REPLICATION AND PERSISTENCE OF COXSACKIEVIRUSES B3 IN HUMAN FIBROBLASTS

Although in some cases a carrier state of Coxsackieviruses in human fi broblasts was described, the persistence mechanism has remained unknow n. Our results demonstrate a replication of Coxsackievirus B3 (CVB3) i n diploid human fibroblasts that is dependent on the virus strain as w ell as on the cell line involved. Two CVB3 Nancy strains could be mult iplied over more than 10 passages in cell line H, whereas CVB3 strains SH''C'' and SH''W'' did not longer form infectious virus following se veral passages in these fibroblasts. None of the CVB3 strains replicat ed in cell lines J and K after a few passages. These results were not influenced by variations of culture conditions such as duration of inc ubation (3 or 7 days), temperature (33 or 37 degrees C) or application of trypsin. In line II, only 3-5 per cent of human fibroblasts were v irus-infected. This was demonstrated by 1. antigen evidence by immunof luorescence, 2. determination of infectious centres, and 3. virus repr oduction in dependence on MOI of the virus. We observed a carrier stat e of CVB3 Nancy strains over 16 cell passages in line H fibroblasts in fected once. As shown in virus passage experiments, only few cells wer e productively infected. An addition of specific anti-CVB3 antiserum t erminated this persistent infection. Generally, no cytopathic effect w as observed. However, in one case a cell destruction by CVB3 Nancy ''P '' at the end of the life-rime of the carrier cells could be found. Th is virus caused a complete cytopathic effect during more than 10 passa ges in line H and could still be neutralized by CVB3-specific antiseru m.