The identified proteins included complement, acute phase proteins, and proteases.
Spore-bound proteins included complement proteins, blood coagulation/fibrinolysis regulators, acute phase proteins, and cell surface and extracellular proteins.
Liver-associated terms included complement activation (2.6×10−4), lipid homeostasis (5.86×10−3) and cholesterol efflux (7.09×10−3).
Affected pro-inflammatory pathways (maps) included, Complement activation, Signaling via ephrins, TOLL-like (TLR) receptors and IL-1.
Those included complement components, adhesion molecules, chemokines and their receptors, and molecules related to antigen presentation [19].
The inflammatory response pathway included complement 1q subcomponent, B chain (C1QB), A chain (C1QA) and C chain (C1QC).
Additional methods used to identify selected isolates included complement fixation (CF) and hemagglutination-inhibition tests (17 ) and panviral microarray-based genotyping (18 ).
This group included complement components, cytokines, chemokines and their receptors, IFN and TNF-related genes, together with three negative regulators of immunity from the SOCS family.
Additional enriched pathways included complement alternate pathway activation (hinting at immune involvement under OFF- state), acute inflammatory response and mitochondrion (Additional file 10: Table S10).
Other upregulated genes included complement subcomponents C1qb (C1qb, 1.6-fold) and C1qc (C1qc, 1.4-fold), Fc receptor homolog S (Fcrls, 1.6-fold) and glial fibrillary aC1qcc protein (GFAP, 1.4-fold).
Similarly to our results, the list of these proteins included complement factors, apolipoprotein A-I, pigment epithelium-derived factor (PEDF) and others.
