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1

Ludwik Hirszfeld Memorial Lecture:HIV-1 reservoirs: major molecular obstacles to viral eradication

100%
Pomerantz R. J.
Archivum Immunologiae et Therapiae Experimentalis
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2004
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vol. 52
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issue 5
297-306
EN
Over the last 18 years of study in one of our laboratories, we have observed the development of residual disease and latent reservoirs as major problems in the long-term therapy of HIV-1-infected individuals on highly active antiretroviral therapy (HAART).It was shown in the early 1990 's that HAART, as it is presently configured, is unlikely to lead to viral eradication due to several mechanisms of viral persistence. The two general mechanisms involved with persistence during HAART include low-level residual, cryptic replication and proviral latently-infected cells. As such, these are key areas of potential study for depletion and, hopefully in the future, eradication of residual disease in patients on suppressive HAART. To deplete these residual disease mechanisms will require multipronged approaches. These will include induction of HIV-1 latent proviruses, suppression of residual viral replication and destruction of long-lived cellular sanctuaries, such astissue-bound macrophages.
2
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Synthesis and anti-HIV properties of novel 6-phenylselenenyl-5-propyluracils

100%
Miazga A., Felczak K., Siwecka M. A., Lipniacki A., Piasek A., Kulikowski T.
Acta Biochimica Polonica
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2007
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vol. 54
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issue 4
863-868
EN
Novel 6-phenylselenenyl-5-propyluracils were synthesized from 5-propyluracil with the use of regioselective synthesis to give 1-[(2-hydroxyethoxy)-methyl]-6-phenylselenenyl-5-propyluracil (6), 1-ethoxymethyl-6-phenylselenenyl-5-propyluracil (9) and 1-benzyloxymethyl-6-phenylselenenyl-5-propyluracil (10). Interaction of these compounds with recombinant HIV-1 reverse transcriptase (RT) was evaluated using a non-isotopic colorimetric method. Compounds 9 and 10 exerted potent HIV RT inhibition (IC50 0.06 and 0.05 µM respectively) while compound 6 showed moderate inhibition (IC50 = 3.5 µM). Potent anti-HIV-1 activity in MT-2 cells inoculated by a syncythia-inducing HIV-1 (cat #3 strain) laboratory isolate was exerted by compounds 9 and 10 (EC50 0.62 µM and 0.025 µM, respectively), while compound 6 showed only moderate activity (IC50 = 4.1 µM). In addition, compound 10 showed very good in vitro therapeutic index (TI > 2046), indicating that it is a potential anti-HIV/AIDS drug.
3

RNA interference:a potential novel therapeutic combating HIV-1 in the central nervous system

100%
Pomerantz R. J.
Archivum Immunologiae et Therapiae Experimentalis
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2004
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vol. 52
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issue 6
401-409
EN
RNA interference (RNAi) is a conserved process by which eukaryotic cells protect their genomes utilizing small, double-stranded RNAs to degrade target RNAs. This occurs in a sequence-specific manner and is different from the interferon effect of larger doublestranded RNAs. Post-transcriptional gene silencing by these nucleic acids can lead to degradation of either cellular or viral RNAs. It has been recently shown that doublestranded, small interfering RNAs (siRNAs) of 21 to 25 nucleotides can be transfected into relevant cells to target specific RNAs. In addition, utilizing hairpin motifs, siRNAs can be expressed intracellularly using molecular therapeutic vectors. This potent approach has been utilized to both inhibit pathogens, including viruses, as well as to dissect cellular molecular mechanisms via a potent knockout effect. At this time in the HIV-1-pandemic, one of the remaining, most enigmatic, and still vitally important areas of HIV-1 pathogenesis occurs in the central nervous system (CNS). HIV-1-induced encephalopathy remains difficult to treat in the developing world and in parts of the developed world, even in the era of highly active anti-retroviral therapy. As such, novel approaches which could lead to intracellular immunization, and life-long resistance against HIV-1 encephalopathy would be of important impact worldwide. Thus, we now seek to combine our background in molecular therapeutics and RNAi with our long-standing interest in HIV-1 neuropathogenesis to target the CNS using siRNAs.
4
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Pochodzenie i zróżnicowanie genetyczne ludzkiego wirusa niedoboru odporności typu 1

88%
Ziach-Terlecka M., Wąsik T.
Annales Academiae Medicae Silesiensis
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2013
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vol. 67
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issue 6
400-409
EN
Multiple transmission of simian immunodeficiency virus (SIV) into the human population started the pandemic of human immunodeficiency virus (HIV-1). The extraordinary variability of human immunodeficiency virus HIV-1 resulting from the high rate of genome mutations and the recombination between different strains resulted in the emergence of a genetically diverse viral strains. Genetic differences between HIV-1 isolates are now the basis for the classification of the virus. Tracking the spread of the HIV-1 genetic variants allows for the monitoring of the development of the epidemic, and provides important information about the time and possible routes of virus introduction into different countries, geographical regions or populations with different transmission routes of infection. On the other hand, the vast viral genetic diversity complicates the diagnosis of infection, can affect the susceptibility of HIV-1 to drugs and is a major obstacle in research aimed at creating an effective vaccine. In this paper the current knowledge on the origin of virus, the genetic diversity of HIV-1, as well as its impact on the course of infection and development of the epidemic is presented.
PL
Pandemia ludzkiego wirusa niedoboru odporności (human immunodeficiency virus – HIV) została zapoczątkowana przez wielokrotną transmisję małpiego wirusa upośledzenia odporności (simian immunodeficiency virus – SIV) do populacji ludzkiej. Niezwykła zmienność HIV-1 wynikająca z dużej częstości mutacji pojawiających się w genomie oraz możliwości rekombinacji między materiałem genetycznym różnych szczepów wirusa zaowocowała wykształceniem zróżnicowanych pod względem genetycznym wariantów. Genetyczne różnice między izolatami HIV-1 stanowią obecnie podstawę klasyfikacji wirusa, a śledzenie rozprzestrzeniania poszczególnych wariantów pozwala na monitorowanie rozwoju epidemii i dostarcza ważnych informacji na temat czasu i sposobu transmisji wirusa do różnych krajów, regionów geograficznych lub populacji. Z drugiej strony olbrzymia różnorodność form genetycznych wirusa utrudnia diagnostykę infekcji, może wpływać na wrażliwość HIV-1 na leki i stanowi poważną przeszkodę w badaniach zmierzających do stworzenia skutecznej szczepionki. W niniejszej pracy przedstawiono aktualny stan wiedzy na temat pochodzenia wirusa, genetycznego zróżnicowania HIV-1 i wpływu tego czynnika na przebieg zakażenia i rozwój epidemii.
5

CD8+ T cell suppressor factors and the control of infection, replication and transcription of human imunodeficiency virus

75%
Copeland K. F. T.
Archivum Immunologiae et Therapiae Experimentalis
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2001
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vol. 49
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issue 1
13-18
EN
CD8+ T cells have been shown to produce factors which modulate HIV-1 replication in both T cells and monocytic cells. Examination of the literature reveals that this modulation may occur by the production of -chemokines which block viral entry. However, another CD8+ T cell-derived activity targets the replication of HIV-1 at the level of transcription. CD8+ T cell factors strongly suppress replication and transcription in T cells and T cell lines, and in contrast, the factors enhance both replication and transcription in cells of the monocyte/macrophage lineage. The enhancement of transcription and replication by CD8+ T cell factors is induced by increased production of TNF by the macrophages. The enhancement is sensitive to pertussis toxin, indicating a G protein-coupled pathway. Thus, CD8+ T cells produce factors which mediate effects on transcription and replication of HIV-1 in a cell type-dependent manner. In this review a summary of the effects of chemokines and CD8-derived factors on HIV-1 transcription and replication is presented. The virus-host cell interactions that participate in the persistent replication of HIV in macrophages and the suppression of these functions in T cells require definition.The identification of CD8+ T cell factors which exert these controls on HIV-1 may lead to promising new therapies for HIV infection.
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