BK virus (BKV) and JC virus (JCV) are widespread human polyomaviruses, and their pathogenic potential during immunodeficiency has been clearly documented. Primary infection usually occurs asymptomatically (or with only mild respiratory symptoms) during childhood, after which the polyomaviruses persist latently in various organs, mainly in the urogenital system, brain and circulating leukocytes. Reactivation of both viruses is common, and frequently associated with asymptomatic viruria. The natural history of infection is well established, but it is still not clear how BKV and JCV are transmitted, although the hypotheses include respiratory, oral-fecal and urinary transmission. Furthermore, on the basis of the frequency of Polyomavirus (PV) infection in childhood, and as has been previously demonstrated in the case of animal homologue polyomaviruses such as the Murine and Simian polyomaviruses (SV-40), some authors have investigated the possibility of vertical transmission, but with conflicting results. So how are these pathogenic viruses transmitted between humans?
Serologic evidence of vertical transmission of JC and BK polyomaviruses in humans. J Gen Virol. Feb 9 2011
Vertical transmission of JC virus and BK virus has been investigated by few authors, with conflicting results. We performed a combined serological and genomic study of 19 unselected pregnant women and their newborns. Blood and urine samples were collected during each gestational trimester in the pregnant women; umbilical cord blood, peripheral blood, urine, and nasopharyngeal secretion samples were taken from newborns at delivery, one week and one month of life. Polyomavirus DNA was detected by nested-PCR. Polyomavirus IgG, IgM and IgA specific antibodies were measured in maternal and newborn serum samples using virus-like particle-based ELISA method. BKV and JCV DNA was detected in urine from 4 (21%) and 5 (26%) women, respectively. BKV and JCV seroprevalence in the pregnant women was 84% and 42%, respectively. Using a rise in the IgG level or the transient appearance of an IgA or IgM response as evidence of infection in the newborn we detected BKV and JCV infections in four (21%) and three (16%) newborns respectively. Three infants had serological evidence of infection with both BKV and JCV. In two of the four possible BKV infected newborns, the mothers seroconverted during pregnancy, while another mother was viruric and IgA seropositive. The mother of one of three possible JCV infected newborn was viruric and IgA seropositive, another mother was viruric. These results suggest JC virus and BK virus can be transmitted from mother to newborn during pregnancy or soon after birth.