The detection of hCVs in body compartments beyond the respiratory and enteric tracts is novel and suggests a role of these viruses in organ-related disease. A low detection rate in CSF does not contradict a general potential of these viruses to cause meningoencephalitis, as exemplifi ed by enteroviruses for which lack of detection in CSF despite clear association with disease is not uncommon (10) . Considering links between the related Theilovirus and demyelinating disease in laboratory models (1) outcomes of patients with hCV infection of the central nervous system should be followed up. Such longitudinal studies should include suffi cient numbers of patients because natural infections with Theilovirus in rodents are common and will less frequently result in multiple sclerosis-like disease than in laboratory models (1) . The rarity of hCV detection in our study suggests the assembly of such cohorts to be a diffi cult and lengthy task that could benefi t greatly from international coordination. Despite the absence of histopathologic alterations, the detection of hCV in a child who died of SIDS is remarkable because the related encephalomyocarditis virus constitutes a prototypic model for myocarditis in mammals (11) . Again, the high human seroprevalence against hCV (12) will complicate epidemiologic studies, yet investigations of links between hCV and SIDS are highly justifi ed because diarrhea is an acknowledged risk factor for SIDS (13) .