12 results match your criteria: "Rega Institute and University Hospitals[Affiliation]"

Bioinformatics tools for the investigation of emerging and re-emerging infectious diseases. Introduction.

Infect Genet Evol

July 2009

Katholieke Universiteit Leuven, Laboratory for Clinical and Epidemiological Virology, AIDS Reference Laboratory, Rega Institute and University Hospitals, Leuven, Belgium.

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Recombination confounds the early evolutionary history of human immunodeficiency virus type 1: subtype G is a circulating recombinant form.

J Virol

August 2007

Katholieke Universiteit Leuven, Laboratory for Clinical and Epidemiological Virology, AIDS Reference Laboratory, Rega Institute and University Hospitals, Minderbroedersstraat 10, B-3000 Leuven, Belgium.

Human immunodeficiency virus type 1 (HIV-1) is classified in nine subtypes (A to D, F, G, H, J, and K), a number of subsubtypes, and several circulating recombinant forms (CRFs). Due to the high level of genetic diversity within HIV-1 and to its worldwide distribution, this classification system is widely used in fields as diverse as vaccine development, evolution, epidemiology, viral fitness, and drug resistance. Here, we demonstrate how the high recombination rates of HIV-1 may confound the study of its evolutionary history and classification.

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Hantavirus infections in Europe.

Lancet Infect Dis

December 2003

Laboratory of Clinical and Epidemiological Virology, Department of Microbiology and Virology, Rega Institute and University Hospitals Leuven, Leuven, Belgium.

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The relationship between adherence, virological response to highly active antiretroviral therapy (HAART) and the presence and development of genotypic resistance was assessed in 41 HIV-infected patients on HAART. Four adherence parameters (drug taking adherence, dosing adherence, timing adherence and drug holidays) were scored prospectively using electronic event monitoring. Genotypic resistance at baseline and after therapy failure was scored retrospectively and a genotype-based susceptibility score was calculated.

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HIV drug resistance is one of the major limitations in the successful treatment of HIV-infected patients using currently available antiretroviral combination therapies. When appropriate, drug susceptibility profiles should be taken into consideration in the choice of a specific combination therapy. Guidelines recommending resistance testing in certain circumstances have been issued.

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We evaluated the predictive value of baseline HIV-1 genotypic resistance mutations for failure of a nucleoside reverse transcriptase inhibitor (NRTI) containing therapy. The change in therapy of 88 HIV-1-infected patients was analyzed retrospectively, relating the genotypic resistance profile at baseline to the evolution of viral load and CD4+ T cell counts. Genotypic resistance at baseline and at 6 months was evaluated with the LiPA HIV-1 RT, which detects mutations at codons 41, 69, 70, 74, 184, and 215.

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In a previous study, we have determined the prevalence of serum HGV-RNA in patients with congenital clotting disorders. Twenty-six (15%) of 175 patients investigated were serum HGV-RNA positive. In addition, HGV-RNA was detectable in peripheral blood mononuclear cells (PBMC) in ten percent of the cases, three of these patients were serum HGV-RNA negative.

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The level of HIV-1 RNA in plasma has become one of the most important markers in the follow-up of HIV-infected patients. Three techniques are commercially available: both the Amplicor HIV Monitor and the NASBA HIV-1 RNA QT are target amplification methods, whereas the Quantiplex HIV RNA assay is a branched DNA signal amplification technique. Detection in both target amplification techniques is based on a single primer pair and a single probe in the gag region, whereas multiple probes capture the pol region of the viral RNA in the branched DNA assay.

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Searching for clues to the evolution of the primate T-lymphotropic viruses (PTLVs), which include the human and the simian T-lymphotropic viruses (HTLV and STLV), we have identified another PTLV, which differs sufficiently from the known PTLV-I and PTLV-II types to be designated here PTLV-L. The virus was isolated from a wild-born baboon (Papio hamadryas) from Eritrea. In a cDNA library a 1802-bp-long fragment was identified that extends from the env region, including the complete transmembrane protein gene, to part of the tax/rex gene.

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We set up a PCR laboratory for the diagnosis of HIV-1. Probably due to the variability of the HIV-genome, classical primers that performed well in some laboratories in the past, did not suffice for detection of HIV-1 strains in Belgian hospitals. Two new primer sets amplifying a fragment in the LTR-gag gene and in the env gene, which perform better on strains seen in Belgium, have been developed and evaluated.

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HTLV-II seroprevalence in pygmies across Africa since 1970.

AIDS Res Hum Retroviruses

August 1993

Rega Institute and University Hospitals, Katholieke Universiteit Leuven, Belgium.

HTLV-II-specific antibodies, with patterns similar to those in the Americas, were present in sera collected about 1970 from Bambuti pygmies in Zaire (14/102; 14%) and from pygmies in Cameroon (5/214; 2.3%), and were more prevalent than HTLV-I. In the Central African Republic, 504 pygmies were HTLV negative.

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