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Query: UMLS:C0019693 (HIV)
 170,526 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Several inflammatory, infectious, and neoplastic conditions in HIV-infected patients are distinctive or require a biopsy for diagnosis. Some differ subtly from similar conditions seen in noninfected patients. The exanthem of acute HIV infection cannot be diagnosed specifically on biopsy as its histologic appearance is similar to that of other viral exanthemata. A condition that closely resembles seborrheic dermatitis occurs in HIV-infected patients. Plasma cells, necrotic keratinocytes, and leukocytoclasis may be present, in contrast to findings in sporadic seborrheic dermatitis. Psoriasis and Reiter's disease also occur in HIV-infected patients and can be specifically diagnosed as such. The category "psoriasiform dermatitis of AIDS" thus seems to include several distinct entities and not to be a single disease. Bacillary angiomatosis is a treatable infection caused by a rickettsialike organism similar to Rochalimaea quintana, the agent of trench fever. Cutaneous lesions are characterized by lobules of capillaries with protuberant endothelial cells, neutrophils and their debris, and purplish-staining clumps of organisms, which can be demonstrated with silver stains or electron microscopy. An unusual reaction to atypical mycobacterial infection, in which spindle-shaped macrophages are seen, resembles histoid leprosy. Viral skin diseases that may challenge the dermatopathologist include unusual verrucous reactions to chronic varicella-zoster infection and flat warts caused by the human papillomavirus associated with epidermodysplasia verruciformis. Keratinocytes with foamy basophilic cytoplasm may be a marker for one of these viruses, human papillomavirus type 5. Neoplastic complications of HIV disease include Kaposi's sarcoma and mycosis fungoides. The earliest lesions of the patch stage of Kaposi's sarcoma show a slightly increased number of cells with small ovoid nuclei around preexistent structures, accompanied, in some cases, by sparse infiltrates of lymphocytes and plasma cells. Staining with antisera to type IV collagen may highlight the vascular spaces in these early lesions. Later lesions that resemble hemangiomas may also prove challenging and require level sections to demonstrate the presence of spindle cells and eosinophilic globules. Although HIV is cytotoxic to helper T cells, neoplastic proliferations of them may be seen in HIV-infected patients. These cases of mycosis fungoides do not seem to differ from sporadically occurring ones and occur in patients who seem not to be infected by HTLV-I.
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PMID:Dermatopathologic findings in patients infected with HIV. 173 Jan 73

Previous studies have shown that coinfection of the human T lymphotrophic virus type I (HTLV-I) chronically infected cell line MT4 with human immunodeficiency virus type 1 (HIV-1) results in cells which spontaneously activate complement via the classical pathway. This complement activation was antibody independent, yet required C2, suggesting either direct C1, C4, or C2 activation. Because some animal retroviruses have been shown to bind human C1q directly, the present study investigated the possible direct binding of C1q by HIV coinfected MT4 cells. Coinfected cells bound both C1q present in serum and highly purified C1q. Binding of C1q resulted in formation of active C1 on the cell surface, which could in turn activate complement as shown by C4 consumption. The C1q binding was not HIV-isolate specific since infection of MT4 cells with any of three diverse isolates all induced C1q binding. Purified collagen-like region (CLR) and globular region (GR) fragments of C1q both bound to coinfected cells, suggesting a mechanism of binding by C1q similar to that of fibronectin-C1q binding. However, culture of coinfected cells in serum-free (fibronectin-free) medium did not reduce C1q binding. A second HTLV-I chronically infected line, SLB-1, also displayed increased binding of C1q after HIV infection. The H9 cell line, which is not HTLV-I infected, did not bind C1q after HIV infection. These results suggest that a retrovirus protein expressed by coinfected cells directly binds C1q resulting in classical complement activation. This type of activation may have profound biological effects in persons coinfected with HIV-1 and HTLV-I.
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PMID:Direct binding of complement component C1q to human immunodeficiency virus (HIV) and human T lymphotrophic virus-I (HTLV-I) coinfected cells. 176 60

Scrofula has been called "The Dangerous Masquerader" because of its propensity to mimic other diseases. Scrofula has been mistaken for metastatic carcinoma, regional neoplasms, thyroglossal duct cysts, fungal disease, toxoplasmosis, lymphoma, osteosarcoma, chondrosarcoma, bacterial adenitis, and collagen vascular disease. Because of the enormous number of infectious and neoplastic diseases acquired by the HIV positive population, the diagnosis of scrofula may be further delayed in some patients. In these patients the early diagnosis of scrofula might allow the early identification of HIV infection and the early institution of anti-retroviral therapy. The recommended duration of anti-tuberculosis therapy is also different in HIV positive patients. Therefore, to ensure the patient of the most beneficial therapy, the physician must always consider scrofula in the differential diagnosis of a neck mass, and particularly because of the increases incidence of intrapulmonary tuberculosis in AIDS patients, he must consider the possibility of HIV infection.
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PMID:The re-emergence of scrofula with HIV infection: a review of epidemiology, pathogenesis, diagnosis and treatment. 181 95

Altered T cell adherence after human immunodeficiency virus 1 (HIV-1) infection may contribute to viral pathogenesis in the acquired immune deficiency syndrome. To address this hypothesis, we assessed mechanisms of T cell adherence to extracellular matrix proteins in vitro. We found that after HIV-1 infection, both chronically infected H9 CD4+ T cells and acutely infected primary peripheral blood lymphocytes acquired the ability to adhere to the extracellular matrix glycoprotein fibronectin, to a lesser extent to type IV collagen and laminin, but not to type I collagen. H9 cells chronically infected with two of the three HIV-1 strains studied showed approximately a sevenfold increase in attachment to fibronectin, while the same cells infected with the human retrovirus HIV-2 did not. Adhesion was accompanied by changes in morphology, including marked spreading and increased filopodia. These alterations were not blocked by the protein kinase C inhibitor H-7, which did inhibit TPA-induced T cell attachment to fibronectin. Monoclonal antibodies against both the alpha 5 and the beta 1 subunits of the classical fibronectin receptor as well as an Arg-Gly-Asp (RGD) peptide inhibited attachment, whereas anti-alpha 4 monoclonal antibodies and the CS1 peptide did not. Binding to collagen IV was also inhibited by the anti-beta 1 monoclonal antibody, but not the other antibodies. Cells metabolically labeled with [35S]methionine and analyzed by immunoprecipitation with polyclonal anti-beta 1 integrin antibody showed a 2.5-fold increase in integrin synthesis in infected cells compared to uninfected controls. This increase in synthesis was associated with an increase in cell surface expression of both alpha 5 and beta 1 integrins by FACS (registered trademark of Becton Dickinson for a fluorescence-activated cell sorter) analysis. Enhanced expression of integrins such as alpha 5 beta 1 may cause T cell adherence to a variety of tissues, where released viral gene products may induce some of the tissue-specific manifestations of HIV-1 infection.
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PMID:HIV-1 infection of human T lymphocytes results in enhanced alpha 5 beta 1 integrin expression. 183 Dec 4

Several types of vasculitis have been described in patients with human immunodeficiency virus infection. Erythema elevatum diutinum is a rare variant of cutaneous leukocytoclastic vasculitis which, with the exception of the case reported herein, has been described only once in human immunodeficiency virus-infected patients. Our male patient, a longtime intravenous drug abuser, had cutaneous lesions, closely resembling Kaposi's sarcoma, on the extensor surfaces of the lower extremities. Cutaneous biopsy specimens, however, demonstrated leukocytoclastic vasculitis with fibrinoid necrosis of the vessel walls and areas of basophilic degeneration of collagen bundles in early lesions, whereas late lesions showed dense diffuse fibrosis with proliferation of dermal spindle cells and some foci of residual leukocytoclastic vasculitis. Oral therapy with dapsone resulted in marked clearing of the cutaneous lesions within few days. This case raises the necessity of histologic confirmation for all cases of suspected Kaposi's sarcoma in patients with acquired immunodeficiency syndrome. We discuss the possible pathogenesis of leukocytoclastic vasculitis in human immunodeficiency virus-infected patients.
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PMID:Erythema elevatum diutinum in a patient with acquired immunodeficiency syndrome. Another clinical simulator of Kaposi's sarcoma. 184 81

Changes in immune competent tissues of the HIV-1-infected person reflect to a certain extent the kind and intensity of immunological dysregulations. The diagnostic approach, however, must include immunophenotyping of cells, immunovirological studies of virus distribution in diseased tissues, and functional tests in addition to classical morphology. The latter technique alone just serves as a crude screening method since structural lesions in lymphoid tissues do not permit discrimination from other HIV-independent immune deficiency and autoimmune disorders. Although the overall appearance of lymph nodes in HIV infection and in chronic autoimmune disorders, such as collagen vascular diseases (e.g., rheumatoid arthritis and systemic lupus erythematosus), is similar, immunophenotyping shows a progressive loss of CD4 cells in HIV infection yet a quantitative increase in this cell population in autoimmune disorders (Krueger 1985a). In addition, there are other persistent active infections by lymphotropic viruses (e.g., EBV or HHV-6) which can cause structural and cellular changes in lymphoid tissues closely resembling HIV-induced lesions (Krueger et al. 1988b; Krueger 1985b). The pathological diagnosis therefore nedds to be supplemented by serological studies and--in selected cases--by in situ hybridization for the demonstration of viral genome. Southern blotting for viral DNA can only detect high numbers of viral genome copies in tissue extracts, not in which cell population the virus resides (e.g., malignant cells vs associated "normal" cells), while the polymerase chain amplification reaction, the most sensitive of all (Buchbinder et al. 1988), cannot yet differentiate between latent and (disease-related) active infection. Taking into consideration the above-described precautions in the evaluation of lymphatic lesions, there are a number of characteristic changes which reflect well the sequelae of HIV infection itself and of the ensuing immune dysregulation. Progressive loss of CD4 cells in the paracortex of lymph nodes and in the peripheral blood leads to inversion of the CD4/CD8 ratio. Loss of demonstrable CD4 cells is probably the consequence not only of cell lysis by HIV-1 infection (note: discrepancy between HIV-1 genome positive cell numbers and depletion of CD4 cells) but also of decreased CD4 marker synthesis in infected cells (Stevenson et al. 1987). In this context it is interesting that Fouchard et al. (1986) were able to show HIV expression in CD8 cells and theorized that these developed from infected CD4 cells which subsequently lost the CD4 epitope and expressed CD8.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Immunological dysregulation of lymph nodes in AIDS patients. 204 8

The presence of antibodies against HTLV-I was investigated with ELISA and Western blot techniques in 76 patients with lymphoproliferative syndromes (n = 53), idiopathic subacute myelopathies (n = 4), chronic T-lymphocytosis (n = 3) and collagen vascular diseases (n = 16) diagnosed in the Barcelona area. 9 HIV seropositive patients were included: 7 with lymphoma, 1 with chronic T-lymphocytosis and 1 with polymyositis. Although 3 samples were repeatedly positive with ELISA, none was confirmed with Western blot. These results suggest that in our country, contrasting with areas where HTLV-I infection is endemic, acute and chronic lymphoproliferative diseases, collagen vascular diseases and demyelinating neurologic diseases are not associated with HTLV-I infection. The development of lymphoma in patients seropositive for HIV also could not be related with HTLV-I infection.
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PMID:[HTLV-I in patients from Barcelona with connective tissue diseases, neurologic demyelinating diseases and lymphoproliferative syndromes]. 238 4

Autoimmunity often precedes the onset of AIDS-related complex or AIDS, and a number of autoantibodies have been described in AIDS patients and persons at risk for AIDS. The presence of such antibodies provokes speculation that autoimmunity is a component of AIDS pathogenesis. We report evidence of an autoantibody (anticollagen) common to all homosexual AIDS patients studied. High titer serum reactivity against collagen was detected in all homosexual AIDS patients, and in HIV+ homosexuals (66%), HIV+ i.v. drug users (38%) HIV- homosexuals (32%), HIV+ transfusion recipients (22%), and HIV+ hemophiliacs (13%), but not in HIV- i.v. drug users, HIV- transfusion recipients, HIV- hemophiliacs, rheumatoid arthritis patients, or controls. Anticollagen reactivity does not correlate with serum IgG levels, so it is not merely a reflection of polyclonal B-cell activation. Titration of anticollagen positive sera typically revealed anticollagen antibody titers 100 times those of normal sera. Affinity purification and immunoblot analysis confirmed the antibody nature of the anticollagen reactivity. The anticollagen antibodies react preferentially with primary determinants of types I and III collagen revealed after heat denaturation. Similar antibodies occur infrequently in rheumatoid arthritis patients, more often on SLE, and frequently in graft vs host disease and lepromatous leprosy. Levels of anticollagen activity in HIV+ i.v. drug users and transfusion recipients correlate with serum beta 2-microglobulin levels, suggesting that those persons with anticollagen antibodies are at greater risk of developing AIDS. This correlation, the fact that anticollagen antibodies occurred in all homosexual AIDS patients tested, and the occurrence of antibodies against denatured collagen in immune disorders with features similar to AIDS suggest these antibodies may be related to disease progression. The association of anticollagen autoantibodies with AIDS and certain other infections and immune disorders may reflect common immunopathogenic features in the etiology of these disorders.
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PMID:Distribution of antibodies against denatured collagen in AIDS risk groups and homosexual AIDS patients suggests a link between autoimmunity and the immunopathogenesis of AIDS. 240 40

Kaposi's sarcoma (KS) in human immunodeficiency virus infection (HIV) has become a rather frequent manifestation of the previously rare disease with fatal outcome. Initial lesions of KS were studied by means of histopathology, immunohistology, and electron microscopy in order to define the earliest alterations. The histopathological changes of initial lesions were distinct, consisting of (1) discrete proliferation of capillary vessels, (2) dissection of collagen by proliferating spindle cells which formed slits, (3) atypical spindle cells arranged in an Indian file pattern, and (4) the lack of any inflammatory cellular infiltrate. Double staining with antibodies against vimentin and immunohistochemical markers for endothelial cells revealed that slits forming vimentin-positive spindle cells displayed laminin, factor VIII, and PAL-E. Atypical vimentin-positive spindle cells arranged in an Indian file pattern inconsistently expressed laminin and factor VIII, but not PAL-E. KS cells rarely stained with the lectin UEA I, not even in case of less advanced dedifferentiation. Electron microscopy showed gradual transformation between spindle cells forming slits and those having lost the ability to form incomplete vessel walls. The present findings support the view that KS develops from the endothelial cells of the blood vessels. The proliferation of atypical endothelial cells as early as in initial lesions and the lack of inflammation favors the primary neoplastic genesis of KS.
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PMID:Initial lesions of HIV-related Kaposi's sarcoma--a histological, immunohistochemical, and ultrastructural study. 332 75

Patients with HIV infection often develop glomerular lesions (focal segmental glomerular sclerosis). Because mesangial expansion (enhanced mesangial cell (MC) growth and matrix accumulation) has been demonstrated to precede the development of focal segmental glomerulosclerosis, we studied the effect of the interaction between HIV-1 proteins such as gp160 envelope protein and macrophages on mesangial cell proliferation and matrix synthesis. We determined the effect of control media, serum-free macrophage supernatant (MSP), and serum-free HIV-1 gp 160 protein-treated MSP (gp 160-MSP) on the proliferation of MC and synthesis of collagen type IV (a component of mesangial matrix). MSP (20%) enhanced (P < 0.01) MC proliferation (control, 7.58 +/- 0.29 versus MSP, 9.06 +/- 0.25 x 10(4) cells/ml), whereas gp 160-MSP (20%) inhibited (P < 0.001) MC proliferation (gp160-MSP, 5.58 +/- 0.14 x 10(4) cells/ml). gp160-MSP modulated MC proliferation in a dose-dependent manner; it enhanced cell proliferation at a lower concentration but inhibited cell proliferation at a higher concentration. Anti-TGF-beta antibody attenuated the effect of gp160-MSP on MC proliferation at lower as well as higher concentrations. Bromodeoxyuridine incorporation studies also showed the modulation of MC proliferation by gp160-MSP. Interaction of other HIV proteins such as HIV-1 Gag4 and HIV-1 Tat with macrophages did not affect MC proliferation when compared with MSP alone. gp160-MSP also enhanced (P < 0.001) synthesis of type IV collagen by MC (control, 467.8 +/- 9.0; MSP, 501.0 +/- 25.0; gp160-MSP, 775.5 +/- 39.0 ng/mg protein). The effect of gp160-MSP on collagen synthesis by MC was dose-dependent. Anti-TGF-beta antibody attenuated the gp160-MSP-induced mesangial cell collagen synthesis. The present study provides a basis for speculation that macrophage-gp160 interaction products have the potential to cause expansion of the mesangium.
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PMID:HIV-1 gp160 protein-macrophage interactions modulate mesangial cell proliferation and matrix synthesis. 749 2


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