4.2 Article

Human pegivirus type 1 infection in kidney transplant recipients: Replication kinetics and clinical correlates

期刊

TRANSPLANT INFECTIOUS DISEASE
卷 24, 期 1, 页码 -

出版社

WILEY
DOI: 10.1111/tid.13771

关键词

human pegivirus type 1; immunosuppression; infection; kidney transplantation; outcomes; replication kinetics

资金

  1. Instituto de Salud Carlos III (ISCIII), Spanish Ministry of Science and Innovation [PI15/01953, CP18/00073, CM18/00221, JR18/00053]
  2. European Development Regional Fund
  3. Rio Hortega [CM18/00221]
  4. Instituto de Salud Carlos III [PI15/01953, CP18/00073, CM18/00221, JR18/00053]
  5. research contract Juan Rodes [JR18/00053]
  6. research contract Miguel Servet [CP18/00073]

向作者/读者索取更多资源

The study found that HPgV-1 infection does not appear to influence patient or graft outcomes after kidney transplantation. The infection rate is mainly influenced by the type of organ transplantation and donation method.
Background Increasing evidence suggests that infection with the nonpathogenic human pegivirus type 1 (HPgV-1) exerts a clinical benefit in human immunodeficiency virus (HIV) patients, which could be attributable to immunomodulatory effects. Whether this impact can be extrapolated to kidney transplantation (KT) remains largely unknown. Methods We measured plasma HPgV-1 RNA by real-time polymerase chain reaction targeting the 5 ' untranslated region at various points (pretransplantation, day 7, months 1, 3, 6, and 12) in 199 KT recipients. Study outcomes included posttransplant serious infection, immunosuppression-related adverse event (opportunistic infection and/or de novo cancer), and acute graft rejection. Results HPgV-1 infection was demonstrated in 52 (26.1%) patients, with rates increasing from 14.7% at baseline to 19.1% by month 12 (p-value = .071). De novo infection occurred in 13.8% of patients with no detectable HPgV-1 RNA before transplantation. Double-organ (liver-kidney or kidney-pancreas) transplantation (odds ratio [OR]: 5.62; 95% confidence interval [CI]: 1.52-20.82) and donation after brain death (OR: 2.21; 95% CI: 1.00-4.88) were associated with posttransplant HPgV-1 infection, whereas pretransplant hypertension was protective (OR: 0.23; 95% CI: 0.09-0.55). There were no significant differences in the incidence of study outcomes according to HPgV-1 status. Plasma HPgV-1 RNA levels at different points did not significantly differ between patients that subsequently developed outcomes and those remaining free from these events. No correlation between HPgV-1 RNA and immune parameters or torque teno virus DNA load was observed either. Conclusion Unlike patients living with HIV, HPgV-1 infection does not seem to influence patient or graft outcomes after KT.

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