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Query: UMLS:C0021311 (Infection)
 38,178 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Infection with the human immunodeficiency virus (HIV) ultimately results in profound immunodeficiency characterized by severe depletion of CD4+ T helper cells. In symptomatic infection a general perturbance of immune function is observed. Here recent insights in the sequence of events in progression to AIDS is reviewed. Following seroconversion a rapid persistent loss of inducible B cell function is observed. In addition, in long term infection, antigen-presenting cell functions of monocytes and dendritic cells are increasingly affected. T-cell non-responsiveness, preceding CD4 cell loss, appears to be induced through several different, sequential mechanisms. In early infection, the in-vivo deletion of memory cells can account for the in-vitro decreased responsiveness. Later on in infection, when the balance between memory and naive T cells is normalized, both CD4 and CD8 cells are non-responsive to nominal antigen and low dose anti-CD3 monoclonal antibodies. This anergy is at the level of IL-2 gene expression since early signal transduction events following CD2 and CD2 receptor occupancy are normal. This state of anergy, probably due to inappropriate activation in vivo, may be related to programmed cell death (PCD) observed in vitro for both CD8 and CD4 cells reflecting a systemic interference with maturation and differentiation of T cells. In progression to symptomatic infection, the proportion of non-responsive CD8 cells with immature or activated phenotypes increases and in about fifty percent of the cases, CD4 cell decline may accelerate in association with emergence of syncytium-inducing HIV variants. During this progressive stage, anti-CD3 reactivity is severely decreased, and alloantigen reactivity and finally the capacity to respond to phytohemagglutinin (PHA) are affected. These functional parameters appear useful for staging of HIV-infected individuals and for evaluation of anti-viral therapy.
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PMID:Immunological abnormalities in the natural history of HIV infection: mechanisms and clinical relevance. 135 68

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.
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PMID:Detection of human immunodeficiency virus type 2 in brain tissue. 135 28

Infection with human immunodeficiency virus type 1 leads to a persistent but progressive cytopathic process that culminates in the near complete destruction of the CD4+ subset of T cells. The levels of human immunodeficiency virus type 1 replication and virus burden increase throughout the clinical course of disease reflecting a balance between the viral and cellular regulatory influences as well as the ability of the host immune system to eliminate infected T cells. Human immunodeficiency virus type 1 replication is dependent on the state of cellular activation and involves both inducible host cell derived transcription factors and at least three virus-derived gene products. Further study of the mechanism of action of these factors, particularly those encoded by the virus, may facilitate the future development of highly specific and effective therapies for human immunodeficiency virus type 1.
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PMID:Molecular insights into human immunodeficiency virus type 1 pathogenesis. 135 48

Infection by the human immunodeficiency virus is associated with polyclonal B cell activation and increased levels of serum IgA. In order to characterize the molecular species of serum IgA, we have measured total IgA, IgA1, and IgA2 in sera from 60 HIV-1-infected patients and 40 healthy controls. In addition, secretory IgA (S-IgA), secretory IgM (S-IgM), free immunoreactive secretory component (SC), and the distribution of monomeric and polymeric IgA were determined. The data confirm the elevation of total serum IgA levels in HIV-1-infected patients, and both IgA1 and IgA2 concentrations are elevated. Furthermore, the data show a substantial increase in serum levels of both monomeric and polymeric IgA. Serum S-IgA levels were significantly increased in CDC group II patients versus controls and more frequently elevated in CDC group IV patients. The highest S-IgA levels were found among patients with the lowest blood CD4+ cell counts. Serum S-IgA levels were not correlated with serum levels of either total IgA or polymeric IgA. Serum S-IgM levels were also increased in HIV-1-infected patients and positively correlated with serum S-IgA levels. Conversely, serum levels of free SC were not altered. An increase in serum S-IgA was not related to human hepatitis B virus infection and/or to hepatic dysfunction or to diarrhea or overt intestinal infection. The data indicate that secretory Ig (S-IgM and S-IgA), which are likely to be produced at mucosal sites, increase in the serum of HIV-1-infected patients.
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PMID:Secretory immunoglobulins in serum from human immunodeficiency virus (HIV)-infected patients. 135 13

The gastrointestinal tract is considered to be a major route of infection for human immunodeficiency virus (HIV). Infection of human colon epithelial cells by HIV is not blocked by anti-CD4 antibodies known to block infection of lymphoid cells (J. Fantini, N. Yahi, and J. C. Chermann, Proc. Natl. Acad. Sci. USA 88:9297-9301, 1991), suggesting the presence of an alternate receptor for HIV on these cells. In this report, we show that (i) a monoclonal antibody specifically directed against galactosyl ceramide inhibited the infection of HT29 cells by two markedly different strains of HIV-1, as assessed by polymerase chain reaction amplification and reverse transcriptase assay; (ii) this antibody strongly labeled the surface of HT29 cells by immunofluorescence and electron microscopic immunolocalization; (iii) the labeling was preferentially but not totally restricted to the basolateral membrane domain of differentiated colonic cells, in agreement with the ability of HIV to infect both the apical and basolateral surfaces of these epithelial cells; and (iv) in thin-layer chromatography-immunostaining experiments with neutral glycolipids prepared from HT29 cells, the antibody specifically reacted with a ceramide monoglycoside fraction corresponding to galactosyl ceramide. We did not detect this glycolipid in lymphoid cells, and anti-galactosyl ceramide antibodies consistently failed to inhibit HIV infection of these cells. These data suggest that galactosyl ceramide (or a derivative) is an essential component of the receptor for HIV on the surface of HT29 cells.
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PMID:Galactosyl ceramide (or a closely related molecule) is the receptor for human immunodeficiency virus type 1 on human colon epithelial HT29 cells. 137 11

Acquired immunodeficiency syndrome (AIDS) is caused by infection with a pathogenic human retrovirus known as human immunodeficiency virus (HIV). Approximately 1 million people are currently infected with HIV in the United States, with 8 to 10 million infected individuals worldwide. The virus is transmitted predominantly through genital sexual contact, although orogenital spread has been rarely reported. Heterosexual transmission has been most common in the Third World, whereas male homosexual transmission has predominated in the United States and western Europe. Transmission through homosexual contact has been steadily declining over the past 5 years as transmission through illicit intravenous drug use and promiscuous unprotected heterosexual activity has increased. Sexually transmitted diseases that cause inflammatory or ulcerative lesions of the genital tract act as important cofactors in increasing the risk of transmission through sexual contact. Perinatal transmission of HIV occurs in approximately 30% of infants born to infected mothers. Transmission to infants through breast-feeding has also been documented. Health care workers have been infected with HIV through accidental high-risk percutaneous or mucous membrane exposures, albeit at a low transmission rate of 0.3%. Infection of patients by infected health care professionals is a rare event, having been reported only once in 10 years of the epidemic. Infection with HIV results in a chronic lifelong infection. The major targets for HIV are CD4+ T-helper lymphocytes and cells of monocyte/macrophage lineage. Infection of the T-helper lymphocyte ultimately results in the death of the cell. Over time (measured in years), a progressive destruction of the T-helper lymphocyte population occurs, which results in profound immune suppression. Infection of monocytes/macrophages is not cidal, but these cells do have functional alterations as a result of the infection, which may contribute to the immune deficiency. In addition, chronically infected tissue macrophages may act as an important reservoir for HIV, particularly in the central nervous system. Infection of the T-helper lymphocytes and monocytes/macrophages is mediated through attachment of HIV through a specific binding interaction between CD4 expressed in the plasma membrane of these cells and a surface glycoprotein on the virus, gp120. Once the virus nucleocapsid (core particle) enters the cytoplasm of the target cell, the viral RNA genome is reverse transcribed by a reverse transcriptase enzyme into proviral DNA. This proviral DNA migrates into the nucleus where it integrates into the host cellular genome, which results in a chronically infected cell.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:AIDS: Part I. 139 37

Infection from human immunodeficiency virus (HIV) is well known for the particular host susceptibility to a variety of opportunistic infections and unusual malignant neoplasms. Although no tumor develops exclusively in concomitance with HIV infection, malignancies in these patients have different clinical behaviour, response to treatment and prognosis than the pattern observed in HIV negative hosts. Kaposi's sarcoma (EKS) and non-Hodgkin's lymphoma (NHL) are tumors per se diagnostic of AIDS in patients with HIV infection. From 1987 to 1991, 210 HIV positive patients underwent ENT examination without symptom-related selection: 128 were intravenous drug users, 50 homosexual males, 22 heterosexuals, 4 intravenous male homosexual drug users, 3 blood recipients and 3 subjects without known risk factors. Sixteen were allocated in group II, 37 in III, 9 in IV A, 2 in IV B, 31 in IV C1, 37 in IV C2, 48 in IV D and 30 in IV E. Fourteen had head and neck EKS localization. All were males, with a median age of 40 of which 11/14 were homosexuals. The concomitant involvement of skin and mucosa was the most common manifestation and the palate was the most frequently affected mucosal site. Twenty-four had NHL localized within the head and neck: 21 males and 4 females with a average age of 38, 10 intravenous drug users, 9 homosexual males, 3 heterosexuals, 1 blood recipient, 1 subject without known risk factors. Extranodal localization was the most frequent characteristic while the gums were the most commonly involved site. The main characteristics of head and neck manifestations of EKS and NHL are reported with references to literature. The majority of HIV infected patients with EKS or NHL have ENT localizations, perhaps because lymphatic tissue, a HIV target, is well represented in this area and contamination by infectious agents (such as Epstein-Barr virus and cytomegalovirus, probably involved in the pathogenesis of EKS and NHL) can easily occur in the head and neck. The otolaryngologist should be aware of the various, and sometimes misleading, characteristics of these diseases.
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PMID:[The cervicofacial manifestations of Kaposi's sarcoma and of non-Hodgkin's lymphomas in HIV-infected patients]. 141 19

We report two cases and review the characteristics of pyomyositis. The courses of patients who presented with pyomyositis at the Maricopa Medical Center (Phoenix) are detailed. Ninety-eight reported cases over the last 20 years in North America, found through a MEDLINE search, are summarized. Infection with the human immunodeficiency virus (HIV) may predispose the patient to pyomyositis. The onset is usually insidious with progression to large purulent collections and significant morbidity. The diagnosis is frequently suggested by findings of imaging studies. Staphylococcus aureus is responsible for most cases in tropical areas but is less frequently associated with cases in North America. Since infection with HIV predisposes patients to bacterial infections, pyomyositis will occur more frequently in this patient population. Increased awareness of the disease will improve management. Following aspiration or surgical drainage, therapy with broad-spectrum empirical antibiotics may be considered initially in the treatment of pyomyositis.
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PMID:Pyomyositis in North America: case reports and review. 142 Jun 80

Infections with Geotrichum species, although rare, are sometimes seen in immunocompromised hosts. We report a case of oral geotrichosis in a patient seropositive for human immunodeficiency virus who had erythematous mandibular and maxillary gingiva but was otherwise free of any active systemic disease. Geotrichum candidum was shown by both culture and histopathology to be present in the lesion and was deduced to be the causative organism. The patient responded well to several weeks of treatment involving oral topical administration of nystatin vaginal tablets.
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PMID:Oral Geotrichum candidum infection associated with HIV infection. A case report. 143 44

Infection with human immunodeficiency virus (HIV) results in progressive deterioration of the cell-mediated immune system characterized by T-helper-cell dysfunction and loss in the face of signs of generalized immune-system activation. The final stage of HIV disease, AIDS, has a myriad of opportunistic infections and malignancies as its hallmarks. The causal relationship between HIV and this complex disease pattern is clear but the mechanisms by which it occurs are not well understood. There are a number of new developments in our understanding of the natural history of HIV infection from a laboratory standpoint. Our review of this information raises further questions as to the validity of the conventional "cytopathic" model and all its direct descendants. In response to these conflicts, we have developed and present an alternative hypothesis in which AIDS pathogenesis, in all its manifestations, is seen as the outcome of one central process, excess immune activation generated by the interaction of virus with the CD4 receptor. The implications of this hypothesis on therapy of HIV infections are discussed.
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PMID:The natural history and pathogenesis of HIV infection. 144 66


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