Protective association between JC polyoma viruria and kidney disease. Issue 1 (January 2019)

• Record Type: Journal Article
• Authors: Divers, Jasmin; Langefeld, Carl D.; Lyles, Douglas S.; Ma, Lijun; Freedman, Barry I.
• Is Part Of: Current opinion in nephrology and hypertension. Volume 28:Issue 1(2019)
• Publication Date: 2019-01
• Subjects: African American -- apolipoprotein L1 -- chronic kidney disease -- focal segmental glomerulosclerosis -- HIV-associated nephropathy -- JC polyomavirus; Hypertension -- Periodicals; Nephrology -- Periodicals; Hypertension -- Indexes; Hypertension -- Periodicals; Kidney Diseases -- Indexes; Kidney Diseases -- Periodicals; Nephrology -- Periodicals; 616.132
• DOI: 10.1097/MNH.0000000000000464
• Languages: English
• ISSNs: 1062-4821

Abstract

Abstract : Purpose of review: The presence of viruses in urine (urine virome) typically reflects infection in the kidneys and urinary tract. The urinary virome is associated with HIV-associated nephropathy and chronic glomerulosclerosis. There are many associations of this microbiome with human diseases that remain to be described. This manuscript reviews emerging data on relationships between kidney disease and urinary tract infection/colonization with JC polyomavirus (JCPyV). Recent findings: Approximately 30% of the adult population sheds JCPyV in the urine. Further, urinary tract infection with one polyomavirus strain appears to inhibit secondary infections. The presence of urinary JCPyV and BK polyomavirus (BKPyV) replication were measured with polymerase chain reaction in African Americans to assess relationships with apolipoprotein L1 gene ( APOL1 )-associated nephropathy. Urinary JCPyV was associated with paradoxically lower rates of nephropathy in those with APOL1 high-risk genotypes. Subsequent studies revealed African Americans with JCPyV viruria had lower rates of nondiabetic nephropathy independent from APOL1 . Summary: Urinary tract JCPyV replication is common and associates with lower rates of nephropathy. This relationship is observed in diverse settings. Results support a host immune system that fails to eradicate nonnephropathic viruses and is also less likely to manifest renal parenchymal inflammation resulting in glomerulosclerosis.