Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0021051 (immunodeficiency)
 71,517 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The tyrosine protein kinase p56lck, specifically expressed in lymphoid cells, undergoes modifications of its autophosphorylation and kinase activity when these cells are triggered by mAbs to the T cell determinants. The kinase activity and the autophosphorylation of p56lck were analysed following triggering Jurkat cells with the human immunodeficiency virus (HIV) glycoprotein gp160 which interacts with CD4: both the autophosphorylation and the kinase activity are increased within 1-5 min following addition of gp160, this increase is maximum at 5 min and is followed by a gradual return to the basal level within 2 h. Similar to observations made with anti-CD4 mAbs the increase in kinase activity of p56lck is not associated with changes in the gel mobility nor is it associated with T cell activation. Triggering of T cells with a combination of anti-CD3 mAbs which activate T cells but not p56lck and gp160 greatly potentiated the increase of p56lck autophosphorylation and kinase activity.
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PMID:Interaction of human immunodeficiency virus glycoprotein 160 with CD4 in Jurkat cells increases p56lck autophosphorylation and kinase activity. 153 87

An enlargement of the thymus suggesting a tumor was discovered in a 28-year-old man who had early-stage acquired immune deficiency syndrome. A biopsy was performed. The adipose involuted thymus, with persistence of many Hassall's corpuscles, was judged to be a large lymphoid follicular hyperplasia. This follicular hyperplasia was similar to that previously described for lymph nodes, spleen, and other lymphoid tissues at earlier stages of human immunodeficiency virus infection, before the development of acquired immune deficiency syndrome. Human immunodeficiency virus RNA and p24 human immunodeficiency virus protein were detected in the hyperplastic germinal centers (lymphocytes and follicular dendritic infected cells), and also in many cells that may have been either lymphocytes and/or epithelial cells in the interfollicular areas. The tissue was negative for Epstein-Barr virus DNA sequences, as determined by the polymerase chain reaction. These observations identify the first state of infection of the thymus in a human immune deficiency virus-infected adult, preceding the severe involution with lymphoid depletion observed in all fatal cases of acquired immunodeficiency syndrome in which the thymus has been analyzed.
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PMID:Thymic pseudotumorous enlargement due to follicular hyperplasia in a human immunodeficiency virus sero-positive patient. Immunohistochemical and molecular biological study of viral infected cells. 154 67

We studied visual impairment caused by benign lymphoid infiltration of the vitreous bilaterally, as a complication of a primary immunodeficiency, X-linked immunodeficiency with increased IgM in an 8-year-old boy. Immunophenotyping of a vitreous aspirate showed a mixed cell population, including lymphocytes (T helper, suppressor-cytotoxic T cells, and B cells) and macrophages. Cultures of the vitreous were negative for bacterial or fungal pathogens. The vitreous infiltrates have been resistant to treatment with corticosteroids and cytotoxic agents.
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PMID:Cellular infiltration of the vitreous in a patient with X-linked immunodeficiency with increased IgM. 155 Jan 86

Patients infected with the human immunodeficiency virus (HIV) are subject to infections and neoplasms, which frequently result in palpable or radiologically identified masses. Fine-needle aspiration (FNA) offers a rapid, simple, and cost effective approach for diagnosis of these masses. During a 2-yr period, 396 aspirates were performed on 362 HIV-infected patients within the LAC-USC Medical Center. Adequate material was obtained from 84% of the FNA, allowing the etiology of the mass to be determined in 90% of the cases by means of a combination of cytologic, microbiologic, and immunocytochemical procedures. Significant pathologic processes identified in these patients by means of FNA included reactive lymphoid proliferations (35%), abnormal lymphoid proliferations (12%), infections (12.5%), cystic (5.5%) and inflammatory processes (5%), nonlymphoid malignancies (4%), and salivary gland pathology (1%). We conclude that FNA is an appropriate initial diagnostic procedure in HIV positive patients presenting with mass lesions.
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PMID:A review of the fine-needle aspiration cytology findings in human immunodeficiency virus infection. 155 65

Immunodeficiency with hyper-IgM (HIM) is a rare disorder characterized by recurrent infections associated with low IgG and IgA, and normal to increased IgM serum levels. Both primary and secondary forms of HIM syndrome have been reported. Among primary HIM syndrome, evidence for genetic heterogeneity is provided by the occurrence of the disease as X-linked, autosomal recessive, or autosomal dominant trait. The most common clinical manifestations include upper and lower respiratory tract infections, otitis, diarrhoea, oral ulcers, lymphoid hyperplasia, and autoimmunity. Recurrent neutropaenia is a frequent finding. Immunological abnormalities consist of lack of IgG and IgA secretion, and failure to respond to vaccination. Lymph nodes show absence of germinal centres. Few patients with a concurrent T-cell defect, and clinical expression of combined immune deficiency, have been reported. The gene responsible for the X-linked HIM syndrome (HIGM1) has been tentatively assigned to Xq24-27. However, carrier detection and prenatal diagnosis are not yet possible. Pathogenetic hypotheses include failure of B-cell differentiation, and defective regulation of immunoglobulin isotype switching due to abnormal T-cell-mediated signals. Treatment is mainly based upon regular administration of intravenous immunoglobulins. Steroids may be useful in the treatment of neutropaenia and of severe autoimmune manifestations.
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PMID:Immunodeficiency with hyper-IgM (HIM). 155 97

The histopathologic investigation of children with congenital immunodeficiency, and its relation to functional parameters and clinical data have been a major contribution to the present knowledge on the histophysiologic aspects of normal immune system function. Based on thorough knowledge in histophysiologic and dynamic aspects of lymphoid organs, the histopathologic evaluation in cases of suspected immunodeficiency today forms an integral part of the assessment of the immune status. Apart from conventional histologic techniques, advanced technology such as immunohistochemistry and in situ hybridization is applied. This enables analysis of the basic cellular components in various lymphoid tissue compartments, and evaluation of the consequences of the deficiency by the assessment of microorganisms and neoplasia. This review focuses on the histopathologic contribution to immunodeficiency evaluation. Sections deal with (1) the description of alterations in the various lymphoid tissues (bone marrow, thymus, lymph node, spleen, and gastrointestinal tissue); (2) histopathology of infection and malignancy; (3) pathology of some types of congenital immunodeficiency; (4) histopathologic methods and reagents; and (5) an autopsy protocol for immunodeficiency.
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PMID:Pathology of congenital immunodeficiencies. 156 87

Simian immunodeficiency virus (SIV) is a designation for a group of related but unique lentiviruses identified in several primate species. A viral isolate from a rhesus macaque (i.e., SIVmac) causes a fatal AIDS-like disease in experimentally infected macaques, and several infectious molecular clones of this virus have been characterized. This report presents the complete nucleotide sequence of molecularly cloned SIVmac1A11, and comparisons are made with the sequence of molecularly cloned SIVmac239. SIVmac1A11 has delayed replication kinetics in lymphoid cells but replicates as well as uncloned SIVmac in macrophage cultures. Macaques infected with virus from the SIVmac1A11 clone develop antiviral antibodies, but virus does not persist in peripheral blood mononuclear cells and no disease signs are observed. SIVmac239 infects lymphoid cells, shows restricted replication in cultured macrophages, and establishes a persistent infection in animals that leads to a fatal AIDS-like disease. Both viruses are about 98% homologous at the nucleotide sequence level. In SIVmac1A11, the vpr gene as well as the transmembrane domain of env are prematurely truncated, whereas the nef gene of SIVmac239 is prematurely truncated. Sequence differences are also noted in variable region 1 (V1) in the surface domain of the env gene. The potential implications of these and other sequence differences are discussed with respect to the phenotypes of both viruses. This animal model is critically important for investigating the roles of specific viral genes in viral/host interactions that cannot be studied in individuals infected with the human immunodeficiency virus (HIV).
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PMID:Genetic and biological comparisons of pathogenic and nonpathogenic molecular clones of simian immunodeficiency virus (SIVmac). 157 Nov 98

The Acquired Immunodeficiency Syndrome (AIDS) has involved the pediatric age group and is especially prevalent in babies born of mothers who are intravenous drug abusers or prostitutes. Approximately 30% of children born to mothers who are seropositive for the human immunodeficiency virus (HIV) will develop HIV infection. There are several important differences in children and adults with AIDS. The incubation period of the disease is shorter, and initial clinical manifestations occur earlier in children. In addition, certain infections are more common in children, and the different types of malignancy, especially Kaposi's sarcoma, are unusual in the pediatric age group. The altered immune system involves both T cells and humoral immunity and increases susceptibility to a variety of infections, particularly opportunistic organisms. In this publication the complications of pediatric AIDS involving the lungs, cardiovascular system, gastrointestinal tract, genitourinary system, and neurological system are described. The most common pulmonary complications in our experience are Pneumocystis carinii pneumonia and pulmonary lymphoid hyperplasia. The spectrum of cardiovascular involvement in pediatric AIDS includes myocarditis, pericarditis, and infectious endocarditis. Gastrointestinal tract involvement is usually due to opportunistic organisms that produce esophagitis, gastritis, and colitis. Abdominal lymphadenopathy is a common finding either due to disseminating Mycobacterium avium-intracellulare infection or nonspecific lymphadenopathy. Although cholangitis is more commonly seen in adults, it may occur in children with AIDS and, in most cases, is due to related opportunistic infections. Genitourinary infections may be the first evidence of HIV disease. Cystitis, pyelonephritis, renal abscesses, and nephropathy with renal insufficiency are complications of pediatric AIDS. A variety of neurological abnormalities may occur in pediatric AIDS. The most common cause of neurological dysfunction in children with AIDS is HIV neuropathy. We present the many complications of AIDS in children demonstrated by a variety of imaging modalities, emphasizing the importance of diagnostic imaging in children with this disease.
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PMID:Radiology of AIDS in the pediatric patient. 157 31

Penicillium marneffei is a rare human pathogen predominantly affecting residents of South-east Asia. We report four fatal cases from Hong Kong in human immunodeficiency virus-infected patients. The diagnosis was established by histological examination and confirmed by isolation of the fungus. The infection was disseminated with involvement of lymph nodes, liver, spleen, lung, intestine and bone marrow. The involved organs showed an exclusively anergic tissue reaction characterized by a diffuse infiltrate of fungi-laden macrophages, multiple co-existing opportunistic infections and lymphoid cell depletion. This organism has to be distinguished from Histoplasma capsulatum and Pneumocystis carinii. Establishment of the diagnosis is important not only because this infection is potentially curable, but also it is a likely indicator disease of AIDS in South-east Asia. Penicilliosis marneffei should be suspected in any symptomatic HIV-positive patient who comes from or has visited endemic areas of South-east Asia.
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PMID:Disseminated Penicillium marneffei infection in HIV-infected subject. 157 8

Neurological disease resulting from lentivirus (including human immunodeficiency virus) infections is usually caused by a strain of virus that replicates productively in microglia in vivo and in macrophage cultures in vitro. We undertook this study using the model of simian immunodeficiency virus in macaques (SIVmac) to test the hypothesis that macrophage tropism is a prerequisite for neurotropism of the virus. Using molecularly cloned SIVmac239, a virus which is lymphocyte- but not macrophagetropic, we showed that this virus failed to infect brain after intracerebral (i.c.) inoculation into two macaques. Rather, these inoculations resulted in disseminated infection in lymphoid organs and the bone marrow. Two sequential passages of infected bone marrow cells inoculated i.c. into new macaques resulted in severe neurological disease and classical neuropathological lesions. Virus obtained from affected brain answered the hypothetical question: it was neurotropic and macrophagetropic. New findings in the study were that both lymphocyte- and macrophage-tropic viruses were present in the animals, but the viruses localized in different tissues: the lymphotropic virus in the spleen, lymph nodes, and plasma and the macrophagetropic virus in the brain and lungs. To determine whether the brain virus was preferentially neurotropic and whether it had neuroinvasive properties, infectious brain homogenate was inoculated into one animal i.c. and into two others peripherally. The i.c. inoculated animal developed fatal encephalitis 5 months later, and examination of tissues showed cell-free virus only in brain homogenates. Only microglia were infected despite persistent viremia and infection in bone marrow cells. The two macaques inoculated peripherally remained healthy and were euthanized at 6 months. Virus replication was detected only in the bone marrow cells and peripheral blood mononuclear cells. No infection in any macrophage population in visceral organs was detected, and the virus did not invade the brain. The strictly microglial specificity of this virus suggested that different macrophage populations in the body may select specific phenotypes of lentivirus from the quasispecies of virus in the bone marrow. This could provide the basis for specific disease affecting different organ systems.
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PMID:Derivation of neurotropic simian immunodeficiency virus from exclusively lymphocytetropic parental virus: pathogenesis of infection in macaques. 158 23


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