Human polyomavirus JC and BK persistent infection.

Primary contact with the human polyomaviruses (HPV) is followed by lifelong persistence of viral DNA in its host. The most prominent organs affected are the kidney, the Central Nervous System (CNS)and the hematopoietic system. Under impairment of immune competence limited activation of virus infection can be followed by prolonged virus multiplication, severe destruction of tissue and disease. The mechanisms responsible for activation episodes of the asymptomatic persistent infection are not understood and questions on cellular localization, routes of dissemination of HPV infection and its activation are controversially discussed. The type of interaction of HPVs with target organs and patients groups is highly differentiated. Organ-specific activation above basic level argues for strong dependence on the respective immune states of risk group patients. However, since immune impairment generally plays an important role in the activation of polyomavirus infection, amplification of virus deoxyribonucleic acid (DNA) and activation of virus replication is also a normal event that is probably subject to immunomodulation in the healthy individual. It also becomes clear that BKV and JCV infection is differentially regulated by mechanisms depending on the balance of immune control as well as on organ-specific signalling.

Haemorrhagic cystitis and polyomavirus JC infection in ataxia telangiectasia.

We report the case of a young adolescent with ataxia telangiectasia (AT) and life-threatening haemorrhage from the bladder due to a combination of bladder wall telangiectasis, immunosuppressive therapy and an infection with polyomavirus JC. BK and JC are both members of the polyomavirus family. BK virus is a known cause of haemorrhagic cystitis in bone-marrow and nephropathy in kidney transplant patients, whereas JC virus is mainly associated with progressive multifocal leukoencephalopathy and only rarely found in haemorrhagic cystitis. Although opportunistic infections are uncommon in AT and virus replication was described as being down-regulated in ATM (AT mutated protein)-deficient cells, clinicians should be aware that severe haematuria in a patient with AT and undergoing immunosuppressive therapy is suggestive for polyomavirus JC-induced haemorrhagic cystitis.