Polyomavirus-Specific Cellular Immunity: From BK-Virus-Specific Cellular Immunity to BK-Virus-Associated Nephropathy?

Abstract

In renal transplantation, BK-virus (BKV)-associated nephropathy has emerged as a major complication, with a prevalence of 1-10% and graft loss in >50% of cases. BKV is a member of the polyomavirus family and rarely induces apparent clinical disease in the general population. However, replication of polyomaviruses, associated with significant organ disease, is observed in patients with acquired immunosuppression. Monitoring of specific immunity combined with viral load could be used to individually assess the risk of viral reactivation and virus control. We review the current knowledge on BKV-specific cellular immunity and, more specifically, in immunocompromised patients. In the future, immune-based therapies could allow us to treat and prevent BKV-associated nephropathy.

Keywords: BK-virus; anti-viral immunity; polyfunctionality; polyomavirus; renal transplantation.

Figure 1

BK-virus-associated nephropathy (A–C): intranuclear viral inclusion in epithelial cells (B,C). Histological analysis of a kidney section from a patient with BKV nephropathy (Trichrome Masson staining). At low magnification (x10), note an extensive fibrosis (green staining) with an important inflammation (Nucleus of leukocytes appeared in black). At higher magnification (x25), the nucleus of some tubular cells is modified by the presence of a large intranuclear viral inclusion which appeared in white (see arrows). Interstitial infiltration is made by several mononuclear cells.