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Article ; Online: Hepatitis C virus: life cycle in cells, infection and host response, and analysis of molecular markers influencing the outcome of infection and response to therapy.

Dustin, L B / Bartolini, B / Capobianchi, M R / Pistello, M

Clinical microbiology and infection : the official publication of the European Society of Clinical Microbiology and Infectious Diseases

2016 Volume 22, Issue 10, Page(s) 826–832

Abstract: Hepatitis C virus (HCV) is a major global health burden accounting for around 170 million chronic infections worldwide. Since its discovery, which dates back to about 30 years ago, many details of the viral genome organization and the astonishing genetic ...

Abstract	Hepatitis C virus (HCV) is a major global health burden accounting for around 170 million chronic infections worldwide. Since its discovery, which dates back to about 30 years ago, many details of the viral genome organization and the astonishing genetic diversity have been unveiled but, owing to the difficulty of culturing HCV in vitro and obtaining fully susceptible yet immunocompetent in vivo models, we are still a long way from the full comprehension of viral life cycle, host cell pathways facilitating or counteracting infection, pathogenetic mechanisms in vivo, and host defences. Here, we illustrate the viral life cycle into cells, describe the interplay between immune and genetic host factors shaping the course of infection, and provide details of the molecular approaches currently used to genotype, monitor replication in vivo, and study the emergence of drug-resistant viral variants.
MeSH term(s)	Antiviral Agents/pharmacology ; Antiviral Agents/therapeutic use ; Drug Resistance, Viral ; Genotype ; Hepacivirus/pathogenicity ; Hepacivirus/physiology ; Hepatitis C/drug therapy ; Hepatitis C/genetics ; Hepatitis C/immunology ; Host-Pathogen Interactions ; Humans ; Virulence Factors/genetics ; Virulence Factors/immunology ; Virus Replication
Chemical Substances	Antiviral Agents ; Virulence Factors
Language	English
Publishing date	2016-10
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	1328418-6
ISSN	1469-0691 ; 1470-9465 ; 1198-743X
ISSN (online)	1469-0691
ISSN	1470-9465 ; 1198-743X
DOI	10.1016/j.cmi.2016.08.025
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Zs.A 4541: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MO 284: Show issues

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Article ; Online: Hepatitis C virus: life cycle in cells, infection and host response, and analysis of molecular markers influencing the outcome of infection and response to therapy

Dustin, L.B. / Bartolini, B. / Capobianchi, M.R. / Pistello, M.

Clinical Microbiology and Infection. 2016,

2016

Abstract	Hepatitis C virus (HCV) is a major global health burden accounting for around 170 million chronic infections worldwide. Since its discovery, which dates back to about 30 years ago, many details of the viral genome organization and the astonishing genetic diversity have been unveiled but, owing to the difficulty of culturing HCV in vitro and obtaining fully susceptible yet immunocompetent in vivo models, we are still a long way from the full comprehension of viral life cycle, host cell pathways facilitating or counteracting infection, pathogenetic mechanisms in vivo, and host defences. Here, we illustrate the viral life cycle into cells, describe the interplay between immune and genetic host factors shaping the course of infection, and provide details of the molecular approaches currently used to genotype, monitor replication in vivo, and study the emergence of drug-resistant viral variants.
Keywords	Broadly reactive neutralizing antibodies ; Cell culture-derived HCV ; Direct antiviral agents ; Drug resistance ; Genotype ; Hepatitis C virus ; Host response ; monitoring drug resistance ; Pathogenesis ; Quantitative molecular assays
Language	English
Publishing place	Elsevier Ltd
Document type	Article ; Online
Note	Pre-press version
ZDB-ID	1328418-6
ISSN	1469-0691 ; 1470-9465 ; 1198-743X
ISSN (online)	1469-0691
ISSN	1470-9465 ; 1198-743X
DOI	10.1016/j.cmi.2016.08.025
Database	NAL-Catalogue (AGRICOLA)

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Zs.A 4541: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MO 284: Show issues

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Article: The immunological relay race: B cells take antigen by synapse.

Dustin, M L / Dustin, L B

Nature immunology

2001 Volume 2, Issue 6, Page(s) 480–482

MeSH term(s)	Animals ; Antigen Presentation ; Antigen-Presenting Cells/immunology ; B-Lymphocytes/immunology ; Humans ; Mice ; Receptors, Antigen, B-Cell/metabolism ; Receptors, Antigen, T-Cell/metabolism ; Synapses/immunology ; T-Lymphocytes/immunology
Chemical Substances	Receptors, Antigen, B-Cell ; Receptors, Antigen, T-Cell
Language	English
Publishing date	2001-06
Publishing country	United States
Document type	News
ZDB-ID	2016987-5
ISSN	1529-2916 ; 1529-2908
ISSN (online)	1529-2916
ISSN	1529-2908
DOI	10.1038/88666
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Zs.A 5294: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article: T-B cell interaction inhibits spontaneous apoptosis of mature lymphocytes in Bcl-2-deficient mice.

Nakayama, K / Dustin, L B / Loh, D Y

The Journal of experimental medicine

1995 Volume 182, Issue 4, Page(s) 1101–1109

Abstract: Bcl-2 expression is tightly regulated during lymphocyte development. Mature lymphocytes in Bcl-2-deficient mice show accelerated spontaneous apoptosis in vivo and in vitro. Stimulation of Bcl-2-deficient lymphocytes by anti-CD3 antibody inhibited the ... ...

Abstract	Bcl-2 expression is tightly regulated during lymphocyte development. Mature lymphocytes in Bcl-2-deficient mice show accelerated spontaneous apoptosis in vivo and in vitro. Stimulation of Bcl-2-deficient lymphocytes by anti-CD3 antibody inhibited the spontaneous apoptosis not only in T cells but also in B cells. The rescue of B cells was dependent on the presence of T cells, mainly through CD40L and interleukin (IL)-4. Furthermore, we generated Bcl-2-deficient mice transgenic for a T cell receptor or an immunoglobulin, both specific for chicken ovalbumin, to test for antigen-specific T-B cell interaction in the inhibition of the spontaneous apoptosis. The initial T cell activation by antigenic peptides presented by B cells suppressed apoptosis in T cells. Subsequently, T cells expressed CD40L and released ILs, leading to the protection of B cells from spontaneous apoptosis. These results suggest that the antiapoptotic signaling via CD40 or IL-4 may be largely independent of Bcl-2. Engagement of the Ig alone was not sufficient for the inhibition of B cell apoptosis. Thus, the physiological role of Bcl-2 in mature lymphocytes may be to protect cells from spontaneous apoptosis and to extend their lifespans to increase the opportunity for T cells and B cells to interact with each other and specific antigens in secondary lymphoid tissues. Bcl-2, however, appears to be dispensable for survival once mature lymphocytes are activated by antigen-specific T-B cell collaboration.
MeSH term(s)	Animals ; Apoptosis ; B-Lymphocytes/immunology ; CD3 Complex/metabolism ; CD40 Antigens/metabolism ; Cell Communication/drug effects ; Cells, Cultured ; Flow Cytometry ; Immunoglobulins/genetics ; Immunoglobulins/immunology ; Interleukin-4/pharmacology ; Mice ; Mice, Mutant Strains ; Mice, Transgenic ; Models, Immunological ; Proto-Oncogene Proteins/deficiency ; Proto-Oncogene Proteins/genetics ; Proto-Oncogene Proteins c-bcl-2 ; Receptors, Antigen, T-Cell/genetics ; Receptors, Antigen, T-Cell/immunology ; T-Lymphocytes/immunology
Chemical Substances	CD3 Complex ; CD40 Antigens ; Immunoglobulins ; Proto-Oncogene Proteins ; Proto-Oncogene Proteins c-bcl-2 ; Receptors, Antigen, T-Cell ; Interleukin-4 (207137-56-2)
Language	English
Publishing date	1995-10-01
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S.
ZDB-ID	218343-2
ISSN	1540-9538 ; 0022-1007
ISSN (online)	1540-9538
ISSN	0022-1007
DOI	10.1084/jem.182.4.1101
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Ua VI Zs.107: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
Zs.MG 45: Show issues

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Article ; Online: Genome-wide association study of hepatitis C virus- and cryoglobulin-related vasculitis.

Zignego, A L / Wojcik, G L / Cacoub, P / Visentini, M / Casato, M / Mangia, A / Latanich, R / Charles, E D / Gragnani, L / Terrier, B / Piazzola, V / Dustin, L B / Khakoo, S I / Busch, M P / Lauer, G M / Kim, A Y / Alric, L / Thomas, D L / Duggal, P

Genes and immunity

2014 Volume 15, Issue 7, Page(s) 500–505

Abstract: The host genetic basis of mixed cryoglobulin vasculitis is not well understood and has not been studied in large cohorts. A genome-wide association study was conducted among 356 hepatitis C virus (HCV) RNA-positive individuals with cryoglobulin-related ... ...

Abstract	The host genetic basis of mixed cryoglobulin vasculitis is not well understood and has not been studied in large cohorts. A genome-wide association study was conducted among 356 hepatitis C virus (HCV) RNA-positive individuals with cryoglobulin-related vasculitis and 447 ethnically matched, HCV RNA-positive controls. All cases had both serum cryoglobulins and a vasculitis syndrome. A total of 899 641 markers from the Illumina HumanOmni1-Quad chip were analyzed using logistic regression adjusted for sex, as well as genetically determined ancestry. Replication of select single-nucleotide polymorphisms (SNPs) was conducted using 91 cases and 180 controls, adjusting for sex and country of origin. The most significant associations were identified on chromosome 6 near the NOTCH4 and MHC class II genes. A genome-wide significant association was detected on chromosome 6 at SNP rs9461776 (odds ratio=2.16, P=1.16E-07) between HLA-DRB1 and DQA1: this association was further replicated in additional independent samples (meta-analysis P=7.1 × 10(-9)). A genome-wide significant association with cryoglobulin-related vasculitis was identified with SNPs near NOTCH4 and MHC Class II genes. The two regions are correlated and it is difficult to disentangle which gene is responsible for the association with mixed cryoglobulinemia vasculitis in this extended major histocompatibility complex region.
MeSH term(s)	Case-Control Studies ; Chromosomes, Human, Pair 6/genetics ; Cryoglobulinemia/etiology ; Cryoglobulinemia/genetics ; Cryoglobulins/analysis ; Female ; Genes, MHC Class II ; Genome-Wide Association Study ; Hepatitis C/complications ; Humans ; Male ; Polymorphism, Single Nucleotide ; Proto-Oncogene Proteins/genetics ; Receptor, Notch4 ; Receptors, Notch/genetics ; Vasculitis/etiology ; Vasculitis/genetics
Chemical Substances	Cryoglobulins ; NOTCH4 protein, human ; Proto-Oncogene Proteins ; Receptor, Notch4 ; Receptors, Notch
Language	English
Publishing date	2014-07-17
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2060566-3
ISSN	1476-5470 ; 1466-4879
ISSN (online)	1476-5470
ISSN	1466-4879
DOI	10.1038/gene.2014.41
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Article: Docosahexaenoic acid, a constituent of rodent fetal serum and fish oil diets, inhibits acquisition of macrophage tumoricidal function.

Dustin, L B / Shea, C M / Soberman, R J / Lu, C Y

Journal of immunology (Baltimore, Md. : 1950)

1990 Volume 144, Issue 12, Page(s) 4888–4897

Abstract: Macrophage (M phi) activation is deficient in the fetus and neonate, at times when the serum concentration of docosahexaenoic acid (DHA; 22:6n3) is approximately 10-fold higher than in the adult. We tested the effects of highly purified DHA on M phi ... ...

Abstract	Macrophage (M phi) activation is deficient in the fetus and neonate, at times when the serum concentration of docosahexaenoic acid (DHA; 22:6n3) is approximately 10-fold higher than in the adult. We tested the effects of highly purified DHA on M phi activation in vitro. M phi were stimulated with rIFN-gamma plus either of two second or "triggering" signals, LPS or heat-killed Listeria monocytogenes. M phi activation was assayed as the lysis of P815 mastocytoma cells, which are resistant to TNF-alpha. DNA inhibited the activation of peritoneal M phi and the M phi line RAW264.7 in a dose-dependent manner at concentrations between 20 and 160 microM. These concentrations are found in fetal and neonatal rodent sera. Another polyunsaturated fatty acid, arachidonic acid (20:4n6), was much less inhibitory. In contrast to its profound effect on tumoricidal activation, DHA did not inhibit phagocytosis and catabolism of 125I-heat-killed Listeria monocytogenes. Increasing the rIFN-gamma or second signals reduced the inhibition of tumoricidal activation by DHA but not M phi incorporation of 14C-DHA. When the rIFN-gamma and second signals were separated in time, DHA was far more inhibitory if delivered with the triggering signal than if delivered with the rIFN-gamma. However, the incorporation of 14C-DHA was the same under these two conditions. In M phi treated with DHA during LPS stimulation, the inhibition was time-dependent, requiring more than 2 h. Although DHA inhibits cyclooxygenase activity, its inhibition of M phi activation was not reversed with the following cyclooxygenase products: PGE2, a stable TXA2 analog (U-46, 619) or a stable PGI2 analog (Iloprost). Although DHA is metabolized by lipoxygenases, the inhibition was not reversed by the lipoxygenase inhibitors 5, 8, 11, 14-eicosatetraynoic acid and nordihydroguaiaretic acid. Altogether, the data indicate that DHA, at concentrations present in fetal and neonatal sera, inhibits M phi activation and may contribute to the previously observed deficits in M phi function in the fetus and neonate.
MeSH term(s)	Cytotoxicity, Immunologic/drug effects ; Docosahexaenoic Acids/pharmacology ; Fish Oils ; Immunity, Cellular/drug effects ; In Vitro Techniques ; Interferon-gamma/pharmacology ; Lipoxygenase/metabolism ; Listeria monocytogenes/immunology ; Macrophage Activation/drug effects ; Macrophages/drug effects ; Peritoneal Cavity/cytology ; Phagocytosis/drug effects ; Prostaglandin-Endoperoxide Synthases/metabolism ; Recombinant Proteins
Chemical Substances	Fish Oils ; Recombinant Proteins ; Docosahexaenoic Acids (25167-62-8) ; Interferon-gamma (82115-62-6) ; Lipoxygenase (EC 1.13.11.12) ; Prostaglandin-Endoperoxide Synthases (EC 1.14.99.1)
Language	English
Publishing date	1990-06-15
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S.
ZDB-ID	3056-9
ISSN	1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
ISSN (online)	1550-6606
ISSN	0022-1767 ; 1048-3233 ; 1047-7381
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Ud II Zs.37: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
Zs.MG 28: Show issues

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Article: Antigen-driven differentiation of naive Ig-transgenic B cells in vitro.

Dustin, L B / Bullock, E D / Hamada, Y / Azuma, T / Loh, D Y

Journal of immunology (Baltimore, Md. : 1950)

1995 Volume 154, Issue 10, Page(s) 4936–4949

Abstract: We have established a culture system in which naive B cells bearing a transgenic, chicken OVA (cOVA)-specific Ig differentiate to plasma cells in vitro after interaction with cOVA plus cOVA-specific helper T cells. B cell-enriched populations from Ig- ... ...

Abstract	We have established a culture system in which naive B cells bearing a transgenic, chicken OVA (cOVA)-specific Ig differentiate to plasma cells in vitro after interaction with cOVA plus cOVA-specific helper T cells. B cell-enriched populations from Ig-transgenic mice, but not from nontransgenic mice, proliferated after presenting nanomolar concentrations of cross-linked cOVA to DO11.10 (cOVA plus IAd-specific) T cells. After 6 to 9 days of culture with Ag and specific T cells, the B cells acquired a plasma cell phenotype and secreted the transgene-derived Ig at high levels. Engagement of B cell surface Ig was not essential for primary B cell differentiation. Differentiating B cells enlarged, clustered, and acquired two plasma cell markers, Syndecan and CD43. B cell CD45 isoform expression changed: the B220 isoform was lost in a T cell-dependent manner, whereas the CD45RB isoform was gained in a T-independent manner. Although unstimulated B cells survived less than 72 h in vitro, those in Ag-stimulated cultures showed reduced early death, a surge of proliferation at 3 to 5 days, and increased death late in the culture. Using a large population of naive B cells of defined antigenic specificity permits us to study a primary immune response to an Ag, rather than to less physiologic polyclonal stimuli. Because all steps of differentiation occurred in vitro, they are easily accessible for study. This coculture system provides an opportunity to observe Ag-specific T cell-B cell collaboration.
MeSH term(s)	Animals ; Antigen Presentation/immunology ; B-Lymphocytes/immunology ; Cell Communication/immunology ; Cell Death/immunology ; Cell Differentiation/immunology ; Cell Line ; Epitopes/immunology ; Epitopes/metabolism ; Flow Cytometry ; Immunoglobulin M/biosynthesis ; Leukocyte Common Antigens/biosynthesis ; Lymphocyte Activation/immunology ; Lymphocyte Cooperation/immunology ; Mice ; Mice, Transgenic ; Ovalbumin/immunology ; Plasma Cells/immunology ; Recombinant Proteins/immunology ; T-Lymphocytes/immunology
Chemical Substances	Epitopes ; Immunoglobulin M ; Recombinant Proteins ; Ovalbumin (9006-59-1) ; Leukocyte Common Antigens (EC 3.1.3.48)
Language	English
Publishing date	1995-05-15
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3056-9
ISSN	1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
ISSN (online)	1550-6606
ISSN	0022-1767 ; 1048-3233 ; 1047-7381
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Ud II Zs.37: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
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Article: High strength binding of P815 mastocytoma cells is not necessary for their lysis by macrophages which have been primed and triggered in vitro.

Lu, C Y / Lombardi, M J / Shea, C M / Dustin, L B

Journal of immunology (Baltimore, Md. : 1950)

1988 Volume 141, Issue 4, Page(s) 1083–1090

Abstract: We have examined the hypothesis that binding of P815 mastocytoma cells is a necessary step in lysis of these cells by macrophages which are both "primed" and "triggered" in vitro, Macrophages "primed" by conditioned media containing IFN-gamma, or by rIFN- ...

Abstract	We have examined the hypothesis that binding of P815 mastocytoma cells is a necessary step in lysis of these cells by macrophages which are both "primed" and "triggered" in vitro, Macrophages "primed" by conditioned media containing IFN-gamma, or by rIFN-gamma have an increased ability to bind P815. However, adding either heat-killed Listeria or endotoxin to trigger the primed macrophages has opposite effects on lysis and binding of P815. Lysis is increased. Binding is dramatically decreased. This is true when centrifugal forces of 200 x g, 400 x g, and 800 x g are used to disrupt P815-macrophage binding. Although 100% of P815 cells bound by cytotoxic macrophages are lysed, a large additional population of unbound P815 is also lysed. Detailed kinetic studies indicate that macrophages do not rapidly bind and lyse several cycles of P815. There is an initial lag period of 4 to 6 h before P815 lysis can be detected, and completion of lytic events then occurs within 12 to 14 h. Lysis of P815 bound to cytotoxic macrophages is slightly slower than lysis of the total population of bound and unbound P815. In contrast, D3.1, a cloned CD4+ T cell line, is tightly bound to macrophages but not lysed efficiently. When macrophages are simultaneously confronted with P815 and macrophage-bound D3.1, only the former are lysed. Altogether, the data indicate that P815-macrophage binding, as operationally defined by our assay, is not a necessary step for lysis. These results, by use of macrophages primed and triggered in vitro, are in contrast to previously reported experiments examining P815 binding and lysis by macrophages activated in vivo by infection with bacillus Calmette-Guérin.
MeSH term(s)	Animals ; Cell Communication/drug effects ; Cell Line ; Cell Separation ; Centrifugation ; Cytotoxicity, Immunologic/drug effects ; Female ; Interferon-gamma/pharmacology ; Kinetics ; Macrophage Activation/drug effects ; Macrophages/immunology ; Macrophages/metabolism ; Macrophages/physiology ; Male ; Mast-Cell Sarcoma/immunology ; Mast-Cell Sarcoma/metabolism ; Membranes, Artificial ; Mice ; Mice, Inbred BALB C ; Micropore Filters ; Recombinant Proteins/pharmacology ; Trypsin
Chemical Substances	Membranes, Artificial ; Recombinant Proteins ; Interferon-gamma (82115-62-6) ; Trypsin (EC 3.4.21.4)
Language	English
Publishing date	1988-08-15
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, U.S. Gov't, P.H.S.
ZDB-ID	3056-9
ISSN	1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
ISSN (online)	1550-6606
ISSN	0022-1767 ; 1048-3233 ; 1047-7381
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Ud II Zs.37: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
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Article: Expression of dominant-negative src-homology domain 2-containing protein tyrosine phosphatase-1 results in increased Syk tyrosine kinase activity and B cell activation.

Dustin, L B / Plas, D R / Wong, J / Hu, Y T / Soto, C / Chan, A C / Thomas, M L

Journal of immunology (Baltimore, Md. : 1950)

1999 Volume 162, Issue 5, Page(s) 2717–2724

Abstract: The Src-homology domain 2 (SH2)-containing cytoplasmic tyrosine phosphatase, SHP-1 (SH2-containing protein tyrosine phosphatase-1), interacts with several B cell surface and intracellular signal transduction molecules through its SH2 domains. Mice with ... ...

Abstract	The Src-homology domain 2 (SH2)-containing cytoplasmic tyrosine phosphatase, SHP-1 (SH2-containing protein tyrosine phosphatase-1), interacts with several B cell surface and intracellular signal transduction molecules through its SH2 domains. Mice with the motheaten and viable motheaten mutations are deficient in SHP-1 and lack most mature B cells. To define the role of SHP-1 in mature B cells, we expressed phosphatase-inactive SHP-1 (C453S) in a mature B cell lymphoma line. SHP-1 (C453S) retains the ability to bind to both substrates and appropriate tyrosine-phosphorylated proteins and therefore can compete with the endogenous wild-type enzyme. We found that B cells expressing SHP-1 (C453S) demonstrated enhanced and prolonged tyrosine phosphorylation of proteins with molecular masses of 110, 70, and 55-60 kDa after stimulation with anti-mouse IgG. The tyrosine kinase Syk was hyperphosphorylated and hyperactive in B cells expressing SHP-1 (C453S). SHP-1 and Syk were coimmunoprecipitated from wild-type K46 cells, K46 SHP-1 (C453S) cells, and splenic B cells, and SHP-1 dephosphorylated Syk. Cells expressing SHP-1 (C453S) showed increased Ca2+ mobilization, extracellular signal-regulated kinase activation, and homotypic adhesion after B cell Ag receptor engagement. Thus, SHP-1 regulates multiple early and late events in B lymphocyte activation.
MeSH term(s)	Animals ; B-Lymphocytes/immunology ; Enzyme Precursors/biosynthesis ; Intracellular Signaling Peptides and Proteins ; Lymphocyte Activation ; Mice ; Mice, Inbred C57BL ; Phosphorylation ; Protein Phosphatase 1 ; Protein Tyrosine Phosphatase, Non-Receptor Type 11 ; Protein Tyrosine Phosphatase, Non-Receptor Type 6 ; Protein Tyrosine Phosphatases/physiology ; Protein-Tyrosine Kinases/biosynthesis ; Rabbits ; Receptors, Antigen, B-Cell/physiology ; Signal Transduction ; Syk Kinase ; Tumor Cells, Cultured ; Tyrosine/metabolism
Chemical Substances	Enzyme Precursors ; Intracellular Signaling Peptides and Proteins ; Receptors, Antigen, B-Cell ; Tyrosine (42HK56048U) ; Protein-Tyrosine Kinases (EC 2.7.10.1) ; Syk Kinase (EC 2.7.10.2) ; Syk protein, mouse (EC 2.7.10.2) ; Protein Phosphatase 1 (EC 3.1.3.16) ; Protein Tyrosine Phosphatase, Non-Receptor Type 11 (EC 3.1.3.48) ; Protein Tyrosine Phosphatase, Non-Receptor Type 6 (EC 3.1.3.48) ; Protein Tyrosine Phosphatases (EC 3.1.3.48) ; Ptpn11 protein, mouse (EC 3.1.3.48) ; Ptpn6 protein, mouse (EC 3.1.3.48)
Language	English
Publishing date	1999-03-01
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S.
ZDB-ID	3056-9
ISSN	1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
ISSN (online)	1550-6606
ISSN	0022-1767 ; 1048-3233 ; 1047-7381
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Diverse hepatitis C virus glycoproteins mediate viral infection in a CD81-dependent manner.

McKeating, J A / Zhang, L Q / Logvinoff, C / Flint, M / Zhang, J / Yu, J / Butera, D / Ho, D D / Dustin, L B / Rice, C M / Balfe, P

Journal of virology

2004 Volume 78, Issue 16, Page(s) 8496–8505

Abstract: We recently reported that retroviral pseudotypes bearing the hepatitis C virus (HCV) strain H and Con1 glycoproteins, genotype 1a and 1b, respectively, require CD81 as a coreceptor for virus-cell entry and infection. Soluble truncated E2 cloned from a ... ...

Abstract	We recently reported that retroviral pseudotypes bearing the hepatitis C virus (HCV) strain H and Con1 glycoproteins, genotype 1a and 1b, respectively, require CD81 as a coreceptor for virus-cell entry and infection. Soluble truncated E2 cloned from a number of diverse HCV genotypes fail to interact with CD81, suggesting that viruses of diverse origin may utilize different receptors and display altered cell tropism. We have used the pseudotyping system to study the tropism of viruses bearing diverse HCV glycoproteins. Viruses bearing these glycoproteins showed a 150-fold range in infectivity for hepatoma cells and failed to infect lymphoid cells. The level of glycoprotein incorporation into particles varied considerably between strains, generally reflecting the E2 expression level within transfected cells. However, differences in glycoprotein incorporation were not associated with virus infectivity, suggesting that infectivity is not limited by the absolute level of glycoprotein. All HCV pseudotypes failed to infect HepG2 cells and yet infected the same cells after transduction to express human CD81, confirming the critical role of CD81 in HCV infection. Interestingly, these HCV pseudotypes differed in their ability to infect HepG2 cells expressing a panel of CD81 variants, suggesting subtle differences in the interaction of CD81 residues with diverse viral glycoproteins. Our current model of HCV infection suggests that CD81, together with additional unknown liver specific receptor(s), mediate the virus-cell entry process.
MeSH term(s)	Amino Acid Sequence ; Animals ; Antigens, CD/metabolism ; Cell Line ; Cell Line, Tumor ; Cells, Cultured ; HIV-1/genetics ; HIV-1/metabolism ; Hepacivirus/classification ; Hepacivirus/genetics ; Hepacivirus/pathogenicity ; Hepacivirus/physiology ; Hepatocytes/virology ; Humans ; Liver ; Lymphocytes/virology ; Mice ; Molecular Sequence Data ; Organ Specificity ; Tetraspanin 28 ; Viral Envelope Proteins/chemistry ; Viral Envelope Proteins/genetics ; Viral Envelope Proteins/metabolism
Chemical Substances	Antigens, CD ; CD81 protein, human ; Cd81 protein, mouse ; E1 protein, Hepatitis C virus ; Tetraspanin 28 ; Viral Envelope Proteins ; glycoprotein E2, Hepatitis C virus (157184-61-7)
Language	English
Publishing date	2004-08
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S.
ZDB-ID	80174-4
ISSN	1098-5514 ; 0022-538X
ISSN (online)	1098-5514
ISSN	0022-538X
DOI	10.1128/JVI.78.16.8496-8505.2004
Database	MEDical Literature Analysis and Retrieval System OnLINE

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