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JC Virus and APOL1 Risk Alleles in Black South Africans With Hypertension-Attributed CKD
Nolubabalo U Nqebelele1, Caroline Dickens1, Therese Dix-Peek1
1Department of Internal Medicine, Faculty of Health Sciences, University of the Witwatersrand, Johannesburg, South Africa.
Insights
The absence of John Cunningham virus (JCV) DNA in urine was strongly linked to chronic kidney disease (CKD). Further research is needed to confirm JCV
Area of Science:
- Nephrology
- Virology
- Genetics
Background:
- Polyomaviruses, including John Cunningham (JC) and BK viruses, are common human infections acquired in childhood.
- Individuals with specific apolipoprotein L1 (APOL1) risk variants and chronic kidney disease (CKD) showed a lower prevalence of kidney disease when JC viruria was present.
- This study investigated polyomavirus infection rates and their impact on CKD, particularly concerning APOL1 risk alleles.
Purpose of the Study:
- To determine the prevalence of polyomavirus infections in individuals with CKD, their relatives, and controls.
- To evaluate the association between JC viruria, APOL1 risk variants, and the presence of CKD.
- To explore potential renoprotective effects of JC virus (JCV) in the context of CKD and APOL1 genetics.
Main Methods:
- Sixty-four South African patients with hypertension-attributed CKD (eGFR ≤60 ml/min/1.73 m²), 44 first-degree relatives, and 56 unrelated controls were enrolled.
- Urine samples were analyzed for viral DNA, and blood samples for genomic DNA, using automated extraction platforms.
- Viral load was quantified using commercial kits, and APOL1 G1/G2 variants were genotyped via polymerase chain reaction-restriction fragment length polymorphism.
Main Results:
- JC viruria prevalence was significantly lower in CKD patients (3%) compared to controls (36%) and first-degree relatives (20%) (P < 0.001).
- Despite similar socioeconomic status, CKD patients exhibited less JC viruria than their healthy first-degree relatives.
- The absence of JCV DNA in urine strongly predicted the presence of CKD (OR 43.43; 95% CI 7.39-255.20; P < 0.001).
Conclusions:
- A significant association exists between the absence of JC viruria and the presence of CKD.
- Larger studies are required to elucidate the renoprotective role of JCV and its interplay with APOL1 risk variants in CKD pathogenesis.
Introduction:
The polyomaviruses, John Cunningham (JC) and BK, infect humans, with primary infection occurring in childhood. First-degree relatives of African American individuals with nondiabetic chronic kidney disease (CKD) who had 2 apolipoprotein L1 (APOL1) risk variants had a lower prevalence of kidney disease in the presence of JC viruria. This study determined the prevalence of polyomavirus infections and their effects, in the presence APOL1 risk alleles, on CKD.
Methods:
Sixty-four black South African individuals with hypertension-attributed CKD with an estimated glomerular filtration rate (eGFR) ≤60 ml/min per 1.73 m2, 44 first-degree relatives, and 56 unrelated controls were included. Viral DNA was extracted from urine and genomic DNA from blood using the Maxwell automated platform. Viral-load quantification was determined using Genesig polyomavirus kits. Genotyping of the APOL1 G1 and G2 variants was by polymerase chain reaction-restriction fragment length polymorphism.
Results:
The prevalence of JC viruria was significantly higher in controls (36%) and first-degree relatives (20%) than in patients with CKD (3%, P < 0.001). Although patients with CKD and their first-degree relatives had similar socioeconomic status scores, we found a lower prevalence of JC viruria in patients with CKD compared with their first-degree relatives, who had normal kidney function. The absence of John Cunningham virus (JCV), DNA was a strong predictor of CKD (odds ratio [OR] 43.43; 95% confidence interval [CI] 7.39-255.20; P < 0.001).
Conclusion:
There was a strong association between the absence of JC viruria and CKD. Studies with a larger sample are essential to determine the renoprotective effects of JCV and its interactions with APOL1.
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