Immune Complexes in Viral Infection

Casali, Paolo; Oldstone, Michael B. A.

doi:10.1007/978-3-642-68949-9_2

Cited by 16 publications

(6 citation statements)

References 148 publications

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“…With respect to the role of hepatitis virus infection in dengue-related hepatitis, there has been no evidence to suggest that the course of illness is influenced by concomitant hepatitis virus or that hepatitis B infection acts as co-factor for hepatic damage in dengue infections (Kuo et al, 1992;Seneviratne et al, 2006). The length of illness associated with hepatitis is about 2-3 weeks with peak elevations in AST on the 7th or 8th day of illness (Casali and Oldstone, 1983;de Souza et al, 2002), and this is consistent with our findings. Liver enzyme abnormalities usually return to normal during the 2-3 weeks of illness (Seneviratne et al, 2006).…”

Section: Discussionsupporting

confidence: 92%

Fulminant hepatitis in dengue haemorrhagic fever

Ling¹,

Wilder-Smith²,

Leo³

2007

Journal of Clinical Virology

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Section: Discussionsupporting

confidence: 92%

Fulminant hepatitis in dengue haemorrhagic fever

Ling¹,

Wilder-Smith²,

Leo³

2007

Journal of Clinical Virology

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“…Consistent with previously documented studies (2,5,18,42,43), our results indicated that positive human sera had very low titers of BDV antibodies. The possible contribution of immune complexes to this phenomenon cannot be excluded (11). The low serum dilutions (1:20) used in the Western blot assay probably contributed to the nonspecific staining of some proteins present in the extracts used as sources of target antigens.…”

Section: Discussionmentioning

confidence: 99%

Detection of Borna disease virus (BDV) antibodies and BDV RNA in psychiatric patients: evidence for high sequence conservation of human blood-derived BDV RNA

Sauder¹,

Müller²,

Cubitt³

et al. 1996

J Virol

129

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In several vertebrate species, Borna disease virus (BDV), the prototype of a new group of animal viruses, causes central nervous system disease accompanied by diverse behavioral abnormalities. Seroepidemiological data indicate that BDV may contribute to the pathophysiology of certain human mental disorders. This hypothesis is further supported by the detection of both BDV antigens and BDV RNA in peripheral blood mononuclear cells (PBMCs) of patients with psychiatric disorders and the isolation of BDV from such PBMCs.Here we describe serological and molecular epidemiological studies on psychiatric patients and healthy individuals from the area of Homburg, Germany. Using a novel Western blot (immunoblot) assay, we found a BDV seroprevalence of 9.6% among 416 neuropsychiatric patients, which is significantly higher than the 1.4% found among 203 healthy control individuals. Human sera displayed a prominent immunoreactivity against the virus nucleoprotein, the p40 antigen. Reverse transcriptase-mediated PCR analysis of RNA extracted from PBMCs of a subset of 26 of the neuropsychiatric patients revealed that 50% were BDV RNA positive. Three of the 13 BDV RNA-positive patients also had BDV-positive serology, whereas one patient with serum antibodies to BDV p40 antigen did not harbor detectable BDV RNA in PBMCs. BDV p40 and p24 sequences derived from human PBMCs exhibited both a high degree of inter-and intrapatient conservation and a close genetic relationship to animal-derived BDV sequences.

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“…In certain viral diseases immune complexes (IC) are formed when antibodies are produced and react with viral antigen molecules which persist in the host or are released from infected cells into extracellular fluids. In a second pathogenic pathway, viruses induce a polyclonal B-cell proliferation with production of antibodies with a broad spectrum of specificity including autoantibodies, thus leading to formation of IC which involve both viral and self antigens (Theofilopoulos and Dixon, 1980;Trautwein, 1982;Casali and Oldstone, 1983;Sissons and Borysiewicz, 1985 ). Some of the persistent viral infections are associated with virus-induced IC deposits and IC-mediated tissue injury.…”

Section: Virus-induced Immune Complex Diseasementioning

confidence: 99%

Immune mechanisms in the pathogenesis of viral diseases: a review

Trautwein¹

1992

Veterinary Microbiology

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Three immunopathological mechanisms may determine the pathogenesis of viral diseases in animals. (1) A variety of viruses causes transient or prolonged immunosuppression by infecting lymphoreticular tissues and interacting with components of the immune system. (2) In persistent viral infections effective immune responses may result in tissue damage. The mechanisms involved are T-cell-mediated destruction of infected cells and delayed-type hypersensitivity. (3) In a number of viral diseases pathogenic immune complexes are formed when antibodies are produced and react with viral antigen molecules persisting in the host. The selected examples of immune dysfunction are the focus of this review.

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Immune Complexes in Viral Infection

Cited by 16 publications

References 148 publications

Fulminant hepatitis in dengue haemorrhagic fever

Fulminant hepatitis in dengue haemorrhagic fever

Detection of Borna disease virus (BDV) antibodies and BDV RNA in psychiatric patients: evidence for high sequence conservation of human blood-derived BDV RNA

Immune mechanisms in the pathogenesis of viral diseases: a review

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