Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

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

Perinatal human immunodeficiency virus (HIV) infection is undoubtedly a multifactorial process. Neither the quantity of viremia nor the level of neutralizing antibody in the infected mother is alone predictive of HIV transmission to her offspring. Additional cofactors may include the ability of maternal immunity to control the host cell range and rate of viral replication. The placenta probably constitutes an effective barrier to viral transmission unless disrupted by processes such as syphilis. Prevention of such breaks in the trophoblast barrier and efforts to stimulate maternal and newborn HIV-specific immunity may further decrease the perinatal transmission rate.
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PMID:Perinatal human immunodeficiency virus infection: ruminations on mechanisms of transmission and methods of intervention. 160 37

A competitive polymerase chain reaction (PCR)-based assay for the quantitative detection of human immunodeficiency virus type 1 (HIV-1) viremia was developed and optimized. This method consists of the reverse transcription and subsequent amplification in the same tube of two similar RNA templates, the wild-type template to be quantified and a known amount of the internally deleted synthetic template, both with identical primer recognition sites. The same strategy also proved to be useful in the quantitative assay of HIV-1-specific cellular transcripts and proviral DNA sequences from peripheral blood mononuclear cells by using competitor DNA. The method might be of interest in the study of the precise level of HIV-1 activity during the different clinical phases of the infection and in the simple, fast, and methodologically correct molecular investigation of patients treated with specific antiviral compounds.
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PMID:Absolute quantitation of viremia in human immunodeficiency virus infection by competitive reverse transcription and polymerase chain reaction. 162 31

Feline leukemia virus is a naturally occurring, contagiously transmitted and oncogenic immunosuppressive retrovirus of cats. The effects of FeLV are paradoxical, causing cytoproliferative and cytosuppressive disease (eg, lymphoma and myeloproliferative disorders vs immunodeficiency and myelosuppressive disorders). In the first few weeks after virus exposure, interactions between FeLV and hemolymphatic system cells determine whether the virus or the cat will dominate in the host/virus relationship--persistent viremia and progressive infection or self limiting, regressive infection will develop. The outcome of these early host/virus interactions is revealed in the diagnostic assays for FeLV antigenemia and viremia. The latter, in turn, predict the outcome of FeLV infection in cats. Known host resistance factors include age and immune system functional status. Known virus virulence factors are magnitude of exposure and virus genotype. Molecular analysis of FeLV strains indicated that natural virus isolates exist as mixtures of closely related virus genotypes and that minor genetic variations among FeLV strains can impart major differences in pathogenicity. The genetic coding regions responsible for cell targeting and specific disease inducing capacity (eg, thymic lymphoma, acute immunosuppression, or aplastic anemia) have been mapped to the virus surface glycoprotein and/or long terminal repeat regions for several FeLV strains. Infection by specific FeLV strains leads to either malignant transformation or cytopathic deletion of specific lymphocyte and hemopoietic cell population, changes that prefigure the onset of clinical illness. Another notable feature of the biology of FeLV is that many cats are able to effectively contain and terminate viral replication, an important example of host immunologic control of a retrovirus infection and a process that can be selectively enhanced by vaccination. Thus, FeLV infection serves as a natural model of the multifaceted pathogenesis of retroviruses and as a paradigm for immunoprophylaxis against an immunosuppressive leukemogenic retrovirus.
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PMID:Feline leukemia virus infection and diseases. 166 70

A group of 15 cats experimentally infected with a Swiss isolate of feline immunodeficiency virus (FIV) and a group of 15 FIV-negative control cats were inoculated with an FeLV vaccine containing recombinant FeLV-envelope. High ELISA antibody titer developed after vaccination in FIV-positive and FIV-negative cats. Vaccinated and nonvaccinated controls were later challenge exposed by intraperitoneal administration of virulent FeLV subtype A (Glasgow). Although 12 of 12 nonvaccinated controls became infected with FeLV (10 persistently, 2 transiently), only 1 of 18 vaccinated (9 FIV positive, 9 FIV negative) cats had persistent and 2 of 18 had transient viremia. From these data and other observations, 2 conclusions were drawn: In the early phase of FIV infection, the immune system is not depressed appreciably, and therefore, cats may be successfully immunized; a recombinant FeLV vaccine was efficacious in protecting cats against intraperitoneal challenge exposure with FeLV.
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PMID:Vaccination of cats experimentally infected with feline immunodeficiency virus, using a recombinant feline leukemia virus vaccine. 166 1

Human immunodeficiency virus (HIV) infection causes a number of clinical syndromes and many laboratory abnormalities, often heralding the development of the life-threatening opportunistic infections or malignancies that are known as the acquired immunodeficiency syndrome (AIDS). Drawing heavily on the results of prospective cohort studies, particularly those that my colleagues at the National Cancer Institute and I have conducted, this paper reviews the relationship of AIDS to clinical signs and symptoms, immunologic measures, and viral assays. The risk of AIDS in the next 3 years is at least 25 to 50% for HIV-infected subjects who have oral candidiasis, unexplained fever, unexplained weight loss, a CD4+ lymphocyte count below 200 cells/microliter, or combinations of these. Elevated serum levels of beta 2 microglobulin and neopterin also appear to be strong predictive markers of AIDS, but further work is needed in diverse HIV-infected populations, such as intravenous drug users and persons in pattern II countries, such as Haiti and central Africa. Elevated levels of interferon or HIV-p24 antigen in the serum are insensitive but highly specific AIDS markers that may have predictive value independent of CD4 lymphocyte levels. Several potentially valuable immunologic (immunoglobulin levels, tumor necrosis factor, soluble interleukin 2) and virologic (HIV viremia) assays remain to be thoroughly evaluated or technically simplified. Data from prospective cohort studies have provided clinical and laboratory markers of AIDS risk that have proved essential for therapeutic trials and other clinical decisions. As effective treatments for HIV infection and its complications begin to emerge, these marker data will also prove invaluable for mathematic modeling of the scope, course, and public health response to the epidemic.
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PMID:Prognostic markers for AIDS. 166 94

Sixty-eight adults and nine children infected with human immunodeficiency virus type 1 (HIV-1) were evaluated consecutively for the presence and amount of cell-free infectious virus in their plasma. Viremia was detected in 18 of 68 adults and in five of nine children; titers ranged from 10 to 100,000,000 TCID/ml plasma. Among the adults, none of 19 asymptomatic patients, 4 of 34 AIDS-related complex patients, and 14 of 15 AIDS patients had cell-free infectious virus in their plasma. None of 35 adult subjects with CD4+ lymphocyte counts greater than 400/mm3 were viremic, whereas 3 of 17 with 200-400 CD4+ lymphocytes/mm3 and 15 of 16 individuals with less than 200 CD4+ lymphocytes/mm3 were plasma viremic. In contrast to adults, each of five children infected with HIV-1 in utero or during the perinatal period were plasma viremic regardless of their CD4+ lymphocytes counts (range, 42-2227/mm3), duration of infection, or clinical stage; however, children infected by HIV-1 at older ages were less frequently plasma viremic. Therapy with zidovudine led to a 10- to 10(6)-fold decline in plasma HIV-1 TCID in all eight subjects studied before and after treatment.
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PMID:High-level viremia in adults and children infected with human immunodeficiency virus: relation to disease stage and CD4+ lymphocyte levels. 167 46

To assess the role of maternal viraemia in vertical transmission of HIV and the extent to which viraemia occurs during the various stages of pregnancy, we have attempted to detect human immunodeficiency virus (HIV) in 44 pregnant HIV-1 infected women during 47 pregnancies (30 continued, 17 aborted) and in 30 children and 12 fetuses. Infectious HIV was detected at some time during pregnancy in 59% of women from plasma and in 83% from either peripheral blood mononuclear cells or plasma. HIV was not isolated from any of the newborn babies (0/27) at birth. The mothers had a significantly higher frequency of viraemia during pregnancy than their children had by 6 months of age (p = 0.002); by this time HIV was recovered from 5 (26%) of 19 infants. HIV was not detected by virus isolation, in-situ hybridisation, or polymerase chain reaction (PCR) in 10 fetuses; the other 2 fetuses were positive either by in-situ hybridisation or by PCR but neither result could be confirmed in a second organ or by the other methods of detection. The findings show that there is no consistent spread of HIV across the placenta during maternal viraemia, and indicate that in most cases transmission occurs close to or at delivery.
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PMID:HIV in pregnant women and their offspring: evidence for late transmission. 167 66

It has been shown that only a small fraction of CD4+ T cells are infected with human immunodeficiency virus type 1 (HIV-1) in vivo, particularly early in the course of infection. An even smaller proportion of cells have been shown to be expressing virus. Recent studies suggest that plasma viremia in asymptomatic HIV-infected individuals, representing active viral replication, is more common than was previously believed (range 23-100% of patients). To determine the in vivo state of HIV expression, samples of peripheral blood of 49 HIV-infected individuals at all stages of disease were examined. All subjects were positive for viral DNA by standard polymerase chain reaction (PCR), and a modified PCR was utilized to detect HIV-specific mRNAs (gag, major splice junction, env, and tat/rev). Patient's plasma was also assayed for p24 antigen and viremia. The results were as follows: (formula: see text) Overall, the findings suggest that active viral expression occurs at all stages of HIV infection. In particular, the presence of gag mRNA was determined in only 2 of 14 patients with T4% greater than 30% but in 20 of 35 patients with T4% less than or equal to 30% (p less than 0.05), demonstrating a direct association between the presence of message for a structural protein, and more advanced immunosuppression. Determination of the expression of certain HIV-specific messages from within a patient's cells adds a new dimension to understanding the pathogenesis of HIV infection. The presence of HIV-specific mRNAs, and in particular gag message, in many healthy seropositives may further argue for early initiation of antiviral therapy.
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PMID:Frequent detection of HIV-1-specific mRNAs in infected individuals suggests ongoing active viral expression in all stages of disease. 167 96

The detection of infectious immune complexes in plasma after human immunodeficiency virus (HIV) infection may be useful as a surrogate marker of progression of disease and may help in understanding the pathogenesis of AIDS. Polyethylene glycol (PEG) precipitates of plasma were tested for the presence of HIV p24 antigen and infectious virus. Results were compared with data from cell and plasma cultures, plasma p24 antigen, CD4 cell counts, and stage of disease. PEG precipitation increased the detection rate of the p24 antigen assay from 38.3% to 58.7%. There was a significant correlation between precipitable p24 antigen and plasma viremia, changes in CD4 cell counts, and progression of disease. The sensitivity of the PEG-precipitable p24 antigen assay versus traditional p24 antigen testing was 59.0% and the specificity 91.7%. The assay was reproducible and may be a useful determinant of viral load, clinical progression, and antiretroviral efficacy.
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PMID:Detection of infectious immune complexes in human immunodeficiency virus type 1 (HIV-1) infections: correlation with plasma viremia and CD4 cell counts. 168 Jan 37


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