Coxsackie B
            <sub>4</sub>
            Viral Infection of the Human Kidney

Burch, George E.; Harb, Joseph M.; Hiramoto, Y.

doi:10.1016/s0022-5347(17)59835-3

Cited by 7 publications

(3 citation statements)

References 9 publications

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“…The involvement of kidney in patients infected with enterovirus had been reported since the 1960s. Burch and Colcolough [ 8 ] detected coxsackievirus B antigen in the kidney and heart of a patient with nephritis and pancarditis, and several reports of similar findings have since been described [ 9 – 11 ]. Coxsackieviruses B were reported to infect human glomerular and tubular cell lines, produce cytopathologic changes, and impair the phagocytic and contractile activity of mesangial cells [ 24 ].…”

Section: Discussionmentioning

confidence: 95%

Risk of Nephrotic Syndrome following Enteroviral Infection in Children: A Nationwide Retrospective Cohort Study

Lin

Yang

et al. 2016

PLoS ONE

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PurposeNephrotic syndrome is a common chronic illness encountered during childhood. Infections have been identified as a cause of nephrotic syndrome. The aim of this study was to evaluate the association between enteroviral infection and nephrotic syndrome.MethodsA nationwide retrospective cohort study was conducted by analyzing data from the National Health Insurance Research Database in Taiwan. Children aged <18 years with enteroviral infection were enrolled. Non-enterovirus-infected children were randomly selected as the comparison cohort. The primary endpoint was the occurrence of nephrotic syndrome.MethodsThis study included 280,087 enterovirus-infected children and 280,085 non-enterovirus-infected children. The mean age of the enterovirus-infected children was 2.38 years, and 53.7% of these children were boys. The overall incidence densities of nephrotic syndrome for enterovirus- and non-enterovirus-infected children were 2.65 and 2.21 per 10,000 person-years, respectively. The enterovirus-infected cohort had a higher cumulative incidence of nephrotic syndrome than did the non-enterovirus-infected cohort (log-rank test, p = 0.01). Multivariable analyses revealed that children with enteroviral infection were significantly associated with an increased risk of nephrotic syndrome compared with those without enteroviral infection (adjusted hazard ratio, 1.20; 95% confidence interval, 1.04–1.39; p = 0.01), particularly in children infected with coxsackievirus. Subgroup analyses revealed that enterovirus-infected girls, children of blue-collar workers, and children without allergies had a higher risk of nephrotic syndrome than did children in the non-enterovirus-infected cohort.ConclusionThis study revealed a significant association between enteroviral infection and nephrotic syndrome. Additional studies elucidating the role and pathogenesis of enterovirus in nephrotic syndrome are warranted.

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Section: Discussionmentioning

confidence: 95%

Risk of Nephrotic Syndrome following Enteroviral Infection in Children: A Nationwide Retrospective Cohort Study

Lin

Yang

et al. 2016

PLoS ONE

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“…Later on, CVB4 glomerulonephritis characterized by viruria, proteinuria, haematuria, leukocyturia, high blood pressure and an elevated blood urea nitrogen in a 9-year-old boy was published by Bayatpour et al [8]. Burch et al found CVB4 by immunofluorescence in the kidney of a 19-year-old male who had died from acute dilated cardiomyopathy [9]. Furthermore, Aronson and Phillips [10] reported six adult patients with acute oliguric renal failure who concurrently showed a significant rise of CVB5 antibody titre levels.…”

Section: Human Case Reportsmentioning

confidence: 99%

Coxsackie B viruses and the kidney—a neglected topic

Frey

2006

Nephrology Dialysis Transplantation

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Coxsackie B viruses types 1-6 (CVB1-6) occur worldwide and cause a broad spectrum of diseases, including myocarditis and aseptic meningitis. Although renal damage due to CVB has been suspected since the 1950s, these agents are only rarely searched for in today's clinical nephrological practice. Nevertheless, CVB can infect mesangial cells. Furthermore, infections with these viruses lead to a histological picture resembling mesangioproliferative glomerulonephritis and IgA-nephropathy in mice. In the present article, we provide an overview of this largely neglected topic, and of the slowly and steadily increasing evidence suggesting a link between coxsackieviral infections and kidney diseases.

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“…CVB3 is primarily known for its etiologic role in Keshan's disease in children and young adults (23), but previous work has demonstrated that coxsackieviruses also are found in older adults and are likely grossly under diagnosed in this population (24,25). In addition, coxsackieviruses are known to cause pathology in humans in multiple other organs (24,(26)(27)(28)(29)(30)(31).…”

mentioning

confidence: 99%

An aged host promotes the evolution of avirulent coxsackievirus into a virulent strain

Gay

Belisle

Beck

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

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The emergence of new, more pathogenic viruses necessitates elucidation of factors that promote viral evolution. Aging, a potential factor, is associated with increased susceptibility to viral infections. We used the enterovirus coxsackievirus B3 (CVB3) to investigate the effects of host age on pathogenicity and viral gene sequence. Old mice infected with a normally amyocarditic strain of CVB3, CVB3͞0, had significantly higher mean heart viral titers compared with CVB3͞0-infected adult mice. To determine whether a change in the CVB3͞0 viral population could contribute to the higher titers observed in the old infected mice, CVB3͞0 was passed once through an old or adult host and the changes in pathogenicity and viral genome were examined after subsequent infection of old or adult mice. Adult mice infected with CVB3͞0 that was passed through an old host (CVB3͞0 Old ) exhibited significantly higher heart viral titers, pathology, and weight loss than adult mice infected with either stock CVB3͞0 or CVB3͞0 passed through an adult host (CVB3͞0 Adult ). Sequence analysis of virus isolated from CVB3͞0 Old -infected mice revealed 13 specific and reproducible nucleotide changes. These changes result in a sequence that matches the virulent CVB3͞20 strain and are associated with promoting cardiovirulence. In contrast, we observed only one nucleotide change, low heart viral titers, and no heart and liver pathology in adult mice infected with CVB3͞0 Adult . These results demonstrate that the aged host promotes rapid selection of a pathogenic variant of CVB3 from an avirulent strain and introduces a host-virus paradigm for studies of viral infection in the aged.aging ͉ myocarditis ͉ oxidative stress ͉ pathology ͉ viral selection

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Coxsackie B ₄ Viral Infection of the Human Kidney

Cited by 7 publications

References 9 publications

Risk of Nephrotic Syndrome following Enteroviral Infection in Children: A Nationwide Retrospective Cohort Study

Risk of Nephrotic Syndrome following Enteroviral Infection in Children: A Nationwide Retrospective Cohort Study

Coxsackie B viruses and the kidney—a neglected topic

An aged host promotes the evolution of avirulent coxsackievirus into a virulent strain

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Coxsackie B 4 Viral Infection of the Human Kidney

Cited by 7 publications

References 9 publications

Risk of Nephrotic Syndrome following Enteroviral Infection in Children: A Nationwide Retrospective Cohort Study

Risk of Nephrotic Syndrome following Enteroviral Infection in Children: A Nationwide Retrospective Cohort Study

Coxsackie B viruses and the kidney—a neglected topic

An aged host promotes the evolution of avirulent coxsackievirus into a virulent strain

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Coxsackie B ₄ Viral Infection of the Human Kidney