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Título: | Hepatitis C virus replication in Caucasian HIV controllers |
Autor: | Ruiz-Mateos, Ezequiel CSIC ORCID; Machmach, K.; Romero-Sánchez, M. C.; Ferrando-Martínez, Sara; Viciana, Pompeyo CSIC; Val, Margarita del CSIC ORCID; Muñoz-Fernández, María Ángeles CSIC ORCID; Genebat, Miguel CSIC; Leal, Manuel CSIC | Palabras clave: | Elite controllers Hepatitis C virus HIV HIV controllers |
Fecha de publicación: | 2011 | Editor: | Wiley-Blackwell | Citación: | Journal of Viral Hepatitis 18(7): e350–e357 (2011) | Resumen: | Whether HIV controllers, patients who spontaneously control HIV viraemia, are able to control hepatitis C virus (HCV) infection, in terms of spontaneous clearance or lower HCV replication, is not well understood. To assess to what extent Caucasian HIV controllers are able to control HCV replication and potential associated factors, plasma HIV-1 and HCV RNA levels, anti-HCV antibodies, HCV genotype and human leucocyte antigens (HLA) typing were determined in samples from 75 HIV controllers (33 viraemic controllers, <1000 HIV-1 RNA copies/mL, and 42 elite controllers, <40 HIV-1 RNA copies/mL) and compared with 261 HIV-infected noncontrollers. We did not find differences in the HCV spontaneous clearance rates between groups. However, we interestingly found a lower HCV viral load in HIV controllers, alongside a different distribution of HCV genotypes in relation to the comparison group. In addition, HLA-B57 was associated with a lower HCV viral load in the control group and HIV controllers, and conversely, HLA-B35 with higher HCV viral load in HIV controllers. The subrepresentation of HCV genotype 1 and the overrepresentation of HLA-B57 only partly explained the lower HCV viral load found in HIV controllers. In fact, HIV controller status was independently associated with lower HCV viral load, together with HCV genotype non-1, the presence of HLA-B57 and absence of HLA-B35. Caucasian HIV controllers are able to better control HCV replication, in terms of lower HCV viral load levels. These findings support the idea that some common host mechanisms are involved in the defence against these two persistent infections. | Versión del editor: | http://dx.doi.org/10.1111/j.1365-2893.2010.01431.x | URI: | http://hdl.handle.net/10261/74972 | DOI: | 10.1111/j.1365-2893.2010.01431.x | ISSN: | 1352-0504 |
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