Analysis of virus replication in ageing human fibroblast cultures.

SINCE Swim and Parker1 and Hayflick and Moorhead2 documented the limited life span of diploid human fibroblasts in cell culture, many investigators have used these cells as possible models of cellular senescence. Most normal human fibroblasts exhibit marked cellular changes and eventually cease growth after fifty to seventy cell divisions. Hayflick3 and Martin et al.4 demonstrated an inverse relationship between the life span of cultured human diploid fibroblasts and the age of the donor. Furthermore, fibroblasts from children with premature ageing diseases have a markedly reduced potential for cell division4. Many investigators have studied human fibroblasts to determine whether their finite life span is related to ageing, and to determine the mechanism of ‘senescence’ in these cells5. There is no firm evidence, however, that fibroblast ‘ageing’ or limited fibroblast division potential is necessarily involved in the tissue and organ changes associated with ageing of individuals. Many types of cells which are obviously important in ageing of the whole organism undergo little or no division in adults (for example, neurones), and others which divide rapidly (for example, intestinal epithelium) have not been shown to behave as fibroblasts do, either in culture or in the organism.