Viral type I interferon binding protein

We investigated if signs of active Epstein–Barr virus and cytomegalovirus infections associate with certain autoantibodies and a marker of type I interferon activity in patients with systemic lupus erythematosus. IgM and IgG plasma levels against Epstein–Barr virus early antigen diffuse and cytomegalovirus pp52 were applied as humoral markers of ongoing/recently active Epstein–Barr virus and cytomegalovirus infections, respectively. Plasma galectin-3 binding protein served as a surrogate marker of type I interferon activity. The measurements were conducted in 57 systemic lupus erythematosus patients and 29 healthy controls using ELISAs. Regression analyses and univariate comparisons were performed for associative evaluation between virus serology, plasma galectin-3 binding protein and autoantibodies, along with other clinical and demographic parameters. Plasma galectin-3 binding protein concentrations were significantly higher in systemic lupus erythematosus patients ( P = 0.009) and associated positively with Epstein–Barr virus early antigen diffuse-directed antibodies and the presence of autoantibodies against extractable nuclear antigens in adjusted linear regressions (B = 2.02 and 2.02, P = 0.02 and P = 0.002, respectively). Furthermore, systemic lupus erythematosus patients with anti-extractable nuclear antigens had significantly higher antibody levels against Epstein–Barr virus early antigen diffuse ( P = 0.02). Our study supports a link between active Epstein–Barr virus infections, positivity for anti-extractable nuclear antigens and increased plasma galectin-3 binding protein concentrations/type I interferon activity in systemic lupus erythematosus patients.

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Resistance to Oncolytic Myxoma Virus Therapy in Nf1−/−/Trp53−/− Syngeneic Mouse Glioma Models Is Independent of Anti-Viral Type-I Interferon

PLoS ONE ◽

10.1371/journal.pone.0065801 ◽

2013 ◽

Vol 8 (6) ◽

pp. e65801 ◽

Cited By ~ 10

Author(s):

Franz J. Zemp ◽

Brienne A. McKenzie ◽

Xueqing Lun ◽

Lori Maxwell ◽

Karlyne M. Reilly ◽

...

Keyword(s):

Type I Interferon ◽

Myxoma Virus ◽

Type I ◽

Syngeneic Mouse ◽

Viral Type ◽

Mouse Glioma

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Degradation of CREB-binding protein and modulation of type I interferon induction by the zinc finger motif of the porcine reproductive and respiratory syndrome virus nsp1α subunit

Virus Research ◽

10.1016/j.virusres.2012.12.012 ◽

2013 ◽

Vol 172 (1-2) ◽

pp. 54-65 ◽

Cited By ~ 36

Author(s):

Mingyuan Han ◽

Yijun Du ◽

Cheng Song ◽

Dongwan Yoo

Keyword(s):

Zinc Finger ◽

Type I Interferon ◽

Binding Protein ◽

Respiratory Syndrome Virus ◽

Type I ◽

Zinc Finger Motif ◽

Creb Binding Protein ◽

Interferon Induction

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Functional assay of type I interferon in systemic lupus erythematosus plasma and association with anti–RNA binding protein autoantibodies

Arthritis & Rheumatism ◽

10.1002/art.21890 ◽

2006 ◽

Vol 54 (6) ◽

pp. 1906-1916 ◽

Cited By ~ 195

Author(s):

Jing Hua ◽

Kyriakos Kirou ◽

Christina Lee ◽

Mary K. Crow

Keyword(s):

Systemic Lupus Erythematosus ◽

Lupus Erythematosus ◽

Rna Binding ◽

Type I Interferon ◽

Binding Protein ◽

Rna Binding Protein ◽

Functional Assay ◽

Type I ◽

Systemic Lupus

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Type I Interferon Induces Inhibitory 16-kD CCAAT/ Enhancer Binding Protein (C/EBP)β, Repressing the HIV-1 Long Terminal Repeat in Macrophages: Pulmonary Tuberculosis Alters C/EBP Expression, Enhancing HIV-1 Replication

Journal of Experimental Medicine ◽

10.1084/jem.188.7.1255 ◽

1998 ◽

Vol 188 (7) ◽

pp. 1255-1265 ◽

Cited By ~ 86

Author(s):

Yoshihiro Honda ◽

Linda Rogers ◽

Koh Nakata ◽

Ben-Yang Zhao ◽

Richard Pine ◽

...

Keyword(s):

Pulmonary Tuberculosis ◽

Alveolar Macrophages ◽

Protein C ◽

Type I Interferon ◽

Binding Protein ◽

Type I ◽

Enhancer Binding Protein ◽

Hiv 1

We have previously observed that HIV-1 replication is suppressed in uninflamed lung and increased during tuberculosis. In vitro THP-1 cell–derived macrophages inhibited HIV-1 replication after infection with Mycobacterium tuberculosis. Suppression of HIV-1 replication was associated with inhibition of the HIV-1 long terminal repeat (LTR) and induction of ISGF-3, a type I interferon (IFN)–specific transcription factor. Repression of the HIV-1 LTR required intact CCAAT/enhancer binding protein (C/EBP) sites. THP-1 cell–derived macrophages infected with M. tuberculosis, lipopolysaccharide, or IFN-β induced the 16-kD inhibitory C/EBPβ isoform and coincidentally repressed HIV-1 LTR transcription. C/EBPβ was the predominant C/EBP family member produced in THP-1 macrophages during HIV-1 LTR repression. In vivo, alveolar macrophages from uninflamed lung strongly expressed inhibitory 16-kD C/EBPβ, but pulmonary tuberculosis abolished inhibitory C/EBPβ expression and induced a novel C/EBP DNA binding protein. Therefore, in vitro, proinflammatory stimulation produces an IFN response inhibiting viral replication by induction of a C/EBPβ transcriptional repressor. THP-1 cell–derived macrophages stimulated with type I IFN are similar to alveolar macrophages in the uninflamed lung in vivo. In contrast, the cellular immune response in active pulmonary tuberculosis disrupts this innate immunity, switching C/EBP expression and allowing high level viral replication.

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