At the same time, it must be taken into account that TGF-β is present from the very onset of the infection, once macrophages phagocyte apoptotic bodies [46], thus downregulating the CMI and favoring the fibrosis, an activity that increases its intensity as the infection progresses, together with the presence of IL-4, which has also been shown to be profibrotic, which also appears at latest time points [47]. This evidence concerns the gene IL4 and infection.