Iowa City, IA, United States
Iowa City, IA, United States

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Gajurel K.,University of Iowa | Stapleton J.T.,University of Iowa | Stapleton J.T.,The Iowa City Veterans Affairs Medical Center
Seminars in Nephrology | Year: 2016

Hepatitis viruses are named for their primary clinical illness, inflammation of the liver. Currently, six types of viruses are designated hepatitis viruses (A, B, C, D, E, and G), although only five of these cause hepatitis. Hepatitis viruses are composed of RNA and DNA viruses from different families and with different virologic properties, some of which typically cause acute hepatitis while others cause acute and chronic hepatitis. In addition to their role in liver disease, members of this group of viruses may cause a variety of pathologic changes in the kidney and other organs, and chronic infection may lead to cirrhosis in addition to raising a variety of important issues in the management of kidney transplant recipients. In this brief report, we review the virologic and clinical properties of each of the hepatitis viruses, and highlight the role of each virus in renal disease and kidney transplantation. © 2016


PubMed | The Iowa City Veterans Affairs Medical Center
Type: Journal Article | Journal: Antiviral therapy | Year: 2012

GB virus C (GBV-C) coinfection is associated with reduced immune activation and a block in CD4(+) T-cell proliferation following interleukin-2 (IL-2) therapy in HIV-infected individuals. We examined peripheral blood mononuclear cells (PBMCs) from HIV-infected subjects with and without GBV-C viraemia to determine if GBV-C correlated with reactivation of latent HIV, T-cell proliferation or T-cell survival following in vitro activation with phytohaemagglutinin A and IL-2 (PHA/IL-2).HIV-infected subjects whose HIV viral load was suppressed on combination antiretroviral therapy (cART) for >6 months were studied. PBMCs were cultured with and without PHA/IL-2 and monitored for HIV reactivation, proliferation and survival. GBV-C viraemia and in vitro replication were detected by real-time RT-PCR. HIV reactivation was determined by measuring HIV p24 antigen in culture supernatants. Proliferation was measured by counting viable cells and survival measured by flow cytometry.Of 49 HIV-infected individuals, 26 had GBV-C viraemia. Significantly less HIV reactivation and PBMC proliferation following in vitro activation with PHA/IL-2 was observed in samples from GBV-C viraemic subjects compared with non-viraemic controls. Following 5 weeks in culture, GBV-C replication was associated with preservation of CD4(+) and CD8(+) T-cells compared with non-viraemic controls.GBV-C appears to inhibit immune activation and IL-2 signalling pathways, which might contribute to a reduction in reactivation of latent HIV from cellular reservoirs. In addition, GBV-C viraemia was associated with a reduction in activation-induced T-cell death. GBV-C-associated T-cell effects could contribute to the observed protective effect of GBV-C coinfection in HIV-infected individuals.

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