Spontaneous clearance of HCV infection can be predicted by several factors, including symptomatic acute infection, favorable IFNL3 polymorphisms and gender.
In our study, we explored the possibility that variants in HCV cell entry factors might be involved in resistance to HCV infection. Here, we conducted an extensive functional study to characterize the ability of these two natural variants to prevent HCV entry. Hence, our study highlights the complexity of HCV resistance mechanisms supporting the fact that this process probably not primarily involves HCV entry factors and that other unknown host factors may be implicated. This is an open access article distributed under the terms of the Creative Commons Attribution License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
(mh=Qcdu6qaL14Cu_8-Q)8.jpg "SEX ESCORT Amiens")
Competing interests: The authors have declared that no competing interests exist. Hepatitis C is a global health problem with more than million infected people worldwide [ 1 ]. An estimated additional two million people are newly infected per year, most of them through contaminated needle injections [ 2 ]. However, this seroprevalence can be very different, depending on the population studied.
Its genome encodes an approximately amino acid polyprotein which is maturated into structural, E1 and E2 glycoproteins and the capsid protein core, and non structural proteins [ 5 ]. E1 and E2 envelope glycoproteins are known to play a key role in HCV entry into hepatocytes, the major target of HCV, by interacting with a series of cellulars factors. Indeed, HCV entry is a complex multistep process requiring many specific entry factors. HCV infection begins with the attachment of the viral particle to the cell surface of hepatocytes through attachment factors such as glycosaminoglycans and low density lipoproteins receptor [ 6 , 7 ].
This attachment allows the contact between the viral particle and specific cell entry factors, including the tetraspanin CD81 [ 8 ], the scavenger receptor class B type 1 SRB1 [ 9 ] and the tight junction proteins claudin-1 CLDN1 [ 10 ] and occludin OCLN [ 11 , 12 ].
