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  1. 16 Archivum Immunologiae et Therapiae Experimentalis

  2. 5 Acta Biochimica Polonica

  3. 4 Folia Histochemica et Cytobiologica

  4. 2 Cellular and Molecular Biology Letters

  5. 2 Polish Journal of Microbiology

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  1. 5 Mozer-Lisewska I.

  2. 4 Zeromski J.

  3. 3 Borowski P.

  4. 3 Kowala-Piaskowska A.

  5. 2 Adamek A.

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  1. 1 2021

  2. 2 2019

  3. 1 2016

  4. 3 2014

  5. 2 2013

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1

Mechanism of inhibition of the protein kinase C by nonstructure protein 3 of hepatitis C virus

100%
Hartjen P., Reinholz M., Baier A., Borowski P.
Cellular and Molecular Biology Letters
|
2005
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tom 10
|
nr Suppl.2
2
Content available remote

Association between PNPLA3[G]/I148M variant, steatosis and fibrosis stage in hepatitis C virus - genetics matters

86%
Crisan D., Grigorescu M., Crisan N., Craciun R., Lupsor M., Radu C., Grigorescu M. D., Suciu A., Epure F., Avram L., Leach N.
Journal of Physiology and Pharmacology
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2019
|
tom 70
|
nr 4
3

Seronegative hepatitis C virus infection

86%
Kazmierczak J., Pawelczyk A., Cortes C. K., Radkowski M.
Archivum Immunologiae et Therapiae Experimentalis
|
2014
|
tom 62
|
nr 2
4

Functional attributes of responding T cells in HCV infection: the recent advances in engineering functional antiviral T cells

86%
Pasetto A., Aleman S., Chen M.
Archivum Immunologiae et Therapiae Experimentalis
|
2014
|
tom 62
|
nr 1
5

The inhibition of protein kinase C by hepatitis C virus non-structural protein 3 depends on its conformational status

86%
Borowski P., Hartjen P.
Cellular and Molecular Biology Letters
|
2003
|
tom 08
|
nr 2A
6

Biochemical phenotypes of Candida albicans isolated from the upper respiratory tract of patients with chronic hepatitis C

72%
Biernasiuk A., Halm A., Kiciak S., Modrzewska R.
Bulletin of the Veterinary Institute in Puławy
|
2009
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tom 53
|
nr 1
43-46
The aim of this paper was to analyse the biochemical phenotypes of Candida albicans colonising the upper respiratory tract in 100 patients with chronic hepatitis C from group I (without antiviral therapy) and from group II (treated with peginterferon and ribavirin). The ability of the assimilation of carbon from various substrates (assimilation phenotypes) or activity of hydrolytic enzymes (biotypes) of 61 C. albicans isolates were estimated using API 20 C AUX and API ZYM microtests, respectively. Among 30 isolates of C. albicans from the group I, seven assimilation phenotypes and six biotypes were determined, while among 31 isolates from the group II - eleven assimilation phenotypes and five biotypes. The most frequently isolated assimilation phenotype in both groups of patients with API numerical profile of 2576174 comprised about 50%-70% of all phenotypes. The predominant biotype E belonging to the classification of Williamson comprised about 39%-50% of all biotypes. Our results and those from the literature suggest that C. albicans biotypes but not assimilation phenotypes may be related with some diseases. However, this requires further detailed studies.
7

Cloning, expression and identification by immunohistochemistry of humanized single-chain variable fragment antibody against hepatitis C virus core protein

72%
Lun Y., Cheng J., Zhong Y., Yu Z., Wang Q., Wang F., Feng J.
Polish Journal of Microbiology
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2011
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tom 60
|
nr 1
Expression of single-chain variable fragment (scFv) antibodies on the surface of bacteriophage is widely used to prepare antibodies with pre-defined specificities. A phage antibody library containing the gene for scFv antibody against Hepatitis C virus core protein was panned with core protein immobilized on microtiter plate wells. After five rounds of panning 60 phage clones specific to core protein were obtained and one selected clone was sequenced. It was found that the specifically detected antigen consists of 774bp and is capable of encoding 257 amino acids in the patients but not in healthy persons.
8

Hepatitis C - new developments in the studies of the viral life cycle

72%
Rychlowska M., Bienkowska-Szewczyk K.
Acta Biochimica Polonica
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2007
|
tom 54
|
nr 4
703-715
Hepatitis C virus (HCV) is a causative agent of chronic liver disease leading tocirrhosis, liver failure and hepatocellular carcinoma. The prevalence of HCV is estimated as 3% of the world population and the virus is a major public health problem all over the world. For over 16 years, since HCV had been discovered, studies of the mechanisms of the viral life cycle and virus-host interactions have been hampered by the lack of a cell culture system allowing the virus to be grown in laboratory conditions. However, in recent years some new model systems to study HCV have been developed. The major breakthrough of the last two years was the cell culture system for maintaining the virus in an adapted hepatocyte-derived cell line. This review describes the techniques and applications of most of the in vitrosystems and animal models currently used for working with hepatitis C virus
9

Mechanism of cell infection with hepatitis C virus [HCV] - a new paradigm in virus-cell interaction

72%
Budkowska A.
Polish Journal of Microbiology
|
2009
|
tom 58
|
nr 2
93-98
Hepatitis C virus (HCV) is an enveloped, single-stranded RNA virus, belonging to the Flaviviridae family. HCV infection is a major cause of chronic hepatitis worldwide, leading to steatosis, liver cirrosis and hepatocellular carcinoma. Significant advances in understanding the mechanisms of HCV infection have been made since the development of a cell culture system reproducing the complete HCV cell cycle in vitro. HCV represents a new paradigm in interactions between the virus and its target cell, the human hepatocyte, due to the central role of lipoproteins in the HCV life cycle. Very low density lipoproteins are required for virus particle assembly and secretion. Upon the release, the infectious virus circulates in the blood as triglyceride-rich particles and infects cells using lipoprotein-receptor dependent mechanisms. HCV cell entry is a multi-step process: heparan sulphate and/or low-density lipoprotein receptor are cell surface factors mediating an initial virus attachment; subsequent virus interaction with tetraspanin CD81 and the human scavenger receptor SR-BI, the main HCV receptors, triggers virus movement to the tight junctions and its uptake via Claudin-1 and occludin. Another originality of HCV is that initiation of productive infection requires dynamic microtubules. Whereas other viruses use kinesin or dynein-dependent transport, HCV exploits mechanisms driven by microtubule polymerization to efficiently infect its target cell, in which virus nucleocapsid protein might play a particular role. An improved of understanding of the cellular-events involved in HCV cell entry and transport, leading to the initiation of productive HCV infection, may reveal novel targets for anti-viral interventions.
10

Detection and significance of cytotoxic cell subsets in biopsies of HCV-infected human livers

72%
Mozer-Lisewska I., Mania A., Kowala-Piaskowska A., Kluk A., Samara H., Pauli A., Zeromski J.
Archivum Immunologiae et Therapiae Experimentalis
|
2014
|
tom 62
|
nr 2
11

Multi-step regulation of interferon induction by hepatitis C virus

72%
Oshiumi H., Funami K., Aly H. H., Matsumoto M., Seya T.
Archivum Immunologiae et Therapiae Experimentalis
|
2013
|
tom 61
|
nr 2
12

Chronic hepatitis C virus infection and the pathogenesis of hepatocellular carcinoma

72%
Feitelson M.
Archivum Immunologiae et Therapiae Experimentalis. Supplement
|
2001
|
tom 49
|
nr 2
65-74
13

Modulation of the immune system in chronic hepatitis C and during antiviral interferon-free therapy

72%
Urbanowicz A., Zagozdzon R., Ciszek M.
Archivum Immunologiae et Therapiae Experimentalis
|
2019
|
tom 67
|
nr 2
14

Circular dichroism analysis for multidomain proteins: studies of the irreversible unfolding of Hepatitis C virus helicase

72%
Gozdek A., Stankiewicz-Drogon A., Poznanski J., Boguszewska-Chachulska A. M.
Acta Biochimica Polonica
|
2008
|
tom 55
|
nr 1
The non-structural protein 3 (NS3) of Hepatitis C virus (HCV) is a bifunctional enzyme with RNA-dependent NTPase/RNA helicase and serine protease activities, and thus represents a promising target for anti-HCV therapy. These functions are performed by two distinct moieties; the N-terminal protease domain and the C-terminal helicase domain that further folds into three structural subdomains. To obtain lower molecular mass proteins suitable for nuclear magnetic resonance studies of helicase-inhibitor complexes, helicase domains 1, 2, and 1+2 devoid of a hydrophobic β-loop were overexpressed and purified. Circular dichroism studies were carried out to confirm the secondary structure content and to determine thermodynamic parameters describing the stability of the proteins. Both thermal and GuHCl-induced unfolding experiments confirmed the multidomain organization of the helicase. The unfolding transition observed for domain 1+2 was in agreement with the model of two well-resolved successive steps corresponding to the independent unfolding of domains 1 and 2, respectively. In the case of the full-length helicase, the presence of domain 3 remarkably changed the transition profile, leading to fast and irreversible transformation of partially unfolded protein.
15

Inhibition of the helicase activity of HCV NTPase-helicase by 1-beta-D-ribofuranosyl-1,2,4-triazole-3-carboxamide-5'-triphosphate [ribavirin-TP]

72%
Borowski P., Lang M., Niebuhr A., Haag A., Schmitz H., Schulze zur Wiesch J., Choe J., Siwecka M. A., Kulikowski T.
Acta Biochimica Polonica
|
2001
|
tom 48
|
nr 3
In the presented study the ribavirin-TP — an established inhibitor of the NTPase ac­tivity of the superfamily NTPase/helicases II — was investigated as an inhibitor of the unwinding activity of the hepatitis C virus (HCV) NTPase/helicase. The kinetics of the reaction revealed that ribavirin-TP reduces the turnover number of the helicase reac­tion by a mechanism that does not correspond to that of the inhibition of the NTPase activity. Our results suggest that derivatives of ribavirin-TP with enhanced stability towards hydrolytic attack may be effective inhibitors of the enzyme.
16

Existing and future therapeutic options for hepatitis C virus infection

72%
Bretner M.
Acta Biochimica Polonica
|
2005
|
tom 52
|
nr 1
Hepatitis C virus (HCV) infection is an important cause of chronic hepatitis, cirrhosis, hepatocellular carcinoma and liver failure worldwide. Chronic hepatitis C virus infection is treated with interferon-alpha (IFN-alpha), pegylated interferon-alpha (PEG-IFNalpha) alone or in combination with ribavirin; however, a significant fraction of patients either fail to respond or relapse after cessation of therapy. Efforts to identify and develop highly specific and potent HCV inhibitors have intensified recently. Each of the virally encoded replication enzymes has been a focus of studies as well as viral receptors and the host immune system. This review summarizes recent progress in the search for novel anti-HCV agents.
17

NK cells prevalence, subsets and function in viral hepatitis C

58%
Zeromski J., Mozer-Lisewska I., Kaczmarek M., Kowala-Piaskowska A., Sikora J.
Archivum Immunologiae et Therapiae Experimentalis
|
2011
|
tom 59
|
nr 6
18

Immune exhaustion and immune senescence: two distinct pathways for HBV vaccine failure during HCV and/or HIV infection

58%
Yao Z. Q., Moorman J. P.
Archivum Immunologiae et Therapiae Experimentalis
|
2013
|
tom 61
|
nr 3
19

New approaches to the prevention and treatment of viral diseases

58%
Pronin A. V., Narovlyansky A. N., Sanin A. V.
Archivum Immunologiae et Therapiae Experimentalis
|
2021
|
tom 69
|
nr 1
20

Genetic (KIR, HLA-C) and some clinical parameters influencing the level of liver enzymes and early virologic response in patients with chronic hepatitis C

58%
Mozer-Lisewska I., Zwolinska K., Kowala-Piaskowska A. E., Bura M., Rozplochowski B., Pauli A., Zeromski J., Piasecki E., Kusnierczyk P.
Archivum Immunologiae et Therapiae Experimentalis
|
2016
|
tom 64
|
nr 1
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