The current findings suggest that S100A8 and S100A9 aggravate CVB3-induced myocarditis by increasing the accumulation of myeloid cells that can release tissue-damaging granules, are mainly involved in the earlier stages of disease that leads to impaired heart functions, and do not appear to play a role in DCM when the virus is absent [104]. Here, S100A8 is linked to myocarditis.