, a combination of MGCE with PDL was seen, suggesting a spectrum of HIV-induced brain lesions. MGCE is characterized by perivascular accumulations predominantly of rod cells, monohistiocytes and macrophages, all of which are strongly labeled with a monoclonal antibody to macrophages. Most conspicuous are multinucleated giant cells which are also labeled by anti-macrophage antibody, and which can be regarded as evidence of the local presence of HIV, as confirmed by electron microscopical detection of HIV particles in four MGCE brains, and by immunocytochemical detection of HIV proteins in two MGCE brains. PDL is characterized by a triad: diffuse myelin loss, astroglial proliferation, and infiltration by mono- and multinucleated macrophages. HIV-induced lesions can be morphologically differentiated from histopathological brain lesions known in immunosuppression, including what is called here nodular encephalitis ["subacute encephalitis" of the literature, in most cases attributable to cytomegalovirus (CMV) or toxoplasmosis], by their characteristic histopathology including the hallmark presence of multinucleated giant cells, by direct immunocytochemical and electron microscopical demonstration of HIV in the lesions, and by the absence of opportunistic agents (bacteria, fungi, Toxoplasma, CMV, HSV or papovaviruses). Diffuse poliodystrophy (diffuse proliferation of astroglia with swollen nuclei, occasionally minor neuronal loss and rod cell proliferation) was found in the cerebral cortex and other gray matter in half of all brains, including cases with gyral atrophy, and may be another correlate of HIV damage to the brain. Morphological delineation of HIV-induced brain lesions is a necessary prerequisite for a meaningful clinical definition of HIV-induced cerebral disease.

Acquired Immunodeficiency Syndrome↗