Circulating Interferon in Patients with Acute Hepatitis A

Zachoval, R.; Abb, Jochen; Zachoval, Vera; Deinhardt, F.

doi:10.1093/infdis/153.6.1174

Cited by 17 publications

(5 citation statements)

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“…Experimental elimination of HAV infections in human fibroblast cultures by exogenously added IFN-α/β showed that HAV is not resistant to these IFNs [9,181] but reports on the presence of type Ⅰ IFN during the acute phase of HAV infections are controversial. Some indicate that patients do not produce IFN [182][183][184] , while in other reports evidence for the presence of IFN is announced [185][186][187] .…”

Section: Havmentioning

confidence: 99%

Innate and adaptive immune responses against picornaviruses and their counteractions: An overview

Dotzauer

Kraemer

2012

WJV

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Picornaviruses, small positive-stranded RNA viruses, cause a wide range of diseases which is based on their differential tissue and cell type tropisms. This diversity is reflected by the immune responses, both innate and adaptive, induced after infection, and the subsequent interactions of the viruses with the immune system. The defense mechanisms of the host and the countermeasures of the virus significantly contribute to the pathogenesis of the infections. Important human pathogens are poliovirus, coxsackievirus, human rhinovirus and hepatitis A virus. These viruses are the beststudied members of the family, and in this review we want to present the major aspects of the reciprocal effects between the immune system and these viruses.

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Section: Havmentioning

confidence: 99%

Innate and adaptive immune responses against picornaviruses and their counteractions: An overview

Dotzauer

Kraemer

2012

WJV

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“…For instance, interferon ␣ (IFN-␣), which is transiently released during the first wave of innate immunity in response to bacteria and viruses, [2][3][4][5][6][7][8][9][10] has been reported to suppress interleukin-12 (IL-12) production of monocytes and DCs. [11][12][13][14] The superfamily of type I IFNs comprises at least 12 IFN-␣ species and a single IFN-␤ that differentially bind to a common receptor.…”

Section: Introductionmentioning

confidence: 99%

“…9 Usually, this synthesis of type I IFN by activated cells appears to be only transient, 44 resulting in elevated type I IFN serum levels in acute but not in chronic viral infections. [5][6][7] Thus, cell death by coincidence of IFN-␣ priming and bacterial activation seems less likely in chronic viral infections but still could occur, for instance in bacterially colonized tissues (ie, the upper respiratory and the gastrointestinal tract during an acute viral illness).…”

mentioning

confidence: 99%

Type I interferons in combination with bacterial stimuli induce apoptosis of monocyte-derived dendritic cells

Lehner

Felzmann

Clodi

et al. 2001

Blood

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For instance, interferon ␣ (IFN-␣), which is transiently released during the first wave of innate immunity in response to bacteria and viruses, 2-10 has been reported to suppress interleukin-12 (IL-12) production of monocytes and DCs. [11][12][13][14] The superfamily of type I IFNs comprises at least 12 IFN-␣ species and a single IFN-␤ that differentially bind to a common receptor. 15 Alpha IFNs are produced in modest amounts by monocytes, macrophages, and B lymphocytes 9 and in much larger quantities by the precursors of lymphoid DCs (pDC2), 9,16,17 whereas IFN-␤ is mainly produced by fibroblasts. 18 Despite their established protective role in innate immunity because of their antibacterial and antiviral activity, 2,10,[19][20][21] there is increasing evidence that type I IFNs might also act negatively on immunity not only by abrogating IL-12 production but also by impairing DC differentiation 22 and reducing the phagocytic and oxidative activity of monocytes. 23 Other studies showed that lipopolysaccharide (LPS) has suppressive effects on monocytes and monocyte-derived DCs, 4,10 possibly in part mediated by LPS-triggered type I IFN production. A transient presence of endotoxin during the differentiation of monocyte-derived DCs abrogates IL-12 production of the resulting immature DCs on a second stimulation with LPS. 24 If permanently present during DC differentiation, it completely desensitizes the cells to all further LPS-mediated maturation signals. 25 Monocytes from septic patients were found to be hyporesponsive to LPS stimulation ex vivo, and this hyporesponsiveness was reversed during IFN-␥ treatment that also lead to clearance of sepsis, 26 suggesting that monocyte deactivation might be a major mechanism of immunosuppression. Despite these data it is unclear how DCs respond to a combination of type I IFNs and bacterial products. With the use of the culture of monocyte-derived DCs, our study revealed a strong synergistic effect between type I IFNs and products from gramnegative as well as gram-positive bacteria for the induction of apoptosis. This effect occurs if both stimuli are present together during the whole culture but also when the bacterial stimulus is added later to immature DCs generated in the presence of type I IFNs. Materials and methods Monocyte isolation and DC cultureHuman mononuclear cells were obtained from blood containing citrate as anticoagulant from healthy donors by density gradient centrifugation using

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“…We found low serum levels of a-interferon in two chronic HBsAg carriers during episodes of superimposed acute type A hepatitis (19), but were unable to detect interferon in the sera of 49 other patients with sporadic acute viral hepatitis (Davis, G. L., unpublished data). Recently, Zachoval and colleagues (20) detected low levels of ainterferon in 40 of 127 patients with acute type A hepatitis. The probable reason for the inability to detect serum interferon in most patients is that interferon is only produced in sufficient quantity to be detected in the systemic circulation, if at all, during the early (incubation) phase of infection (21).…”

mentioning

confidence: 99%