Variable sources of Bk virus in renal allograft recipients

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Citações na Scopus
6
Tipo de produção
article
Data de publicação
2019
Título da Revista
ISSN da Revista
Título do Volume
Editora
WILEY
Citação
JOURNAL OF MEDICAL VIROLOGY, v.91, n.6, p.1136-1141, 2019
Projetos de Pesquisa
Unidades Organizacionais
Fascículo
Resumo
BK virus is the causative agent of polyomavirus-associated nephropathy, a major cause of kidney transplant failure affecting 1%-10% of recipients. Previous studies that investigated the viral source on the kidney recipient pointed that the donor is implicated in the origin of human polyomavirus BK (BKPyV) infection in recipients, but giving the low genetic variability of BKPyV this subject is still controversial. The aim of this study was to determine if BKPyV replicating in kidney recipients after transplantation is always originated from the donor. Urine and blood samples from 68 pairs of living donors and kidney recipients who underwent renal transplantation from August 2010-September 2011 were screened for BKPyV by real time polymerase chain reaction. Only three recipients presented viremia. When both donors and recipients were BKPyV positive, a larger fragment of VP1 region was obtained and sequenced to determine the level of similarity between them. A phylogenetic tree was built for the 12 pairs of sequences obtained from urine and high level of similarity among all sequences was observed, indicating that homology inferences for donor and recipient viruses must be cautiously interpreted. However, a close inspection on the donor-recipient pairs sequences revealed that 3 of 12 pairs presented considerably different viruses and 4 of 12 presented mixed infection, indicating that the source of BKPyV infection is not exclusively derived from the donor. We report that about 60% of the renal recipients shed BKPyV genetically distinct from the donor, confronting the accepted concept that the donor is the main source of recipients' infection.
Palavras-chave
human polyomavirus BK, renal transplantation, viral source, viruria
Referências
  1. Babel N, 2009, TRANSPLANTATION, V88, P89, DOI 10.1097/TP.0b013e3181aa8f62
  2. Bohl DL, 2005, AM J TRANSPLANT, V5, P2213, DOI 10.1111/j.1600-6143.2005.01000.x
  3. Darriba D, 2012, NAT METHODS, V9, P772, DOI 10.1038/nmeth.2109
  4. GARDNER SD, 1971, LANCET, V1, P1253
  5. Gouy M, 2010, MOL BIOL EVOL, V27, P221, DOI 10.1093/molbev/msp259
  6. Haines HL, 2011, BIOL BLOOD MARROW TR, V17, P1512, DOI 10.1016/j.bbmt.2011.02.012
  7. Hirsch HH, 2005, TRANSPLANTATION, V79, P1277, DOI 10.1097/01.TP.0000156165.83160.09
  8. Hirsch HH, 2003, LANCET INFECT DIS, V3, P611, DOI 10.1016/S1473-3099(03)00770-9
  9. Zalona ACJ, 2011, J MED VIROL, V83, P1401, DOI 10.1002/jmv.22117
  10. Knowles WA, 2006, ADV EXP MED BIOL, V577, P19
  11. Krumbholz A, 2008, INFECT GENET EVOL, V8, P632, DOI 10.1016/j.meegid.2008.05.006
  12. Krumbholz A, 2006, J MED VIROL, V78, P1588, DOI 10.1002/jmv.20743
  13. MOENS U, 1995, VIRUS GENES, V10, P261, DOI 10.1007/BF01701816
  14. Morel V, 2017, J CLIN MICROBIOL, V55, P1177, DOI 10.1128/JCM.01180-16
  15. Pal A, 2006, J VIROL METHODS, V135, P32, DOI 10.1016/j.jviromet.2006.01.018
  16. Pang XLL, 2007, J CLIN MICROBIOL, V45, P3568, DOI 10.1128/JCM.00655-07
  17. Randhawa P, 2004, J CLIN MICROBIOL, V42, P1176, DOI 10.1128/JCM.42.3.1176-1180.2004
  18. Saundh BK, 2013, J INFECT DIS, V207, P137, DOI 10.1093/infdis/jis642
  19. Schmitt C, 2014, J CLIN VIROL, V59, P120, DOI 10.1016/j.jcv.2013.11.009
  20. Schwarz A, 2016, TRANSPLANTATION, V100, P844, DOI 10.1097/TP.0000000000001066
  21. Tamura K, 2011, MOL BIOL EVOL, V28, P2731, DOI 10.1093/molbev/msr121
  22. Thompson JD, 1997, NUCLEIC ACIDS RES, V25, P4876, DOI 10.1093/nar/25.24.4876
  23. Tremolada S, 2010, J CELL PHYSIOL, V222, P195, DOI 10.1002/jcp.21937
  24. Vera-Sempere FJ, 2006, TRANSPL P, V38, P2378, DOI 10.1016/j.transproceed.2006.08.049
  25. Verghese PS, 2015, TRANSPLANTATION, V99, P602, DOI 10.1097/TP.0000000000000354