The hypothesis that the HBoV infection is indeed a trigger for fibrogenesis is confirmed by some more parameters that showed an increased expression in the HBoV positive patient cohort and also in cell culture: TIMP-1 that is also increased in liver fibrosis [44]; and NAP-2 (CXCL7) that was found to be higher expressed in kidney fibrosis [45], while neutralization of NAP-2 (CXCL7) reduces lung fibrosis in the animal model [46]. Here, TIMP1 is linked to pulmonary fibrosis.