B19 virus infection in renal transplant recipients.
BACKGROUND
B19 virus infection with persistent anaemia has been reported in organ transplant recipients. Detection of B19 virus DNA in serum is the best direct marker of active infection.


OBJECTIVE
The present study evaluated the incidence and clinical role of active B19 virus infection in renal transplant recipients presenting with anaemia.


METHODS
Forty-eight such recipients were investigated by nested PCR on serum samples. The controls were 21 recipients without anaemia. Active HCMV infection was also investigated as a marker of high immunosuppression.


CONCLUSIONS
In 11/48 (23%) patients B19 virus DNA was demonstrated in serum versus only 1/21 (5%) of the controls. Ten of these 11 patients had already been seropositive at transplantation and active infection occurred in eight of them during the first 3 months after transplantation. The remaining patient experienced a primary infection 9 months after transplantation. Eight (73%) of these 11 patients displayed a concomitant HCMV infection and four (36%) showed increasing serum creatinine levels but none developed glomerulopathy; 3/11 (27%) recovered spontaneously from anaemia whereas 8/11 (73%) needed therapy. In conclusion, the relatively high occurrence (23%) of B19 virus infection in patients presenting with anaemia, suggests that it should be considered in the differential diagnosis of persistent anaemia in renal transplant recipients. Presence of the viral DNA should be assessed early from transplantation and the viral load should be monitored to follow persistent infection and better understand the relation between active infection and occurrence of anaemia, and to assess the efficacy of IVIG therapy and/or immunosuppression reduction in clearing the virus.
Cavallo
Rossana
R
Virology Unit, Department of Public Health and Microbiology, University of Turin, Via Santena 9, 10126, Turin, Italy. rossana.cavallo@unito.it
Merlino
C
C
Re
D
D
Bollero
C
C
Bergallo
M
M
Lembo
D
D
Musso
T
T
Leonardi
G
G
Segoloni
G P
GP
Ponzi
A Negro
AN
D000740:Anemia / Q000209:etiology* / Q000821:virology; D000911:Antibodies, Monoclonal / Q000009:adverse effects; D000914:Antibodies, Viral / Q000097:blood; D000961:Antilymphocyte Serum / Q000009:adverse effects; D000077552:Basiliximab; D016572:Cyclosporine / Q000009:adverse effects; D003586:Cytomegalovirus Infections / Q000209:etiology / Q000628:therapy / Q000821:virology*; D004279:DNA, Viral / Q000097:blood* / Q000302:isolation & purification; D003937:Diagnosis, Differential; D004198:Disease Susceptibility; D005260:Female; D006801:Humans; D016756:Immunoglobulins, Intravenous / Q000627:therapeutic use; D007166:Immunosuppressive Agents / Q000009:adverse effects; D007375:Interleukin-1 / Q000037:antagonists & inhibitors; D016030:Kidney Transplantation; D008297:Male; D009173:Mycophenolic Acid / Q000009:adverse effects / Q000031:analogs & derivatives; D010322:Parvoviridae Infections / Q000209:etiology / Q000628:therapy / Q000821:virology*; D016732:Parvovirus B19, Human / Q000235:genetics / Q000276:immunology / Q000302:isolation & purification*; D010750:Phosphoproteins / Q000097:blood; D016133:Polymerase Chain Reaction; D011183:Postoperative Complications / Q000821:virology*; D011241:Prednisone / Q000009:adverse effects; D011993:Recombinant Fusion Proteins; D012189:Retrospective Studies; D013601:T-Lymphocytes; D016559:Tacrolimus / Q000009:adverse effects; D019562:Viral Load; D014763:Viral Matrix Proteins / Q000097:blood; D014766:Viremia / Q000821:virology*; D015215:Zidovudine / Q000009:adverse effects
D000911:Antibodies, Monoclonal; D000914:Antibodies, Viral; D000961:Antilymphocyte Serum; D004279:DNA, Viral; D016756:Immunoglobulins, Intravenous; D007166:Immunosuppressive Agents; D007375:Interleukin-1; D010750:Phosphoproteins; D011993:Recombinant Fusion Proteins; D014763:Viral Matrix Proteins; C065418:cytomegalovirus matrix protein 65kDa; D015215:Zidovudine; D016572:Cyclosporine; D000077552:Basiliximab; D009173:Mycophenolic Acid; D011241:Prednisone; D016559:Tacrolimus