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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fifty AIDS patients were investigated for human cytomegalovirus (HCMV) viraemia when potentially HCMV-related clinical symptoms or syndromes were observed. Nine patients underwent prolonged virologic follow-up, while 41 additional patients were examined only once or sporadically. Concentrated preparations of polymorphonuclear leukocytes (PMNL) from 153 blood samples were obtained for monitoring: (1) early virus isolation in cell cultures 24 h p.i. (viraemia); (2) early structural antigen detection in cytospin preparations (antigenemia); and (3) HCMV DNA in blood (DNAemia) through DNA amplification by the polymerase chain reaction (PCR). Viraemia and antigenemia were quantitated, whereas evaluation of DNAemia was only qualitative. A good correlation between levels of viraemia and antigenemia was consistently found except during ganciclovir treatment. HCMV-related clinical symptoms were observed when the number of infected PMNL was greater than 100 per 2 x 10(5) cells examined. All 56 blood samples positive for viraemia and antigenemia were also PCR-positive, whereas 44 samples (39 of which taken from patients with ascertained HCMV infection in blood) were positive by PCR only. Viraemia and antigenemia were often unrelated to HCMV organ syndromes, such as retinitis, in which only DNAemia was often detected. Prolonged ganciclovir treatment kept viraemia, antigenemia and even DNAemia at a low or negative level, yet drug discontinuation led to rapid progression of HCMV infection in blood. In addition, prolonged antiviral treatment could induce appearance of ganciclovir-resistant HCMV strains, requiring alternative foscarnet therapy. In conclusion, determination of viraemia and antigenemia appears essential for correct clinical management and antiviral treatment of disseminated HCMV infections in AIDS patients. However, PCR is the most sensitive method for diagnosis and monitoring of HCMV infections in blood at a pre-clinical stage.
Mol Cell Probes 1991 Oct
PMID:Early virus isolation, early structural antigen detection and DNA amplification by the polymerase chain reaction in polymorphonuclear leukocytes from AIDS patients with human cytomegalovirus viraemia. 166 8

Normal feline bone marrow-derived macrophages released maximum concentrations of interleukin-6, tumor necrosis factor, and interleukin-1 when stimulated with ImuVert (Cell Technology Inc, Boulder, CO, USA) at dosages of 1.0 microgram/ml, 5.0 micrograms/ml, and 10.0 micrograms/ml, respectively. When ImuVert was administered to healthy adult cats, significant elevations in rectal temperature and neutrophil counts were observed 10 and 24 hours after each treatment. Weekly treatment with ImuVert failed to prevent or reverse viremia in cats when initiated prior to or 6 weeks after inoculation with feline leukemia virus.
Mol Biother 1991 Dec
PMID:Evaluation of a biologic response modifier derived from Serratia marcescens: effects on feline macrophages and usefulness for the prevention and treatment of viremia in feline leukemia virus-infected cats. 176 75

Infection with the macaque strain of the simian immunodeficiency virus (SIVmac) induces simian immunodeficiency syndrome in rhesus macaques. This report describes the isolation and identification of antigenic variants of SIVmac in one of the infected monkeys (macaque #22803). Eight naive rhesus monkeys were inoculated with a titered viral stock of the molecularly cloned SIVmac239. Standard serological analysis revealed that all but two were seroconverted. Western blot analysis confirmed the seronegativity of macaque #22803. In addition, sera recovered from this monkey were not able to neutralize the parent SIVmac239. However, virus could be isolated from all of the infected animals, including macaque #22803. Sera recovered were reactive to the autologous virus. The results suggest that the virus from macaque #22803 may have undergone extensive antigenic shift in vivo. To test this hypothesis, a portion of the gag gene was amplified by the polymerase chain reaction (PCR), cloned, and sequenced. Sequence analysis revealed amino acid changes that were clustered between amino acids 200-245. Evaluation of the possible selective pressures contributing to the observed viral mutation revealed that in comparison with the other SIVmac239-infected monkeys, macaque #22803 produced an unusually high T cell proliferative response toward mitogen stimulation before infection, and continued to display a persistently high plasma viremia titer after infection.
Cell Mol Biol Res 1994
PMID:Emergence of antigenic variants of simian immunodeficiency virus (SIVmac) in a seronegative macaque after SIVmac239 infection. 778 84

The nef gene is conserved throughout the primate lentivirus family. Although dispensable in vitro, an important role for nef in vivo is suggested by the failure of SIV nef mutants to establish persistent viraemia. Although the biochemical function of the Nef protein remains equivocal, a consistent theme has emerged with the reproducible observation that Nef expression results in the down-modulation of the cell surface marker CD4. Down-modulation requires amino acid sequences within the cytoplasmic domain of CD4 but occurs by a mechanism distinct from the normal serine phosphorylation-dependent pathway. As CD4 is a transmembrane glycoprotein and Nef a myristoylated protein targeted to the cytoplasmic face of the plasma membrane we considered that a direct interaction between Nef and CD4 might play a role in down-modulation. Here we demonstrate that a baculovirus-expressed Nef-GST fusion protein interacts specifically with CD4. This interaction requires co-expression in the same cell and is dependent on Nef myristoylation. The site of Nef interaction maps to the cytoplasmic domain of CD4, as a deletion mutant lacking this domain fails to interact with Nef. This observation sheds new light on the biochemical function of Nef and offers new opportunities for the future development of HIV chemotherapy.
J Mol Biol 1994 Aug 12
PMID:Myristoylation-dependent binding of HIV-1 Nef to CD4. 805 54

Endogenous proviruses of the Moloney murine leukemia retrovirus (Mo-MuLV) are transcriptionally blocked in early embryos and in general remain silent even when the tissues have become permissive to the expression of newly integrated copies. Eventually, activation in presumably very few cells initiates rapid superinfection leading to viremia and leukemia, but the processes leading to provirus activation are unknown. Differences in the onset and development of viremia between several mouse strains carrying an endogenous Mo-MuLV (Mov lines) are attributed to a chromosomal position effect, but neither cell type nor stage of provirus activation is known for any strain. We have now monitored the appearance of viral transcripts and particles in the Mov13 strain, which carries the Mo-MuLV provirus in inverted orientation in the first intron of a collagen gene (Col1a1) with well-characterized transcriptional activity. We report obligatory tissue- and stage-specific virus activation in osteoblasts and odontoblasts. The significance of this activation pattern is indicated by the fact that of the great variety of cells expressing the wild-type collagen gene, only these two cell types can also transcribe the mutant allele including its viral insert. We propose that this transcription of the proviral genome, albeit in the opposite direction, leads to the activation of the viral promoter.
Mol Cell Biol 1996 Jan
PMID:Tissue- and stage-specific activation of an endogenous provirus after transcription through its integration site in the opposite orientation. 852 19

SIVsm chronically infected cultures were obtained after infection of CEMX174 cells with either SIVsmH3 or SIVsmE660. These phenotypically CD4 cells, formed syncytia but only when cocultivated with CD4+ cells. Single cell clones were derived from these cultures and examined for the production of virus-specific proteins. The majority of the clones expressed SIV p27 antigen and low levels of virus reverse transcriptase activity. Western blot analysis, performed with either monoclonal or polyclonal sera, showed that a chronically infected clone (B7) produced particles which contained envelope (gp135 and gp43), gag precursors and gag proteins (p27, p16 and p8). However, these particles (SIVsmB7) lacked detectable levels of vpx and of integrase, and contained several fusion proteins which expressed viral protease antigens. This defective virus failed to infect established CD4+ cell lines, as well as primary cultures of macrophages and of peripheral blood lymphocytes, obtained both from humans and from rhesus macaques. Lack of infection correlated with lack of viral DNA detection by PCR amplification of genomic DNA extracted from these cell cultures. In addition, SIVsmB7 virus lacked infectivity in vivo. Rhesus macaques inoculated with high concentrations of SIVsmB7 showed no viremia and their PBMC were PCR negative. Thus, B7 cells produced stable, non-infectious virus mutants, which contained env and gag proteins, but lacked detectable amounts of vpx and of enzymes required for virus replication. Due to the high constitutive expression of this virus-like particle, we are now testing this preparation as a vaccine.
Cell Mol Biol (Noisy-le-grand) 1995
PMID:Properties of virus-like particles produced by SIV-chronically infected human cell clones. 857 47

A simple and reliable automated method was developed for the detection of amplified products after PCR, which provides an alternative to the time-consuming Southern blotting and hybridization procedure. For the determination and quantification of hepatitis C viremia, the digoxigenin labelling process was applied during the PCR of the amplicons, followed by an inverse hybridization assay performed with biotinylated probes. The detection of the PCR amplified products could be processed as simply as an ELISA, or by means of an automated analyser.
Cell Mol Biol (Noisy-le-grand) 1995 Nov
PMID:Automated determination of amplified PCR products: application to HCV viremia detection and quantification. 859 74

Certain isolates of the oncoretrovirus feline leukemia virus (FeLV) are strongly cytopathic for hemolymphatic cells. A major cytopathicity determinant is encoded by the SU envelope glucoprotein gp70. Isolates with subgroup C SU gp70 genes specifically induce apoptosis in hemolymphatic cells but not fibroblasts. In vitro exposure of feline T-cells to FeLV-C leads first to productive viral replication, next to virus-induced cell agglutination, and lastly to apogenesis. This in vitro phenomenon may explain the severe progressive thymic atrophy and erythroid aplasia which follow viremic FeLV-C infection in vivo. Inappropriate apoptosis induction has also been hypothesized to explain the severe thymico-lymphoid atrophy and progressive immune deterioration associated with isolates of FeLV containing variant envelope genes. The influence of envelope hypervariability (variable regions 1 [Vr1] and 5 [Vr5] on virus tropism, viremia induction, neutralizing antibody development and cytopathicity is discussed. Certain potentially cytopathic elements in FeLV SU gp70 Vr5 may derive from replication-defective, poorly expressed, endogenous FeLVs. Other more highly conserved regions in FeLV TM envelope p15E may also influence apoptosis induction.
Prog Mol Subcell Biol 1996
PMID:Cytopathic feline leukemia viruses cause apoptosis in hemolymphatic cells. 882 90

The early detection of hepatitis C viraemia (HCV) following liver transplantation is important for monitoring disease recurrence and planning antiviral chemotherapy. In the current study, the sensitivity, specificity, and concordance of three HCV RNA assays were compared using a random sample of 84 plasma specimens from 23 transplant recipients. Two of the assays were prototype commercial tests: Roche Molecular Diagnostic's RT-PCR HCV Amplicor system; and Chiron's Quantiplex HCV-RNA assay. The third was a 'home brew' PCR-liquid hybridization/gel retardation assay developed at the University of Pittsburgh Medical Center (UPMC). On all criteria the PCR-based assays out-performed the Quantiplex assay and displayed an overall concordance of 87%. A high percentage of specimens in the Quantiplex assay gave indeterminate results (12%) or high coefficients of variance (13%). The specificities of all RNA assays were determined using HCV serostatus as the gold standard. Both of the PCR-based assays had specificities of 100%, whereas the Chiron Quantiplex HCV assay had a specificity of 88%, if indeterminates were counted as negatives, and a specificity of 64% if indeterminates were counted as positives. The calculated sensitivities of the PCR-based assays were 56% and 48% for the 'home brew' and the Roche assays, respectively. The UPMC HCV assay, however, was determined to be capable of reproducibly detecting four or fewer chimpanzee infectious doses, suggesting that HCV viraemia was not present in the PCR-negative cases. The sensitivity of the Quantiplex assay was 41% counting indeterminates as negatives and 46% counting them as positives. The high cost of the Quantiplex assay combined with the number of uninterpretable results, the lack of sensitivity, and reduced specificity may limit the usefulness of this assay for monitoring HCV recurrence.
Mol Cell Probes 1996 Oct
PMID:Comparative analysis of three nucleic acid-based detection systems for hepatitis C virus RNA in plasma from liver transplant recipients. 891 Aug 87

In order to detect spring viraemia of carp virus, DNA probes have been constructed using reverse transcription-PCR amplification technique and cDNA cloning in plasmid and phage vectors. The sensitivity and specificity of viral RNA detection was assessed using nonradioactive probes in infected FHM cell culture and in tissues from dead fish. Viral RNA was more frequently detected in the brain and gill than in the abdominal organs.
Mol Gen Mikrobiol Virusol
PMID:[Detection of the spring viremia of carp virus by hybridization with nonradioactive DNA probes]. 892 59


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