PolyomavirusBK（BKV）infectsupto90%ofthegeneralpopulation.Afterprimaryinfection,occurringearlyduringchildhood,astateofnon-replicativeinfectionisestablishedinthereno-urinarytract,withoutcomplicationsforimmunocompetenthosts.Inimmunocompromisedinpiduals,particularlytransplantedpatients,asymptomaticBKVviremiaand/orviruriacanbeobserved.RenalgraftsmayalsobesourcesofinfectionasBKVpreferskidneysratherthanothersolidorgansfortransplantationsuchastheliver.ThemechanismbehindthehigherincidenceofBKVinfectioninkidneytransplantpatients,comparedtoliverorhearttransplantation,isunclearandtheprevalenceofBKVinfectioninnon-renalsolidorgantransplantshasnotbeenyetthoroughlyinvestigated.WeevaluatedtheprevalenceofPolyomavirusBKinfectionamonglivertransplantrecipients.APubMedsearchwasconductedusingthetermsBKVinfectionANDlivertransplantrecipients;BKVANDnon-renalsolidorgantransplant＊;BKVinfectionANDimmunosuppression;thesearchwaslimitedtotitle/abstractandEnglish-languagearticlespublishedfrom2000,toMarch2015.ElevenrelevantstudiessuggestthattheprevalenceofBKVviruriaand/orviremiaamonglivertransplantrecipientsislessthanthatreportedinkidneyorhearttransplantrecipients,exceptwhenchronickidneydisease（CKD）ispresentatthesametime.DataalsosuggestthatviruricandviremicpatientshavehigherlevelsofserumcreatininethanBKVnegativepatients.Moreover,nospecificimmunosuppressivedrugsareassociatedwiththeonsetofBKVnephropathy.ThecomorbidityoftransplantationandCKDcouldplayamajorroleinpromotingBKVreplication.
