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

4000 sera were tested for antibodies against hepatitis C virus (HCV) by means of an ELISA using the C100-3 antigen. 38.9% of patients with non-A, non-B hepatitis following blood transfusion (n = 108) had HCV antibodies. Among patients with chronic liver damage of unknown origin (n = 316) 30.4% were anti-HCV positive, and in 2,506 patients with transitional or chronic elevation of transaminases 14.8% showed HCV antibodies. Haemophiliacs (n = 26) with 65.4% anti-HCV positives and drug addicts (n = 46) with 56.5% anti-HCV positives had the highest prevalence among high risk groups. Addicts dying from drug abuse (n = 216) and HIV 1 positives (n = 127) were anti-HCV positive in 37.5% and 26.0%, respectively. Patients on haemodialysis (n = 331) had antibodies against HCV in 12.4%. Health care workers (n = 217) appear to be at a comparably low risk with only 2.8% anti-HCV positives. Up to now we could not find a single case of intrafamilial spread of HCV in 46 examined cases. We suggest that HCV infectivity of contaminated body fluids and blood is lower than that of hepatitis B virus or human immunodeficiency virus type 1 carriers. In suspected non-A, non-B hepatitis negative test results should be confirmed in a second sample because it may take three to six months after infection before HCV antibodies occur. However, about 10% of chronic HCV infections are not detectable with the presently available test. This may change when new tests become available using HCV specific antigens other than C100-3.
Infection
PMID:Hepatitis C virus antibodies among different groups at risk and patients with suspected non-A, non-B hepatitis. 171 Oct 18

Infection of macaque monkeys with the simian immunodeficiency virus of macaques (SIVmac) results in disease similar to human AIDS. Therefore, the macaque monkey is proving to be an important model for testing the effectiveness of various AIDS vaccine approaches. A detailed analysis of the cellular immune responses is necessary for the evaluation of candidate vaccines. However, this has not been possible in macaques, due, in part, to the unknown nature of the MHC molecules that restrict their T lymphocytes. In our report we demonstrate that a particular MHC class I molecule involved in the rhesus monkey's effector T lymphocyte response to SIVmac is expressed at a high frequency in a colony of rhesus monkeys. SIVmac-infected monkeys that express this MHC class I molecule all develop CTL that are restricted by that molecule and recognize an identical nine amino acid epitope of the SIVmac gag protein. This MHC class I molecule has been defined as an HLA-A homolog by cDNA cloning and sequencing. It has also been expressed in an MHC class I-deficient cell line to demonstrate directly the cloned molecule's capacity to bind and present peptide Ag to CTL. These studies illustrate that AIDS virus-specific CTL can be characterized in detail in the rhesus monkey and lay the foundation for exploring novel approaches to AIDS virus vaccination in this species.
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PMID:Definition of an epitope and MHC class I molecule recognized by gag-specific cytotoxic T lymphocytes in SIVmac-infected rhesus monkeys. 171 Oct 81

Infection of embryonic bovine lung (EBL) cells by bovine immunodeficiency-like virus (BIV) were monitored by reverse transcriptase (RT), syncytia formation and polymerase chain reaction (PCR). Infection can be detected by PCR at 24 h while the presence of syncytia and RT were not detected until much later. The detection of BIV RT can be optimized by changing the pH and salt conditions. The enzyme is very sensitive to changes in pH but can tolerate a wider range of salt and MgCl2 concentrations. Infection of primary human cell cultures by BIV was monitored by both PCR and RT. No active infection of human cells were detectable.
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PMID:Comparative evaluation of bovine immunodeficiency-like virus infection by reverse transcriptase and polymerase chain reaction. 171 14

The gastrointestinal tract is considered to be a major route of infection for the human immunodeficiency virus (HIV). To understand the interaction of HIV with epithelial cells of the intestinal mucosa, we have studied the infection of a human colon cancer cell clone HT-29-D4. The enterocyte-like differentiation of this clone can be modulated in vitro according to the concentration of glucose. We show that: (i) undifferentiated HT-29-D4 cells can be infected by HIV types 1 and 2 (HIV-1 and HIV-2) strains with no subsequent effect on cell growth; (ii) undifferentiated HT-29-D4 cells express a CD4-related antigen bearing epitopes of the immunoglobulin-like variable (V) region domains V1 and V2 of CD4 but lacking the epitope known to be involved in HIV envelope recognition; (iii) differentiated HT-29-D4 cells can be infected by HIV after an interaction with either the apical brush border membrane (luminal side) or the basolateral side (serosal side); (iv) the CD4-like molecule is restricted to the basolateral domain of differentiated cells; and (v) the infection is not inhibited by anti-CD4 monoclonal antibodies (mAbs) OKT4, OKT4A, Leu-3a, Bl4, 13-B-8-2, S-T4 or S-T40. We conclude that epithelial intestinal cells may represent a major site of entry for HIV. Infection of these epithelial cells may occur via the basolateral membrane by HIV-bearing lymphocytes or macrophages of the lamina propria and via the apical membrane by HIV present in the bowel lumen. This infection may remain silent for up to 9 months, and the virus can be rescued by cocultivation with lymphoid cells. These data may give an explanation for the long latent seronegative state that may occur in a HIV-infected individual.
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PMID:Human immunodeficiency virus can infect the apical and basolateral surfaces of human colonic epithelial cells. 171 4

Infection of human peripheral blood lymphocytes by human immunodeficiency virus type 1 (HIV-1) was investigated by means of 1H nuclear magnetic resonance spectroscopy, taking advantage of the presence of signals from fluid lipid domains in the membrane of stimulated lymphocytes. A transient decrease of the lipid methylene signal intensity was observed at the time of HIV internalization, monitoring a general rearrangement of membrane structure associated with virus entry. A similar effect was also observed a few days after infection, when HIV particles are released by infected cells as demonstrated by high reverse transcriptase activity in cell supernatant. Signals arising from choline-based metabolites were also affected by HIV infection, indicating a possible slowing down of phospholipid synthesis.
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PMID:Metabolic and structural effects of HIV infection in human peripheral blood mononuclear cells can be monitored with 1H NMR spectroscopy. 172 52

Human epidermal Langerhans cells play an important role in the immunoregulation of the skin. We measured the numbers of CD(3+)-, CD(8+)-, CD1a(+)-, HLADR(+)-, IL2R(+)-, CD(4+)- and CD68 positive cells in the skin of 8 asymptomatic HIV-infected Persons, 3 Patients with AIDS and 11 healthy volunteers by suction blister technique. Our results indicate increased numbers of CD1a+ cells and increased numbers of CD4+ cells in the epidermis in asymptomatic HIV-infection. At the same time CD68+ cells are decreased already in an early stage of HIV-Infection. The number of CD1a/CD4+ cells is related to the degree of immunodeficiency. This fact might be caused by the activation of MPS.
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PMID:[Lymphocytes, Langerhans cells and CD68-positive monocytes/macrophages in the skin of HIV-infected patients and normal controls]. 172 11

Some neonates with congenital human immunodeficiency virus type 1 (HIV-1) infection exhibit immune dysregulation. This suggests that fetal CD4+ cells, possibly thymocytes, may be infected during gestation. If thymocytes are infected, this may result in a disruption of T-cell differentiation. To examine this hypothesis, normal human fetal thymocytes were established in tissue culture, characterized, and then exposed to HIV-1. On initial isolation, fetal thymocytes were analyzed for phenotypic markers by flow cytometry and assessed for T-cell function by mitogen-stimulated thymidine incorporation. The thymocytes comprised greater than 70% double positive (CD4+, CD8+) cells and responded to T- but not to B-cell mitogens. Thereafter, thymocytes were incubated in either tissue culture medium containing infectious HIV-1 or in control (HIV-free) medium. Infection of fetal thymocytes was determined by light and electron microscopy in combination with immunocytochemistry, molecular hybridization, and an infectious cell center (ICC) assay. After 1 week in culture, the thymocytes exposed to HIV-1 were positive by immunocytochemistry for the HIV-1-associated protein gp41. In addition, the presence of HIV-1 DNA was detected by molecular hybridization confirming infection of these cells. The ICC assay demonstrated the production of infectious HIV-1 particles and budding of mature virions was observed by electron microscopy. These studies demonstrate that human fetal thymocytes can be infected with HIV-1 in vitro and that this infection results in production of infectious virions. These results support the hypothesis that vertical transmission of HIV-1 in vivo may result in the infection of fetal thymocytes, which may contribute to postnatal HIV-1-associated pathologic conditions.
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PMID:HIV-1 infection of human fetal thymocytes. 173 92

Infection with the human immunodeficiency virus type 1 (HIV-1) can cause a spectrum of renal disease, termed acquired immunodeficiency syndrome (AIDS) nephropathy. The most common clinical manifestations of kidney involvement in HIV-1-infected patients are proteinuria and/or nephrotic syndrome, and the histopathological pattern usually reveals focal segmental glomerulosclerosis. We describe an 8-year-old child with AIDS who presented with recurrent gross hematuria. A kidney biopsy demonstrated IgA nephropathy. This unique case indicates that the range of kidney disease in HIV-infected children may be broader than originally thought, and that these patients warrant a complete evaluation of any renal abnormality.
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PMID:IgA nephropathy in a child with human immunodeficiency virus type 1 infection. 176 86

Infection with the human immunodeficiency virus (HIV) results in severe damage to the immune system and consequent disease (AIDS) after a long and variable incubation period (on average 8-10 years). Why the incubation period should be so long is a puzzle. We outline an explanation based on the dynamics of the interplay between the immune response and antigenic variation in the virus population. The essential idea is that AIDS results when the diversity of antigenic variants of HIV in an infected patient exceeds some threshold, beyond which the immune system can no longer cope. The paper develops a simple mathematical model for this process, based on experimental observations, and explores several ramifications.
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PMID:Mathematical biology of HIV infections: antigenic variation and diversity threshold. 180 71

The ability of a variety of epithelial, embryonal, placental, and neuronal cells to express the CD4 antigen and to be infected by human immunodeficiency virus 1 (HIV-1) was examined. Only two (IMR-32 and HeLa-T4) expressed CD4 detectable by indirect immunofluorescence, and both were infectable by HIV-1. Two others, a human laryngeal carcinoma (HEp-2) and human colonic carcinoma (HT-29), did not express CD4 antigen but were infectable by HIV-1. Infection of the HEp-2 cells was detectable four months (and 20 serial passages) later. Infection of HEp-2 cells was not inhibited by anti CD4 monoclonal antibody but was by the lectin concanavalin A. These results suggest the presence of a receptor other than CD4 can be involved in HIV-1 infection.
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PMID:Growth of human immunodeficiency virus I in cultured cells in the absence of the CD4 antigen. 180 30


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