Production of interferon alpha and interferon gamma by peripheral blood leukocytes from patients with chronic hepatitis B virus infection

Abb, Jochen; Zachoval, Vera; Deinhardt, Friedrich; Pape, Gerd R.; Zachoval, Reinhart; Eisenburg, J

doi:10.1002/jmv.1890160209

Cited by 60 publications

(14 citation statements)

References 9 publications

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“…We found that HCV infection did not result in disturbed inducibility of IRFs genes nor of IFN‐α production. These findings are in contrast with those reported in patients with HBV or HIV infections where the IFN system is impaired in PBMC [49–50].…”

Section: Discussioncontrasting

confidence: 99%

Expression of interferon‐α subtypes in peripheral mononuclear cells from patients with chronic hepatitis C: a role for interferon‐α5

Larrea

Alberdi

Castelruiz

et al. 2001

Journal of Viral Hepatitis

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Interferon (IFN)-alpha is a family of antiviral proteins encoded by different genes. The biological significance of the existence of various IFN-alpha subtypes is not clear. We have investigated the interferon system in chronic hepatitis C virus (HCV) infection, a disease that responds to interferon-alpha2 therapy in only a limited proportion of cases. We analysed the expression of interferon regulatory factor (IRF)-1, IRF-2, and IFN-alpha subtypes in nonstimulated and Sendai virus-stimulated peripheral blood mononuclear cells (PBMC) from HCV infected patients and healthy controls. We observed that the IRF-1 mRNA and IRF-1/IRF-2 ratios were increased in PBMC from hepatitis C patients with respect to normal subjects. Sendai virus stimulation of PBMC led to a significant increase in the levels of IRF-1, IRF-2 and IFN-alpha mRNAs and in the production of IFN-alpha protein with respect to basal values in healthy controls as well as in patients with HCV infection. In addition, we found that while natural HCV infection induced increased IFN-alpha5 expression in PBMC, in vitro infection of these cells with Sendai virus caused a raise in the expression of IFN-alpha8 in both patients and normal controls. In summary, our results indicate that virus-induced activation of the IFN system in human PBMC is associated with selective expression of individual IFN-alpha subtypes, IFN-alpha5 being the specific subtype induced in PBMC from patients with chronic HCV infection.

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Section: Discussioncontrasting

confidence: 99%

Expression of interferon‐α subtypes in peripheral mononuclear cells from patients with chronic hepatitis C: a role for interferon‐α5

Larrea

Alberdi

Castelruiz

et al. 2001

Journal of Viral Hepatitis

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“…Submitted for publication. Lopez et al, 1983;Abb and Deinhardt, 1984;Buimovici-Klein et al, 1986;Siegal et al, 1986;Fitzgerald-Bocarsly et al, 1989b;Rossol et al, 1989Tolentino et al, 1975Abb et al, 1985Levin and Hahn, 1982Emodi and Just, 1974Rhodes-Feuillette et al, 1983Preble et al, 1982Yee et al, 1989 Arvin andMiller, 1984 Neighbor et al, Sendai was not found to be correlated in the patient populations, with normal levels of IFN production in response to Sendai virus often seen in patients with grossly deficient NIPC function. Further, we have observed patients with normal Sendai ELISpot responses but very low frequency NIPC.…”

Section: Ifn Production In Aidsmentioning

confidence: 99%

Human natural interferon-α producing cells

Fitzgerald-Bocarsly

1993

Pharmacology & Therapeutics

198

147

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Interferons (IFNs) are critical components of the host immune system, serving as antiviral agents, immunomodulators and inhibitors of cell growth. Among peripheral blood mononuclear cells, the primary IFN-alpha-producing cell is a light density, HLA-DR+ cell negative for cell surface markers typical for T cells, B cells, monocytes, natural-killer or progenitor cells and has been tentatively termed the 'natural IFN-producing cell' or NIPC. Although present in very low frequency (approximately 1:1000 among peripheral blood mononuclear cells), the NIPC are very potent, with an individual cell able to produce 1-2 IU of IFN. In this review, the characteristics, phenotype, regulation and relationship of NIPC to human disease are discussed.

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“…This MHC protein is part of the recognition signal for cytotoxic T cells and is induced by IFN. Some chronic carriers appear to have a decreased ability to produce IFN in vitro and this may contribute to chronic carriage (10,11). We have previously documented nucleotide homology between HBV and sequences regulating the IFN-induced antiviral system (5).…”

Section: Hepatitis B Virus Is Not Cytopathic and Clearance Of Infectmentioning

confidence: 99%

Defective response to interferons in cells transfected with the hepatitis B virus genome

et al. 1989

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The interferon responsiveness of two cell lines transfected with the hepatitis B virus genome was investigated. A cosmid vector containing multiple copies of the hepatitis B virus genome was transfected into FL5-1 cells; it reduced their sensitivity to interferons as measured by inhibition of the cytopathic effect of Sindbis virus challenge. Similar vectors transfected into HeLa cells reduced their sensitivity to interferon as measured by production of beta 2-microglobulin. This resistance to interferon in hepatitis B virus-transfected cells may be a trans-acting phenomenon related to nucleotide homology between hepatitis B virus DNA and sequences regulating the interferon-induced antiviral system. Alternatively, other mechanisms involving transcription or translation products of hepatitis B virus may be responsible. Hepatitis B virus-induced cellular resistance to the action of interferon may be important in maintaining the chronic carrier state.

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Production of interferon alpha and interferon gamma by peripheral blood leukocytes from patients with chronic hepatitis B virus infection

Cited by 60 publications

References 9 publications

Expression of interferon‐α subtypes in peripheral mononuclear cells from patients with chronic hepatitis C: a role for interferon‐α5

Expression of interferon‐α subtypes in peripheral mononuclear cells from patients with chronic hepatitis C: a role for interferon‐α5

Human natural interferon-α producing cells

Defective response to interferons in cells transfected with the hepatitis B virus genome

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