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13. Reduced expression of Jak-1 and Tyk-2 proteins leads to interferon resistance in Hepatitis C virus replicon

Author

Luftig Ronald, Florman Sander, Garry Robert F, Haque Salima, Taylor Lizeth, Hazari Sidhartha, Regenstein Frederic, and Dash Srikanta

Subjects
Infectious and parasitic diseases, RC109-216
Abstract

Abstract Background Alpha interferon in combination with ribavirin is the standard therapy for hepatitis C virus infection. Unfortunately, a significant number of patients fail to eradicate their infection with this regimen. The mechanisms of IFN-resistance are unclear. The aim of this study was to determine the contribution of host cell factors to the mechanisms of interferon resistance using replicon cell lines. Results HCV replicons with high and low activation of the IFN-promoter were cultured for a prolonged period of time in the presence of interferon-alpha (IFN-alpha2b). Stable replicon cell lines with resistant phenotype were isolated and characterized by their ability to continue viral replication in the presence of IFN-alpha. Interferon resistant cell colonies developed only in replicons having lower activation of the IFN promoter and no resistant colonies arose from replicons that exhibit higher activation of the IFN promoter. Individual cell clones were isolated and nine IFN resistant cell lines were established. HCV RNA and protein levels in these cells were not altered by IFN- alpha2b. Reduced signaling and IFN-resistant phenotype was found in all Huh-7 cell lines even after eliminating HCV, suggesting that cellular factors are involved. Resistant phenotype in the replicons is not due to lack of interferon receptor expression. All the cell lines show defect in the JAK-STAT signaling and phosphorylation of STAT 1 and STAT 2 proteins were strongly inhibited due to reduced expression of Tyk2 and Jak-1 protein. Conclusion This in vitro study provides evidence that altered expression of the Jak-Stat signaling proteins can cause IFN resistance using HCV replicon cell clones.

Published
2007
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15. Metastatic pancreatic carcinoma presenting as colon carcinoma

Author

Bellows, Charles, Gage, Thomas, Stark, Matthew, McCarty, Curt, and Haque, Salima

Subjects
Pancreatic cancer -- Diagnosis, Pancreatic cancer -- Care and treatment, Pancreatic cancer -- Case studies, Colon cancer -- Diagnosis, Metastasis -- Diagnosis, Metastasis -- Care and treatment, Metastasis -- Case studies, DNA binding proteins -- Identification and classification, Health
Published
2009

38. PAT-2. Composite gastric carcinoma arising in a background of lymphocytic gastritis

Author

Mac, Mylinh T. and Haque, Salima

Subjects
Care and treatment, Research, Stomach cancer -- Care and treatment -- Research
Abstract

Composite carcinoma is a rare malignant neoplasm composed of two different types of tumor in discrete areas intermingled with each other, probably representing a single neoplasm with multidirectional differentiation. We [...]

Published
2004

39. PAT-5. Langerhans cell histiocytosis in liver: single organ involvement in a child

Author

Buza, Natalia and Haque, Salima

Subjects
Research, Cells (Biology) -- Research, Histiocytosis -- Research, Cells -- Research
Abstract

Langerhans cell histiocytosis (LCH; Histiocytosis X) is a rare neoplastic process that can affect various organ systems. The hepatic manifestation in LCH is rare and usually presents as part of [...]

Published
2004

40. Reply

Author

Haque, Salima, primary, Eisen, Richard N., additional, and Brian West, A., additional

Published
1993
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46. Interferonsα,β,γ each inhibit hepatitis C virus replication at the level of internal ribosome entry site-mediated translation.

Author

Dash, Srikanta, Prabhu, Ramesh, Hazari, Sidhartha, Bastian, Frank, Garry, Robert, Zou, Weiping, Haque, Salima, Joshi, Virendra, Regenstein, Fredric G., and Thung, Swan N.

Subjects
HEPATITIS C virus, LIVER diseases, GENOMES, VIRAL hepatitis, MESSENGER RNA, ANTINEOPLASTIC agents
Abstract

Dash S, Prabhu R, Hazari S, Bastian F, Garry R, Zou W, Haque S, Joshi V, Regenstein FG, Thung SN. Interferonsα,β,γ each inhibit hepatitis C virus replication at the level of internal ribosome entry site-mediated translation.Liver International 2005: DOI: 10.1111/j.1478-3231.2005.01082.x.© Blackwell Munksgaard 2005Interferon (IFN)-α is the standard therapy for the treatment of chronic hepatitis C, but the mechanisms underlying its antiviral action are not well understood. In this report, we demonstrated that IFN-α, -β and -γ inhibit replication of the hepatitis C virus (HCV) in a cell culture model at concentrations between 10 and 100 IU/ml. We demonstrated that the antiviral actions each of each these IFNs are targeted to the highly conserved 5′ untranslated region of the HCV genome, and that they directly inhibit translation from a chimeric clone between full-length HCV genome and green fluorescent protein (GFP). This effect is not limited to HCV internal ribosome entry site (IRES), since these IFNs also inhibit translation of the encephalomyocardititis virus (EMCV) chimeric mRNA in which GFP is expressed by IRES-dependent mechanisms (pCITE-GFP). These IFNs had minimal effects on the expression of mRNAs from clones in which translation is not IRES dependent. We conclude that IFN-α, -β and -γ inhibit replication of sub-genomic HCV RNA in a cell culture model by directly inhibiting two internal translation initiation sites of HCV- and EMCV-IRES sequences present in the dicistronic HCV sub-genomic RNA. Results of thisin vitrostudy suggest that selective inhibition of IRES-mediated translation of viral polyprotein is a general mechanism by which IFNs inhibits HCV replication. [ABSTRACT FROM AUTHOR]

Published
2005
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48. A Cecal Diaphragm Associated with the Use of Nonsteroidal Antiinflammatory Drugs

Author

Haque, Salima, Haswell, James E., Dreznick, Jeffrey T., and West, A. Brian

Abstract

In the small intestine, strictures and diaphragms causing obstructive symptoms are well known to occur in patients using nonsteroidal anti-inflammatory drugs. Recently, two cases of nonsteroidal anti-inflammatory drug (NSAID)-associated diaphragm-like colonic stricture were reported as unexpected findings in patients being investigated for iron-deficiency anemia. We present a third such case that occurred in the cecum in a 49-year-old woman with rheumatoid arthritis who had been taking NSAIDs for 5 years.

Published
1992

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