An analysis of the relationship between caveolin and clathrin molecules and BK virus infection seen after kidney transplantation and HLA tissue type distribution.

BK virus infections which usually remains asymptomatic in healthy adults may have different clinical manifestations in immunocompromised patient population. BK virus reactivation can cause BK virus nephropathy in 8% of kidney transplant patients and graft loss may be seen if not treated. Clathrin or Caveolar system are known to be required for the transport of many viruses from Polyomaviruses family including BK viruses and HLA molecules are speculated to have roles as co-receptors for some virus types. In this study, kidney transplant patients with BK virus viremia were divided into two groups according to the BK virus nephropathy found in kidney biopsy (Group I: Viremia +, Nephropathy + / Group II: Viremia+, Nephropathy -). Both patient groups were evaluated with regard to HLA tissue typing match and HLA tissue types. Kidney biopsies were examined with immunohistochemical staining to determine the distribution and density of the Caveolin-1 and Clathrin molecules. Of the 343 patients, 42 had BKV viremia. While HLA match was not found to be a significant factor for viremia, some of donor or recipient HLA allels was found to be significant in BKV viremia or viruria. Immunohistochemical staining of the 31 pathologic specimens with anti-caveolin-1 immunoglobulin revealed statistically significant difference between group-I and group-II. The number of the specimens stained with anti-caveolin-1 was less in group I. On the other hand, we did not find any difference between the groups regarding the anti-clathrin immunochemical analysis. According to these findings, some HLA types may be regarded as risk factors for BKV infection. Besides, caveolin-1 expression can be considered as a protective factor for kidney involvement. Both results should be verified with high scale studies.