Changes in gene expression in liver tissue from patients with fulminant hepatitis E

Table 4 Pathways whose genes were found to be over-represented among entities differentially expressed in both fulminant hepatitis E and fulminant hepatitis B, and in fulminant hepatitis E but not in fulminant hepatitis B (derived using BioCarta through DAVID resource)

BioCarta pathway	Gene count	P value
In both FH-B vs normal, and FH-E vs normal
Complement pathway	10	0.0002
Intrinsic prothrombin activation pathway	10	0.0002
Nuclear receptors in lipid metabolism and toxicity	13	0.0022
Alternative complement pathway	6	0.0069
Extrinsic prothrombin activation pathway	6	0.0113
Lectin induced complement pathway	6	0.0172
Classical complement pathway	6	0.0172
Acute myocardial infarction	6	0.0248
Vitamin C in the brain	4	0.0385
CBL mediated ligand-induced downregulation of epidermal growth factor receptors	5	0.0543
Catabolic pathways for methionine, isoleucine, threonine and valine	3	0.0955
In FH-E vs normal but not in FH-B vs normal
T cytotoxic cell surface molecules	7	0.0005
T helper cell surface molecules	6	0.0043
Cytotoxic T lymphocyte mediated immune response against target cells	7	0.0022
Co-stimulatory signal during T-cell activation	7	0.0085
Role of epidermal growth factor receptor transactivation by G protein-coupled receptors in cardiac hypertrophy	6	0.0092
T cell receptor signaling pathway	10	0.0049
Lck and Fyn tyrosine kinases in initiation of T cell receptor activation	5	0.0187
Interleukin-7 signal transduction	5	0.0446
Mitochondrial carnitinepalmitoyltransferase system	3	0.0529
T cell receptor and CD3 complex	3	0.0529
Interleukin-17 signaling pathway	5	0.0562