Adult mouse kidneys become permissive to acute polyomavirus infection and reactivate persistent infections in response to cellular damage and regeneration

Atencio, Isabella A.; Shadan, Farhad F.; Zhou, Xin J.; Vaziri, N.D.; Villarreal, Luis P.

doi:10.1128/jvi.67.3.1424-1432.1993

Cited by 139 publications

(70 citation statements)

References 52 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…One possibility is that coviral-induced cellular damage results in high levels of cellular division and differentiation, creating conditions permissive for HBoV replication. A similar mechanism has been shown for polyomavirus infection in mice [18]. In addition, respiratory viral infections may suppress immune system functions to make the host more susceptible to infection with HBoV.…”

Section: Characteristicsupporting

confidence: 58%

Human Bocavirus: A Novel Parvovirus Epidemiologically Associated with Pneumonia Requiring Hospitalization in Thailand

Fry¹,

Lu²,

et al. 2007

View full text Add to dashboard Cite

show abstract

Section: Characteristicsupporting

confidence: 58%

Human Bocavirus: A Novel Parvovirus Epidemiologically Associated with Pneumonia Requiring Hospitalization in Thailand

Fry¹,

Lu²,

et al. 2007

View full text Add to dashboard Cite

show abstract

“…Danger, as originally described by Matzinger et al, is known to augment immune responses (41). In the setting of MPyV infection, it has been reported that renal injury, either by biochemical agents or by ischemia, increased susceptibility to viral replication in the kidney (29). We thus hypothesized that IRI injury would be an important clinical variable that could potentiate PVAN.…”

Section: Discussionmentioning

confidence: 88%

“…Previous studies in nontransplant mouse models have shown that injury mediated by chemical toxins or by renal artery ligation increased the permissivity of kidneys for MPyV replication (29). This, together with the observation that the magnitude of PVAN was greatest in mice infected near the time of transplantation, suggested that ischemia/reperfusion injury (IRI) contributed to the pathology of PVAN.…”

Section: Prolonged Cold Ischemia Does Not Increase the Severity Of Pvanmentioning

confidence: 98%

Adaptive Immunity Rather Than Viral Cytopathology Mediates Polyomavirus-Associated Nephropathy in Mice

Albrecht

Dong

Wang

et al. 2012

American Journal of Transplantation

View full text Add to dashboard Cite

Nephropathy associated with BK polyomavirus causes kidney allograft dysfunction and failure. Understanding the pathogenesis of polyomavirus‐associated allograft nephropathy (PVAN) is hampered by the species specificity of Polyomaviridae family members. Using a mouse polyomavirus (MPyV) kidney transplant model, we investigated clinically relevant variables that may contribute to PVAN. We found that the timing and source (i.e. donor vs. recipient) of MPyV infection and the titer of the viral inoculum have significant effects on the extent of allograft injury, with acute infection of the recipient by high‐titer MPyV inoculums producing the most profound PVAN. In contrast, altering the degree of MHC matching or increasing ischemia/reperfusion injury by prolonging the cold ischemic time of the allograft did not affect the severity of PVAN. Survival correlated positively with serum creatinine levels, but not with viral loads in the kidney allograft. Using splenectomized alymphoplasia mice, which are unable to mount primary adaptive immune responses, we further demonstrate that persistent high viral loads in the kidney are not sufficient to cause advanced PVAN. These findings suggest that the mechanism of PVAN in mice is not a direct consequence of viral cytopathology, but rather involves interplay between viral infection and the recipient antidonor immune response.

show abstract

“…Of the five polyoma viruses infecting humans, BK virus is associated most strongly with the development of disease following transplantation, where viral replication can lead to ureteric stenosis, tubulointerstitial nephritis (polyoma virus nephropathy) or haemorrhagic cystitis [1,20,[32][33][34]. Although BKV reactivation has been reported after most types of solid organ transplantation [35][36][37][38], the incidence is disproportionately high following renal transplantation, due possibly to local tissue damage and ischaemia-reperfusion injury inducing viral replication [39,40]. As the early diagnosis of BKV reactivation may improve outcomes and reduce complications most renal transplant units have introduced surveillance programmes, with associated protocols for immunosuppression reduction or modulation [41].…”

Section: Discussionmentioning

confidence: 99%

Antigen-specific T cell responses to BK polyomavirus antigens identify functional anti-viral immunity and may help to guide immunosuppression following renal transplantation

Chakera

Bennett

Lawrence

et al. 2011

Clinical and Experimental Immunology

View full text Add to dashboard Cite

SummaryInfection with the polyoma virus BK (BKV) is a major cause of morbidity following renal transplantation. Limited understanding of the anti-viral immune response has prevented the design of a strategy that balances treatment with the preservation of graft function. The proven utility of interferongamma enzyme-linked immunospot (ELISPOT) assays to measure T cell responses in immunocompetent hosts was the basis for trying to develop a rational approach to the management of BKV following renal transplantation. In a sample of transplant recipients and healthy controls, comparisons were made between T cell responses to the complete panel of BKV antigens, the Epstein-Barr virus (EBV) antigens, BZLF1 and EBNA1, and the mitogen phytohaemagglutinin (PHA). Correlations between responses to individual antigens and immunosuppressive regimens were also analysed. Antigen-specific T cell responses were a specific indicator of recent or ongoing recovery from BKV infection (P < 0·05), with responses to different BKV antigens being highly heterogeneous. Significant BKV immunity was undetectable in transplant patients with persistent viral replication or no history of BKV reactivation. Responses to EBV antigens and mitogen were reduced in patients with BKV reactivation, but these differences were not statistically significant. The T cell response to BKV antigens is a useful and specific guide to recovery from BKV reactivation in renal transplant recipients, provided that the full range of antigenic responses is measured.

show abstract

Adult mouse kidneys become permissive to acute polyomavirus infection and reactivate persistent infections in response to cellular damage and regeneration

Cited by 139 publications

References 52 publications

Human Bocavirus: A Novel Parvovirus Epidemiologically Associated with Pneumonia Requiring Hospitalization in Thailand

Human Bocavirus: A Novel Parvovirus Epidemiologically Associated with Pneumonia Requiring Hospitalization in Thailand

Adaptive Immunity Rather Than Viral Cytopathology Mediates Polyomavirus-Associated Nephropathy in Mice

Antigen-specific T cell responses to BK polyomavirus antigens identify functional anti-viral immunity and may help to guide immunosuppression following renal transplantation

Contact Info

Product

Resources

About