Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 20 de 29
Filtrar
1.
AIDS ; 3(4): 239-41, 1989 Apr.
Artículo en Inglés | MEDLINE | ID: mdl-2500958

RESUMEN

Using immunohistochemical staining, in situ hybridization and a combination of both, we demonstrate here the replication of HIV in the endometrial stroma. Infected cells do not belong to the T-lymphocyte lineage but rather to a monocyte-macrophage cell type. This report suggests a possible relationship between HIV infection and endometritis. Moreover, HIV replication in endometrial tissues could play a role in heterosexual and materno-fetal transmission.


Asunto(s)
Síndrome de Inmunodeficiencia Adquirida/complicaciones , Endometritis/complicaciones , Endometrio/microbiología , VIH/fisiología , Adulto , Endometrio/patología , Femenino , VIH/genética , Humanos , Técnicas para Inmunoenzimas , Inmunohistoquímica , Macrófagos/microbiología , Monocitos/microbiología , Hibridación de Ácido Nucleico , Sondas ARN , Linfocitos T/clasificación , Replicación Viral
2.
AIDS ; 5(6): 741-5, 1991 Jun.
Artículo en Inglés | MEDLINE | ID: mdl-1679334

RESUMEN

Recent epidemiological and virological data suggest that the incidence of maternofetal transmission of HIV-1 infection is between 20 and 30%. The available evidence points to a possible role of peri- and postnatal contamination, but the isolation of HIV from fetuses shows that transplacental transmission also occurs. We attempted to detect, by means of an immunohistochemical method, HIV proteins in frozen placentas from 75 HIV-1-positive women (30 at term, 45 induced abortions). In addition, in situ hybridization using HIV-specific probes was performed in three cases. Neither HIV proteins nor nucleic acid sequences were detected, but CD4+ mononuclear cells were present in the chorion and villi, regardless of the clinical and biological status of the mother (particularly in the nine cases in which the infants were infected). There are several possible mechanisms involving the placenta in the maternofetal transmission of HIV, including active transport of the HIV-immunoglobulin G complex via Fc receptors on trophoblastic cells, passive transplacental passage of HIV during a viraemic episode, the passage of infected maternal cells, and infection of the placenta itself. The methods we used could not rule out the presence of HIV DNA provirus within the genome of placental cells. In any event, immunohistochemical detection of HIV proteins in the placenta is not a technique suitable for the prenatal diagnosis of HIV infection or for identifying newborns likely to develop HIV infection.


Asunto(s)
Infecciones por VIH/transmisión , VIH-1 , Placenta/microbiología , Complicaciones Infecciosas del Embarazo/microbiología , Proteínas de los Retroviridae/análisis , Adulto , Linfocitos T CD4-Positivos/microbiología , Femenino , Productos del Gen gag/análisis , Antígenos VIH/análisis , Proteína p24 del Núcleo del VIH , Infecciones por VIH/microbiología , Humanos , Inmunohistoquímica , Hibridación de Ácido Nucleico , Placenta/química , Placenta/patología , Embarazo , Estudios Prospectivos , Proteínas del Núcleo Viral/análisis , Proteínas del Envoltorio Viral/análisis , Productos del Gen gag del Virus de la Inmunodeficiencia Humana
3.
Neurology ; 40(6): 944-8, 1990 Jun.
Artículo en Inglés | MEDLINE | ID: mdl-2161093

RESUMEN

We observed 3 cases of progressive multifocal leukoencephalopathy (PML) among frozen CNS samples obtained at autopsy from 102 adult AIDS patients. In 2 patients, PML was associated with severe HIV encephalitis. In those 2 cases, the areas of extensive JC-induced demyelination were massively infiltrated by HIV infected macrophages/microglial cells with evidence for localized increase of HIV encephalitis in PML lesions. Using immunohistochemistry and in situ hybridization, we demonstrated that each virus infects, in a latent or productive fashion, different CNS cell populations. Therefore, the extension of HIV encephalitis could not be related to an intracellular transactivation of 1 virus by the other. However, the results are consistent with dissemination of viral infection by the recruitment of HIV-infected macrophages to damaged areas of the brain. This phenomenon might be generalized to other pathogens that are frequently associated with HIV CNS infection. Early detection and treatment of opportunistic CNS lesions could be important to prevent extension of HIV encephalitis.


Asunto(s)
Infecciones por VIH/complicaciones , Leucoencefalopatía Multifocal Progresiva/etiología , Infecciones Tumorales por Virus/complicaciones , Complejo SIDA Demencia/complicaciones , Adulto , Encéfalo/inmunología , Encéfalo/patología , Antígenos VIH/análisis , Infecciones por VIH/inmunología , Infecciones por VIH/metabolismo , Humanos , Inmunohistoquímica , Virus JC/inmunología , Virus JC/aislamiento & purificación , Leucoencefalopatía Multifocal Progresiva/inmunología , Leucoencefalopatía Multifocal Progresiva/metabolismo , Macrófagos/patología , Masculino , Infecciones Tumorales por Virus/inmunología , Infecciones Tumorales por Virus/metabolismo
4.
Neurology ; 43(8): 1492-9, 1993 Aug.
Artículo en Inglés | MEDLINE | ID: mdl-8351001

RESUMEN

We performed a postmortem morphometric study in six AIDS patients and six controls to determine if a neocortical neuronal loss occurs in HIV-1-associated cognitive/motor complex. Patients were selected during a prospective study including psychometric evaluation and neuroimaging, and none had focal lesions. Two had HIV-1-associated myelopathy with mild cognitive impairment, and four had HIV-1-associated dementia complex. Planimetry did not show any cerebral atrophy. Cortical thickness, mean neuronal size, and mean neuronal densities in Brodmann's areas 4, 9, and 40 were not statistically different in patients and controls. There were no significant changes in neuronal densities of columnar and laminar samples, indicating that there was neither global nor selective neuronal loss. HIV-1-associated cognitive/motor complex is not necessarily related to neocortical neuronal loss, but could be due to subcortical lesions or metabolic dysfunction.


Asunto(s)
Corteza Cerebral/patología , Trastornos del Conocimiento/diagnóstico , Infecciones por VIH/diagnóstico , Trastornos del Movimiento/diagnóstico , Adulto , Corteza Cerebral/diagnóstico por imagen , Trastornos del Conocimiento/etiología , Infecciones por VIH/complicaciones , Infecciones por VIH/diagnóstico por imagen , Infecciones por VIH/patología , Humanos , Hígado/patología , Masculino , Persona de Mediana Edad , Trastornos del Movimiento/etiología , Neuronas/diagnóstico por imagen , Neuronas/patología , Estudios Prospectivos , Radiografía
5.
Eur J Obstet Gynecol Reprod Biol ; 28(2): 133-5, 1988 Jun.
Artículo en Inglés | MEDLINE | ID: mdl-3402652

RESUMEN

PIP: Since an estimated 1-2 million heterosexual women in Africa are infected with human immunodeficiency virus (HIV), maternal-fetal transmission of this virus is a serious issue. At this point, the only accurate data concern the high level of virus transmission from infected mothers to the newborn (at least 40%) and the severity of infection in infants. About 50% of infected infants develop acquired immunodeficiency syndrome, generally at 6 months of age, and die by the age of 3-4 years. There have been no studies large enough to determine the time of HIV transmission--antenatal, prepartum, or postpartum? Also unclear at this point are the consequences of pregnancy for the immunological status for women infected with HIV. Amniocentesis, cord blood punction, and trophoblastic biopsy are potential means of diagnosing HIV infection prenatally; however, there is a risk of infecting the fetus by the techniques themselves, a danger of false negative results and a likelihood that HIV infection can occur later in pregnancy after the tests have been completed.^ieng


Asunto(s)
Síndrome de Inmunodeficiencia Adquirida/transmisión , Intercambio Materno-Fetal , Complicaciones Infecciosas del Embarazo/transmisión , Síndrome de Inmunodeficiencia Adquirida/diagnóstico , Síndrome de Inmunodeficiencia Adquirida/epidemiología , Adulto , África , Europa (Continente) , Femenino , VIH/aislamiento & purificación , Humanos , Masculino , Embarazo , Complicaciones Infecciosas del Embarazo/diagnóstico , Factores de Riesgo , Estados Unidos
6.
Rev Neurol (Paris) ; 149(1): 37-45, 1993.
Artículo en Francés | MEDLINE | ID: mdl-8337560

RESUMEN

In 10 children infected by HIV at birth, who presented early and severe immunodeficiency encephalopathy, the lesions observed in the central nervous system were different from those found in adults. Using standard neuropathological techniques, the main abnormalities were white matter palor and atrophy, pyramidal tract demyelination, moderate perivascular inflammation, numerous calcifications of blood vessels in basal ganglia, white matter and occasional in the cortex, few opportunistic infections including cytomegalovirus ventriculitis, polymorphonuclear microabcessses and aspergillus abscesses; no toxoplasma was detected. An 18-month-old girl presented with an angiocentric lymphoproliferative disorder in central and peripheral nervous system and muscle, with predominance of B cells. In most cases, low levels of HIV replication were detected in brain tissue, as demonstrated by the presence of only few microglial nodules and giant cells, feeble detection of HIV p24 and p17 antigens by immunocytochemistry, in situ hybridization of HIV DNA and RNA and polymerase chain reaction, despite severe clinical encephalopathy. Zidovudine did not improve any patient. In children with severe AIDS encephalopathy, HIV might not be directly implicated in the central nervous system lesions: an intermediate factor such as cytokines or another toxic substance secreted by activated macrophages and/or lymphocytes, could induce severe lesions in the central nervous system and minor pathology of the peripheral nervous system and muscles.


Asunto(s)
Encefalopatías/patología , Infecciones por VIH/patología , Infecciones Oportunistas Relacionadas con el SIDA/complicaciones , Aspergilosis/complicaciones , Atrofia , Encefalopatías/etiología , Preescolar , Femenino , Infecciones por VIH/complicaciones , Infecciones por VIH/congénito , Humanos , Lactante , Recién Nacido , Masculino
7.
Rev Neurol (Paris) ; 143(10): 631-42, 1987.
Artículo en Francés | MEDLINE | ID: mdl-3423582

RESUMEN

Post-mortem study of every patient who died from AIDS in Pitié-Salpêtrire Hospital from June 1984 to November 1985 was performed without regard to the presence of neurological signs and symptoms. Autopsy were performed in 31/48 cases. Patients had been hospitalized in the Departments of Parasitology-Infectious Disease (24 cases) Internal Medicine (4 cases) and Neurology (3 cases). In every case, formalin-fixed material from the brain and the spinal cord were embedded in paraffin (20 samples), stained with hematoxylin-eosin, PAS, Alcian blue, Giemsa, Grocott and Ziehl techniques and Bodian's silver impregnation along with Luxol fast blue, and, in celloïdin (8 samples), stained with hematoxylin-eosin and Loyez' impregnation. There were 30 men (27 caucasian, 1 egyptian, 1 haïtian, 1 senegalese) and one woman (congolese). Twenty eight (28) patients were homosexuals. AIDS was transfusion-associated in two cases. Neurologic complications revealed the disease in 2 cases. Eighteen (18) patients had neurological signs or symptoms before death. Age range at death was 22-58 (mean 38). Brain weight in AIDS (from 1150 gms to 1750 gms-mean 1428 gms) was not statistically different from the mean weight of 100 male patients in the same age range autopsied in the same laboratory during the identical period (mean 1427 gms, standard deviation: 23). Microscopic abnormalities were present in every brain examined. These included non-Hodgkin lymphoma (3 cases), opportunistic infections (21 cases: 13 toxoplasmosis, 4 cytomegalovirus encephalitis, 3 cryptococcal meningitis, 1 infection by mycobacterium avium-intracellulare), and subacute encephalitis (17 cases, 9 isolated, 8 associated with other disorders). The characteristic changes consisted of lympho-monocytic focal infiltrates (so-called microglial nodules) and mild lympho-monocytic perivascular cuffs in 10 cases. Typical giant cells were seen only in one case. Mild demyelinating changes were also seen in only one case. No spinal cord spongiosis, nor Progressive Multifocal Leukoencephalopathy was found. HIV localization was performed on frozen sections utilizing in situ hybridization techniques (2 cases) and immunohistologic techniques (5 cases). HIV, RNA and proteins, was detected in 2 cases with subacute encephalitis. Infected cells were labeled with macrophage markers, and rarely with T4 lymphocyte markers. Infected astrocytes (identified by anti-GFAP serum) or neurons (identified by anti-NSE serum) were never observed. No giant cells were seen in these two cases.


Asunto(s)
Síndrome de Inmunodeficiencia Adquirida/patología , Encefalopatías/patología , Encéfalo/patología , Síndrome de Inmunodeficiencia Adquirida/complicaciones , Adulto , Encefalopatías/etiología , Enfermedades del Sistema Nervioso Central/patología , Femenino , Humanos , Masculino , Persona de Mediana Edad , Estudios Prospectivos
8.
Rev Neurol (Paris) ; 150(2): 123-32, 1994.
Artículo en Francés | MEDLINE | ID: mdl-7863152

RESUMEN

We report the natural history of 17 brain lymphomas (11 primary, 6 disseminated) from a post-mortem series of 130 patients with AIDS. Primary lymphomas appeared lately in the course of AIDS. They were often associated with a severe T-cell immunodepression and with more frequent opportunistic disorders than disseminated lymphomas. Associated Kaposi's sarcomas were surprisingly frequent. All patients presented with neurological manifestations. Heterogeneous features were seen at CT examination. The CSF was abnormal in 12/13 cases, with an increase of protein contents and secretion of immunoglobulins; it contained activated lymphocytes in 5/6 cases of disseminated lymphomas, and malignant cells in only one case. Cellular density never exceeded 8/mm3 for primary lymphomas, and the lymphocytes were considered normal. The pre-mortem diagnosis of cerebral lymphomas was made in five patients, with a time lapse of 1 to 7 months between the first neurological symptoms and death, and of 5 to 30 days between the diagnosis and death. Cerebral biopsy was diagnostic in 4 cases of primary cerebral lymphomas. In only 1/6 patients with disseminated lymphomas, the diagnosis had been made when the patient was still alive, based on CSF and bone marrow lymphomatous infiltrations. The diagnosis of cerebral lymphoma (7 primary, 5 disseminated) was post-mortem in 12 cases. It was made only at microscopic examination in 2/12 cases of primary lymphomas. The histopathological study frequently showed a multicentric involvement, and always an immunoblastic cell type with plasmablastic differentiation and frequent medium size cells. Marked gliosis and significant necrosis were often observed. Neuropathological lesions associated with HIV-1 infection (toxoplasmosis, CMV and HIV-1 encephalitis) were seen in 8 cases with primary lymphomas.


Asunto(s)
Neoplasias Encefálicas/diagnóstico , Linfoma Relacionado con SIDA/diagnóstico , Sarcoma de Kaposi/etiología , Adulto , Neoplasias Encefálicas/etiología , Humanos , Linfoma Relacionado con SIDA/complicaciones , Linfoma Relacionado con SIDA/patología , Masculino , Persona de Mediana Edad , Neoplasias Primarias Múltiples/diagnóstico , Enfermedades del Sistema Nervioso/etiología , Sarcoma de Kaposi/diagnóstico
9.
J Neuroradiol ; 17(4): 233-54, 1990.
Artículo en Inglés, Francés | MEDLINE | ID: mdl-1709207

RESUMEN

Progressive multifocal leukoencephalopathy (PML) is a demyelinating disease which occurs in immunodepressed subjects and is particularly frequent in AIDS. Some authors having drawn attention to the protean aspect of the disease and claimed that AIDS may lose its basic characteristics and affect the grey matter as well as the white matter, we reviewed a series of 8 patients who had been biopsied and/or autopsied and had been examined at least once by MRI. In this series, contrary to what is regularly observed in toxoplasmic abscesses we did not find any lesion of the grey matter or any mass effect. On the other hand, we confirmed that PLM is not multifocal in all cases and that it course may be interrupted by prolonged remissions. The MRI criteria for PML therefore are reliable, provided multiple T2-weighted slices in coronal plane are performed, clearly showing the anatomy of the white fibres affected. However, it must be borne in mind that HIV-infected patients often have other associated brain pathologies, especially when the immune deficiency increases.


Asunto(s)
Síndrome de Inmunodeficiencia Adquirida , Leucoencefalopatía Multifocal Progresiva/patología , Imagen por Resonancia Magnética , Síndrome de Inmunodeficiencia Adquirida/patología , Adulto , Biopsia , Encéfalo/patología , Diagnóstico Diferencial , Encefalitis/patología , Infecciones por VIH/patología , Humanos , Leucoencefalopatía Multifocal Progresiva/diagnóstico , Leucoencefalopatía Multifocal Progresiva/diagnóstico por imagen , Masculino , Microscopía Electrónica , Persona de Mediana Edad , Sensibilidad y Especificidad , Coloración y Etiquetado , Tomografía Computarizada por Rayos X
10.
Bull Acad Natl Med ; 174(6): 807-10; discussion 811, 1990.
Artículo en Francés | MEDLINE | ID: mdl-2271986

RESUMEN

Human immunodeficiency virus type I (HIV), the etiology of AIDS is also the cause of a primary infection of the central nervous system. The AIDS Dementia Complex is a common and important cause of morbidity in patients in advanced stages of infection. Subacute encephalitis demonstrating, the neuropathogenicity of HIV 1 constitute an human model for slow virus encephalitis.


Asunto(s)
Complejo SIDA Demencia , Complejo SIDA Demencia/fisiopatología , Síndrome de Inmunodeficiencia Adquirida/fisiopatología , Encefalitis/fisiopatología , Humanos
12.
Pathobiology ; 59(4): 214-8, 1991.
Artículo en Inglés | MEDLINE | ID: mdl-1883516

RESUMEN

HIV induces severe dementia in about 20% of adult AIDS patients. In children HIV-infected at birth, the incidence of specific neurological complications is still higher since severe encephalopathy occurs in almost all children who develop an early and severe immunosuppression. In all cases, the brain monocytes/macrophages and the microglial cells are the only cells which replicate HIV in the central nervous system (CNS) of these patients, and the appearance of neurological symptoms seems induced by an interaction between HIV-infected macrophages with neurons and glial cells. AIDS encephalopathy is related to two properties of HIV: to the viral tropism for monocytes/macrophages/microglial cells, which allow the brain infection, and to HIV tropism for CD4+ lymphocytes responsible for the appearance of immunosuppression, which trigger viral dissemination in the CNS. However, childhood encephalopathy is not always associated with HIV replication in the CNS at the time of death, and mild dementia in HIV-infected adults were described without signs of HIV replication in autopsy CNS samples. Those findings suggest that persistent, productive viral infection is not required for the development of HIV encephalopathy. Therefore, if the relationship between HIV CNS infection and AIDS encephalopathy in adults and children is clearly demonstrated, the pathogenesis of the neurological disease and the kinetics of HIV replication in the CNS are unclear. In addition, the very high incidence of AIDS encephalopathy in children could be related to HIV infection of microglia which is differentiating in fetal or newborn brain.


Asunto(s)
Complejo SIDA Demencia/microbiología , Adulto , Encéfalo/microbiología , VIH/aislamiento & purificación , Humanos , Lactante , Macrófagos/microbiología , Monocitos/microbiología , Neuroglía/microbiología
13.
Cell ; 57(7): 1155-65, 1989 Jun 30.
Artículo en Inglés | MEDLINE | ID: mdl-2736624

RESUMEN

By in situ hybridization analysis and immunoprecipitations following transfection of COS cells, we show that the Rev protein of the human immunodeficiency virus is necessary for envelope protein expression, which is correlated with the appearance in the cytoplasm of envelope-specific RNA. In the absence of cotransfection with a plasmid expressing Rev, envelope-specific RNA is retained in the nucleus. Several cis-acting sites in the envelope are involved, one of which is between nucleotides 7330 and 7735 and is required for the response to Rev. Other sequences (nucleotides 5797-7330 and 7735-7989) are involved in the apparent retention of the envelope-specific RNA in the nucleus in the absence of Rev and its response element. Because Rev affects the localization of envelope RNA both in the presence and in the absence of the normal splice sites on the RNA, the mechanism of Rev action is independent of splicing.


Asunto(s)
Genes Virales , VIH/genética , ARN Viral/metabolismo , Proteínas del Envoltorio Viral/genética , Compartimento Celular , Núcleo Celular/metabolismo , Citoplasma/metabolismo , Análisis Mutacional de ADN , Regulación de la Expresión Génica , Glicoproteínas/genética , Hibridación de Ácido Nucleico , Procesamiento Postranscripcional del ARN , Empalme del ARN , Secuencias Reguladoras de Ácidos Nucleicos
14.
Acta Neuropathol ; 81(5): 496-502, 1991.
Artículo en Inglés | MEDLINE | ID: mdl-1650111

RESUMEN

In addition to muscle changes due to peripheral nervous system involvement, primary myopathic changes associated with the human immunodeficiency virus (HIV) have also been described. We studied seven cases: two had developed an acquired immunodeficiency syndrome (AIDS), four had seroconverted to HIV but were otherwise asymptomatic, one was HIV seronegative when the biopsy was performed and one was biopsied twice. Besides the HIV no other infectious agent was detected. Muscle biopsies showed: (a) muscle fiber necrosis and regeneration; (b) inflammatory changes with moderate perivascular infiltration; and (c) unusual myofibrillary disorganization. Immunocytochemical techniques using anti-HIV monoclonal antibodies showed the presence of the virus in one biopsy. HIV-RNA was detected by in situ hybridization in the same biopsy. With both techniques the HIV was detected in isolated mononuclear cells in the muscle endomysium and not within the muscle fibers. Muscle involvement associated with HIV infection may be related, at least in some cases, to the presence of the virus in interstitial cells.


Asunto(s)
Síndrome de Inmunodeficiencia Adquirida/patología , Músculos/patología , Síndrome de Inmunodeficiencia Adquirida/microbiología , Adulto , Infecciones por Citomegalovirus/patología , Histocitoquímica , Humanos , Inmunohistoquímica , Microscopía Electrónica , Músculos/microbiología , Hibridación de Ácido Nucleico , Toxoplasmosis/patología
15.
Arthritis Rheum ; 37(6): 846-54, 1994 Jun.
Artículo en Inglés | MEDLINE | ID: mdl-7516162

RESUMEN

OBJECTIVE: To study the distribution of intercellular adhesion molecule receptor (ICAM-R, or ICAM-3), a novel ligand for the leukointegrin lymphocyte function-associated antigen 1 (LFA-1), in normal and rheumatoid synovial membranes and to compare this with the distribution of ICAM-1, ICAM-2, vascular cell adhesion molecule 1 (VCAM-1), and endothelial leukocyte adhesion molecule 1 (ELAM-1). METHODS: We performed immunohistochemical analyses of frozen sections of normal and rheumatoid synovial tissue using monoclonal antibodies to the molecules examined. RESULTS: ICAM-1 staining was detectable on the vascular endothelium and the synovial lining cells of both normal and rheumatoid synovial membranes. A variable proportion of lymphocytes infiltrating rheumatoid tissues expressed ICAM-1, ICAM-2 staining was demonstrable in the vascular endothelium of both normal and inflamed tissues, the latter demonstrating a significantly higher proportion of positive vessels. ELAM-1 staining was not detectable in normal synovial membranes but was seen on the endothelium of a limited number of rheumatoid synovial vessels, usually close to the synovial lining cell layer. VCAM-1 staining was intense in both normal and rheumatoid synovial lining cells, but vascular staining was weak in both. In contrast, ICAM-R staining was not detected in association with any synovial blood vessels, but was widely expressed by lymphocytes and macrophages. Cells of the lining layer did not stain for ICAM-R. CONCLUSION: Although ICAM-R is a ligand for LFA-1 and shares considerable sequence homology with ICAM-1 and ICAM-2, it does not appear to be expressed by the endothelium of normal or inflamed synovial vessels. Intense expression of ICAM-R by rheumatoid synovial lymphocytes and macrophages suggests that it may play a role in processes requiring cell-cell contact, such as antigen presentation and homotypic aggregation.


Asunto(s)
Antígenos CD , Artritis Reumatoide , Moléculas de Adhesión Celular/análisis , Membrana Sinovial/química , Artritis Reumatoide/patología , Selectina E , Endotelio Vascular/química , Humanos , Molécula 1 de Adhesión Intercelular , Linfocitos/química , Membrana Sinovial/patología , Molécula 1 de Adhesión Celular Vascular
16.
J Infect Dis ; 166(4): 888-91, 1992 Oct.
Artículo en Inglés | MEDLINE | ID: mdl-1356128

RESUMEN

Infection due to human immunodeficiency virus (HIV) type 2 is believed to cause a clinical picture similar to that of HIV-1, although extensive data are not available. In 2 patients with West African exposure and neurologic symptoms, HIV-2 was detected in the central nervous system using DNA and RNA polymerase chain reaction, in situ hybridization, and immunohistology. In the first patient, the neurologic disease was most likely due to productive infection with HIV-2. In the second, a combination of neuropathologic abnormalities (including the presence of HIV-2) explained the clinical features. Thus HIV-2, like HIV-1, can be readily detected in brain tissue in patients with neurologic abnormalities, although the exact role of HIV-2 in pathogenesis of AIDS-associated neurologic disease requires further study.


Asunto(s)
Encefalopatías/microbiología , Infecciones por Deltaretrovirus/microbiología , VIH-2/aislamiento & purificación , Adulto , Anciano , Secuencia de Bases , ADN Viral/análisis , Femenino , Humanos , Masculino , Datos de Secuencia Molecular , Reacción en Cadena de la Polimerasa , ARN Viral/análisis
17.
Am J Pathol ; 148(2): 465-72, 1996 Feb.
Artículo en Inglés | MEDLINE | ID: mdl-8579109

RESUMEN

Intercellular adhesion molecule-3 (ICAM-3) was identified as the third counter-receptor for lymphocyte function-associated antigen-1. ICAM-3 is absent on endothelial cells in normal tissues but found on endothelial cells in lymphomas. Here, we examined ICAM-3 expression on vascular endothelial cells in lymphomas, nonlymphoid malignancies, benign tumors, and inflammatory diseases. We compared the expression of ICAM-3 on endothelial cells with the severity of inflammatory infiltrates and with the presence of E-selectin and VCAM-1. We found that ICAM-3 expression on endothelial cells was high on both benign and malignant tumors whereas it was low in inflammatory diseases. In contrast to E-selectin, ICAM-3 expression on endothelial cells was not correlated to the severity of inflammatory infiltrates. In hemangiomas, we showed by Northern blot analysis and immunocytochemistry that ICAM-3 expression was induced and that it was localized in immature areas that sustain the early stages of angiogenesis. Therefore, expression of ICAM-3 on blood vessels does not seem to play a role in the recruitment of leukocytes during inflammation but rather is correlated with angiogenesis and tumor development.


Asunto(s)
Antígenos CD , Antígenos de Diferenciación , Moléculas de Adhesión Celular/biosíntesis , Endotelio Vascular/metabolismo , Inflamación/metabolismo , Linfoma/metabolismo , Neoplasias/metabolismo , Biomarcadores de Tumor , Northern Blotting , Moléculas de Adhesión Celular/análisis , Selectina E/análisis , Selectina E/biosíntesis , Endotelio Vascular/citología , Hemangioma/química , Hemangioma/metabolismo , Enfermedad de Hodgkin/metabolismo , Humanos , Técnicas para Inmunoenzimas , Tejido Linfoide/metabolismo , Linfoma/química , Linfoma no Hodgkin/metabolismo , Neovascularización Patológica/fisiopatología , Molécula 1 de Adhesión Celular Vascular/análisis , Molécula 1 de Adhesión Celular Vascular/biosíntesis
18.
Am J Pathol ; 139(6): 1273-80, 1991 Dec.
Artículo en Inglés | MEDLINE | ID: mdl-1750503

RESUMEN

To investigate the mechanism of simian immunodeficiency virus (SIV) entry into the central nervous system (CNS) and the initial events leading to neuropathogenesis, SIV replication was studied by in situ hybridization in the CNS of 5 Rhesus macaques at 7 days, 1, 2, and 3 months after SIV intravenous inoculation. CNS infection was found to be a frequent and early event, as SIV was detected in the CNS of all the animals studied and as early as 7 days postinoculation. At the earliest stage, the infection localized mainly to perivascular cells. Using combined immunohistochemistry and in situ hybridization, infected cells were shown to express the CD68 marker, suggesting that infected mononuclear phagocytes crossing the blood-brain barrier represent the main source of virus in the CNS. Early viral replication coincided with neuropathologic changes, consisting in gliosis, perivascular infiltrates and rare glial nodules. Immunophenotyping of brain tissue showed that increased macrophage infiltration, microglial reactivity and MHC class II induction occurred within the first week of infection, indicating a possible immunopathologic mechanism in early CNS pathogenesis.


Asunto(s)
Encéfalo/microbiología , Síndrome de Inmunodeficiencia Adquirida del Simio/microbiología , Virus de la Inmunodeficiencia de los Simios/fisiología , Replicación Viral , Animales , Encéfalo/fisiopatología , Femenino , Inmunohistoquímica , Inmunofenotipificación , Macaca mulatta , Sistema Nervioso/patología , Hibridación de Ácido Nucleico , ARN Viral/análisis , Síndrome de Inmunodeficiencia Adquirida del Simio/patología , Virus de la Inmunodeficiencia de los Simios/genética , Virus de la Inmunodeficiencia de los Simios/aislamiento & purificación
19.
Cancer Detect Prev ; 16(5-6): 341-5, 1992.
Artículo en Inglés | MEDLINE | ID: mdl-1473123

RESUMEN

To establish an animal model of AIDS, two different "wild" or "adapted" HIV2 Rod and Eho strains were cultivated on monkey cells from different species (baboons, cynomolgus, Rhesus monkeys). Five different available strains were then injected both by intravenous (i.v.) and intracerebral (i.c.) route into ten Rhesus monkeys. Seven animals seroconverted between days 13 and 230. Reverse transcriptase activity in the lymphocyte culture supernatants was detectable in six of the seven animals that seroconverted, and in one animal that remained seronegative. Lymphopenia and a decrease in the CD4+ cell counts were observed in eight animals. One animal, inoculated with HIV2-Rod "wild type," developed a severe cachexia, with dyspnea, and associated neurological symptoms 150 days after inoculation. This animal was sacrificed on day 220. Pathological examination showed typical lesions of actinomycetes infection in the lungs and in the meninges. Another monkey had significant weight loss associated with lymphadenopathies and pancytopenia. These results suggest that in vivo replication of HIV2 in Rhesus monkeys may induce clinical symptoms of immune deficiency. This method is reproducible and may provide a good model for AIDS.


Asunto(s)
Infecciones por VIH/fisiopatología , VIH-2/patogenicidad , Animales , Relación CD4-CD8 , Modelos Animales de Enfermedad , Anticuerpos Anti-VIH/metabolismo , Infecciones por VIH/microbiología , VIH-2/crecimiento & desarrollo , Macaca mulatta , Replicación Viral
20.
Br J Haematol ; 57(4): 563-9, 1984 Aug.
Artículo en Inglés | MEDLINE | ID: mdl-6743572

RESUMEN

We present the results of the immunohaematological tests performed in an unselected group of patients with acute leukaemia at the time of diagnosis, and when possible the follow-up in remission and/or in relapse. Thirteen out of the 112 patients tested had a positive Coombs test at the time of diagnosis and, in six patients, the Coombs test became positive during remission. All the 19 positive Coombs test were of the complement type with, in 11 cases, an anti-I antibody eluted from the patient's RBC. There was no relationship between the FAB morphologic subtype, the presence of other immune abnormalities, the course of the leukaemia and the immunohaematological abnormalities. Several hypotheses on the possible relationships between the acute leukaemias and the immunohaematological abnormalities are discussed.


Asunto(s)
Prueba de Coombs , Leucemia/inmunología , Adulto , Anciano , Aglutininas/análisis , Autoanticuerpos/análisis , Proteínas del Sistema Complemento , Crioglobulinas , Femenino , Humanos , Masculino , Persona de Mediana Edad , Pronóstico
SELECCIÓN DE REFERENCIAS
DETALLE DE LA BÚSQUEDA