Ouroborus has an interesting post looking at the telomere-shortening effect of chronic infections and chronic stress.
Chronic stress has been associated with decreased telomere length in lymphocytes. The association is robust and has been observed in multiple studies, including one that looked at stress in addition to other risk factors for cardiovascular disease (CVD), so it appears that lymphocyte telomeres are a useful biomarker for some convolution of age and lifetime stress level. The question still remains, however, whether the relationship is correlative or causative.
...To the extent that telomere shortening is a causative force in aging (an idea consistent with correlative data showing an association between critically short telomeres and extreme old age, and bolstered by evidence that telomere length is a heritable determinant of lifespan), this study implies that infection itself contributes to the aging process, at least within the hematopoietic lineage — and that we already have one biomarker, just a PCR away from a peripheral blood sample, to measure the extent of that contribution. __ Ouroborus
The article discusses a study that appears to strengthen the connection between infection and telomere shortening.
Geron and other research groups have studied telomerase with the intent of blocking the enzyme in cancer, but also with the possibility that a telomerase form or analog might be useful in regenerating senescent cells.
Until science can separate the connection between cancer and old age, progress on this front may be slow. Then again, breakthroughs often occur just when you'd given up hope.