BK viruria and viremia in children with systemic lupus erythematosus

Gupta, Nakul; Nguyen, Cuong Q.; Modica, Renee; Elder, Melissa E.; Garin, Eduardo H.

doi:10.1186/s12969-017-0156-2

Cited by 11 publications

(5 citation statements)

References 25 publications

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“…EBV promotes B cell proliferation, and some of the encoded proteins, such as nuclear antigen 1 (EBVN-1), share sequence homology with SLE autoantigens and may induce via antigenic mimicry antibodies that crossreact with the ribonucleoproteins (RNPs) Ro, Sm B/B’ and Sm D1 [ 20 ]. Besides EBV, tentative associations with SLE have been reported for parvovirus B19 [ 21 ], cytomegalovirus [ 22 ], and polyomavirus [ 23 ].…”

Section: Introductionmentioning

confidence: 99%

Lupus acceleration by a MAVS-activating RNA virus requires endosomal TLR signaling and host genetic predisposition

et al. 2018

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Viruses have long been implicated in the pathogenesis of autoimmunity, yet their contribution remains circumstantial partly due to the lack of well-documented information on infections prior to autoimmune disease onset. Here, we used the lymphocytic choriomeningitis virus (LCMV) as a model to mechanistically dissect the impact of viral infection on lupus-like autoimmunity. Virus persistence strongly enhanced disease in mice with otherwise weak genetic predisposition but not in highly predisposed or non-autoimmune mice, indicating a synergistic interplay between genetic susceptibility and virus infection. Moreover, endosomal Toll-like receptors (TLRs) and plasmacytoid dendritic cells (pDCs) were both strictly required for disease acceleration, even though LCMV also induces strong TLR-independent type I interferon (IFN-I) production via RNA helicases and MAVS in conventional DCs. These results suggest that LCMV enhances systemic autoimmunity primarily by providing stimulatory nucleic acids for endosomal TLR engagement, whereas overstimulation of the MAVS-dependent cytosolic pathway in the absence of endosomal TLR signaling is insufficient for disease induction.

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Section: Introductionmentioning

confidence: 99%

Lupus acceleration by a MAVS-activating RNA virus requires endosomal TLR signaling and host genetic predisposition

et al. 2018

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“…Colla et al reported increased BKPyV viruria in adult SLE, and they also reported an association between proteinuria and BKPyV viruria [30]. SLE patients are believed to be at risk of developing infectious complications due to their suppressed immune systems caused by various immunomodulatory drugs [31]. In addition, it has been speculated that there is a relationship between BKPyV reactivation and anti-dsDNA antibody production [32,33].…”

Section: Discussionmentioning

confidence: 99%

BK Polyomavirus Viremia and Viruria Frequency in Children Who are Receiving Immunosuppressive Treatment due to Kidney Diseases

Ugurtay,

Pehlivanoglu,

Meşe

et al. 2024

Preprint

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Background BK polyomavirus (BKPyV) is an important cause of nephropathy, graft dysfunction and loss in patients receiving immunosuppressive therapy after solid organ transplantation, especially kidney transplantation. However, the full spectrum of BKPyV-related kidney diseases in immunocompromised patients remains unclear. The aim of our study was to evaluate the frequency of BKPyV-DNA in blood and urine in patients who received immunosuppressive treatment due to kidney diseases other than kidney transplantation and to compare healthy controls. Methods A total of 46 (25 female) children, who were using immunosuppressive treatment and were under follow-up due to kidney diseases at the pediatric nephrology outpatient clinic and 28 (13 female) healthy controls, were included in the study. BKPyV quantitation was performed in urine and serum samples by real time polymerase chain reaction (PCR). Results Patient group and control group mean ages were 11.3±4.6 and 9.92±4.5 years respectively. There was no statistical difference between the patient and control groups regarding age and sex distribution (p>0.05). Twenty-four (52.2%) patients were receiving methylprednisolone, 14 (30.4%) patients were receiving dual, 1 (2.2%) patient was receiving triple immunosupressive therapy and 7 (15.2%) patients were receiving single immunosupressive therapy other than steroid. BKPyV-DNA was detected in the urine samples of 2 (4.35%) patients while there were no BKPyV-DNA positivity in plasma samples. One of these patients was being followed up with the diagnosis of systemic lupus erythematosus (SLE). Until the sample date, she had received methylprednisolon pulses, oral methylprednisolon, intravenosus immunglobulin, intravenousus cyclophosphamide, mycophenolat mofetil and rituximab. The patient’s current treatment was cyclosporin and oral methylprednisolon. The second patient was diagnosed with steroid-dependent nephrotic syndrome. He had recevied cylophosphamid previously and his current treatment was oral methylprednisolon. Remarkably, both patients had a history of cyclophosphamide treatment. There were no positivity in the plasma and urine samples of the healthy control group. Conclusion The use of steroids alone in immunosuppressive therapy does not appear to be an important risk factor for BKPyV reactivation. It does not seem necessary to perform plasma and urine BKPyV-DNA screening in pediatric patients not receiving intensive immunosuppressive therapy. It has been thought that BKPyV reactivation may be more frequent, especially if the underlying disease is SLE or if cyclophosphamide is used as an immunosuppressive, and BKPyV screening may be performed in these patients. The absence of positivity in any patient in our healthy control group suggests that BKV viruria and viremia are very low in healthy children.

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“…6 Patients with autoimmune diseases, such as SLE, by themselves immunosuppressant, have been found to have higher rates of BKV viremia and viruria. 4,7…”

Section: Discussionmentioning

confidence: 99%

Systemic BK Virus Infection in a Pediatric Patient With Severe Combined Immunodeficiency

et al. 2020

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Human BK virus (BKV) infection is known to occur mostly during childhood with the establishment of latent infection with no tissue damage or clinical manifestations. However, conditions causing immunosuppression can lead to increased virus replication and tissue damage. Although the tissues most commonly involved are the kidneys, bladder, ureters and, to some extent, brain tissue, there are some reports that suggest that BKV may cause multisystemic infections. In this case, a 12-month-old child was seen to suffer from multiple gastrointestinal infections. This prompted a search for immunodeficiencies, which revealed the presence of severe combined immunodeficiency. The child was eventually hospitalized and continued showing recurrent bouts of gastroenteritis as well as lower respiratory infection. After multiple antibiotic courses, he developed acute kidney injury, a hemophagocytic syndrome, and eventually respiratory failure, which led to his death a year later. Autopsy findings revealed the presence of a disseminated BKV infection involving the kidneys, ureters, leptomeninges, and pancreas. Analysis of the literature failed to show any previous case of BKV pancreatitis. The present case suggests that BKV can damage more tissues than previously reported and may be responsible for systemic infections in immunosuppressed patients.

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BK viruria and viremia in children with systemic lupus erythematosus

Cited by 11 publications

References 25 publications

Lupus acceleration by a MAVS-activating RNA virus requires endosomal TLR signaling and host genetic predisposition

Lupus acceleration by a MAVS-activating RNA virus requires endosomal TLR signaling and host genetic predisposition

BK Polyomavirus Viremia and Viruria Frequency in Children Who are Receiving Immunosuppressive Treatment due to Kidney Diseases

Systemic BK Virus Infection in a Pediatric Patient With Severe Combined Immunodeficiency

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