Increasing attention has been recently accorded to BK and JC viruses (BKV a
nd JCV), Both these human polyomavirus (HPV) are members of the papovavirus
family which includes the simian virus SV 40, BKV and JCV infect more than
60% of the population worldwide. After primary infection, they remain harb
oured in the kidneys and may become reactivated in situations of immune imp
airment, HPV were first described in 1971, BIN was isolated in a renal tran
splant patient with ureteral stricture and JCV in a patient with progressiv
e multifocal leukoencephalopathy (PML). BKV was known to be involved in pos
t-bone marrow transplantation (BMT) hemorrhagic cystitis, In renal transpla
ntation, BKV and JCV were initially found in the post-transplant ureteric s
tricture and PML. They are now recognised as a possible cause of transplant
interstitial nephritis, mimicking rejection (satisfying the Banff criteria
for acute rejection) or drug toxicity, In HPV nephritis there is a mixed i
nterstitial inflammatory infiltrate with focal tubular injury; the tubular
epithelium shows marked anisonucleosis, nuclear atypia and basophilic or am
phophilic intranuclear inclusions. Tubulitis is frequent. DNA hybridisation
or gene amplification by polymerase chain reaction usually demonstrate HPV
. Although histology with viral nucleic acid detection may be helpful in di
fferentiating viral infection and rejection, confusion between these compli
cations may lead to either anti-rejection therapy, with the risk of over-im
munosuppression, or reduction of immunosuppression, with the risk of graft
loss. Confusion may also arise with inclusions of other viruses, such as cy
tomegalovirus, herpes virus and adenovirus, Reactivation of BKV and JCV inf
ection was demonstrated in respectively 22.2% and 10.9% of renal transplant
recipients and 55% and 6.7% of BMT patients. Unfortunately, no routine scr
eening is available for these viruses, so this complication is probably und
erestimated, No specific therapy of HPV infection is currently available.