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Impaired interferon induction of human MxA protein in chronic hepatitis B virus infection
Author(s) -
Fernández Mario,
Quiroga Juan Antonio,
Martín Julio,
Cotonat Teresa,
Pardo Margarita,
Horisberger MichelAndre,
Carreño Vicente
Publication year - 1997
Publication title -
journal of medical virology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.782
H-Index - 121
eISSN - 1096-9071
pISSN - 0146-6615
DOI - 10.1002/(sici)1096-9071(199704)51:4<332::aid-jmv12>3.0.co;2-k
Subject(s) - viremia , immunology , interferon , virus , peripheral blood mononuclear cell , virology , alpha interferon , immune system , cytokine , biology , medicine , in vitro , biochemistry
MxA protein is interferon inducible, and its role as an antiviral mediator is being studied in various viral diseases. Several cytokines, including type I interferons (α and B), interleukins 2 and 12, and granulocyte, macrophage, and granulocyte‐macrophage colony‐stimulating factors, were tested for their ability to induce human MxA protein synthesis in peripheral blood mononuclear cells from 15 chronic hepatitis B virus‐infected patients and 6 healthy subjects as controls. Constitutive MxA expression was scarce in patients and controls but increased significantly in response to type I interferons. MxA responsiveness to interferon α was diminished significantly in chronic hepatitis B patients, compared with healthy donors ( P < 0.05); this effect was more marked in patients with high viremia levels. Interleukins 2 and 12, and none of the colony‐stimulating factors tested, induced low, but detectable, MxA protein levels. These results indicate that chronic infection by hepatitis B virus may impair activation of the immune cells and their capacity to respond to type I interferons. J. Med. Virol. 51:332–337, 1997. © 1997 Wiley‐Liss, Inc.