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An In vitro Co-infection Model to Study Plasmodium falciparum-HIV-1 Interactions in Human Primary Monocyte-derived Immune Cells
Published on: August 15, 2012
GB virus C: insights into co-infection
Mark D Berzsenyi1, D Scott Bowden, Stuart K Roberts
1Department of Gastroenterology, Alfred Hospital, Commercial Road, Prahran 3181, Victoria, Australia. M.Berzsenyi@alfred.org.au
Abstract:
GB virus C (GBV-C) is a single stranded positive sense RNA virus, which is a member of the Flaviviridae. It has a close sequence homology and genomic organisation to hepatitis C virus (HCV). However, unlike HCV it is not hepatotrophic. GBV-C replicates within cells of the haemopoietic lineage, in particular lymphocytes. No disease has been associated with GBV-C infection but co-infection with human immunodeficiency virus (HIV) leads to improved morbidity and mortality for the HIV infected individual and slows progression to acquired immunodeficiency syndrome. This potential benefit of GBV-C has been demonstrated in the pre and post highly active anti-retroviral treatment (HAART) eras. GBV-C has been found to decrease HIV replication in in vitro models. The mechanism of the beneficial effect of GBV-C appears to be mediated by alterations in the cellular immune response, the details of which remain unclear. Despite this, there continues to be controversy regarding the influence of GBV-C on HIV as several reports have questioned the beneficial effect. GBV-C does not appear to influence liver related disease in subjects co-infected with HCV or hepatitis B virus (HBV). Combination of HIV and HCV leads to accelerated liver disease. The influence of GBV-C in this situation is yet to be determined. Elucidation of the putative protective effect of GBV-C in HIV co-infection could potentially identify novel targets for anti-HIV therapeutics and lead to the development of disease modifying vaccines.
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