1990
DOI: 10.1016/0140-6736(90)93101-t
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Non-A, non-B hepatitis specific antibodies directed at host-derived epitope: implication for an autoimmune process

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Cited by 221 publications
(76 citation statements)
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“…Consistent with results from previous studies, 10,28,31,32,33 we found that the prevalence of autoantibodies in HCV patients was significantly higher than those in uninfected controls. Our study showed a high prevalence of ASMA, ANA and RF.…”
Section: Discussionsupporting
confidence: 92%
See 1 more Smart Citation
“…Consistent with results from previous studies, 10,28,31,32,33 we found that the prevalence of autoantibodies in HCV patients was significantly higher than those in uninfected controls. Our study showed a high prevalence of ASMA, ANA and RF.…”
Section: Discussionsupporting
confidence: 92%
“…15,21,24,25,26 The mechanisms by which viruses in general, and HCV in particular, trigger or enhance autoimmunity can be explained in various ways. 27,28,29,30 According to one theory, viruses may non-specifically trigger immune regulatory cells, such as lymphocytes or macrophages, inducing them to react with self-antigens in multiple organs, and therefore cause tissue injury as well as extrahepatic diseases. Another theory suggests that viruses alter the antigenic profile of infected cells (such as hepatocytes) by changing, releasing or exposing selfantigens that are usually "hidden" and for which the immune system usually has no tolerance.…”
Section: Discussionmentioning
confidence: 99%
“…In cases of community-acquired infection, 62% develop chronic hepatitis in the USA [5]. Recent data show evidence for the presence of several autoimmune phenomena in patients with HCV infection, such as oligo-or polyarthritis [6,7], primary Sjogren's syndrome [8,9], membranoprolifcrative glomerulonephritis [10], cryoglobulinaemia [11][12][13][14], antinuclear, anti-mitochondrial, and anti-smooth muscle antibodies [11], rheumatoid factors [11,13], autoantibodies targeting a host protein named GOR, cloned from a chimpanzee infected with non-A, non-B hepatitis [15,16], and LKM-1 antibodies in adult palients with concomitant type 2 autoimmune hepatitis [17][18][19][20][21]. Some of the events were related to interferon-alpha {lFN-«) treatment [22] or to concomitant HCV infection due to exposure to human blood products [23].…”
Section: Introductionmentioning
confidence: 99%
“…2 The high HCV mutation rate readily generates variants that contribute to establishing the persistent infection. 3 HCV is known to cause a variety of systemic immunologic reactions or abnormalities such as circulating immune complexes, 4 autoantibodies, 5,6 and autoimmune manifestations. [7][8][9][10] Although the liver is considered the primary site of HCV replication with convincing evidence, 11,12 systemic or extrahepetic immune reactions, as well as intrahepatic responses, can be induced in the course of chronic infection.…”
mentioning
confidence: 99%