Polyomavirus, Adenovirus, and Viral Respiratory Diseases

Abstract

BK polyomavirus (BKPyV) belongs to the genus Polyomavirus of the family Polyomaviridae that comprises 13 different species with human host (Calvignac-Spencer et al. 2016). BKPyV virions are small non-enveloped particles of 40–45 nm in diameter, with an icosahedral symmetry, resistant to heat, and environment exposure (Hirsch and Steiger 2003). Structurally, BKPyV consists of a circular 5.1 kb double-stranded DNA genome within a capsid made of proteins Vp1 on the outside and Vp2 and Vp3 on the inside. The BKPyV genome is divided into three regions: the noncoding control region (NCCR); the early viral gene region (EVGR); the late viral gene region (LVGR). The NCCR is responsible for DNA replication and bidirectional viral gene expression; the EVGR encodes the regulatory nonstructural proteins called small tumor antigen (sTag), large tumor antigen (LTag), and spliced variants called truncated Tag; the LVGR contains the genes for the structural proteins Vp1, Vp2, Vp3, and a small accessory protein of unknown function called agnoprotein. The Vp1 capsid protein is the main target of BKPyV-specific antibodies while LTag is used as target for immunohistochemical diagnosis in tissue samples. BKPyV was isolated for the first time in a patient (B.K.) who underwent a kidney transplant and presented in the urine particular epithelial cells with nuclear viral inclusions called “decoy cells” (Gardner et al. 1971). Subsequently, BKPyV has been associated with hemorrhagic cystitis (HC) after hematopoietic stem cell transplantation (HSCT) (Apperley et al. 1987; Arthur et al. 1986), and nephropathy after kidney transplantation (Binet et al. 1999; Randhawa et al. 1999). Serologic studies showed that up to 90% of the adult population has been exposed to BKPyV during infancy and childhood (Egli et al. 2009). The infection can be asymptomatic or causes flu-like symptoms indistinguishable from other causes of viral community respiratory tract infections. The transmission is thought to be by direct person-to-person contact or by exposure to respiratory secretions. After primary infection, the virus remains latent in renal tubular epithelial and urothelial cells and asymptomatic viruria can be detected in 5–10% of healthy individuals (Hirsch and Steiger 2003; Egli et al. 2009). The urinary shedding increases to 60–80% in patients undergoing HSCT, as well as the BKPyV viruria load increases to less than 3 log10 to >7 log10 copies/mL (Cesaro et al. 2018a; Cesaro et al. 2015).