Chronic hepatitis B (CHB) affects about 248 million people worldwide and can lead to liver cirrhosis, liver failure and hepatocellular carcinoma, especially in many Asian and African countries [
1,
2]. Whereas around 90% of the HBV-infected adults develop acute infection followed by spontaneous viral clearance, 5–10% of infected individuals are not able to clear the virus and develop chronic infection [
3,
4]. Morocco is a country of intermediate endemicity of hepatitis B virus (HBV) and diverse modes of transmission including vertical, intra-familial, sexual or parenteral have been reported [
5]. Several studies have highlighted that host genetic factors could influence the course of the disease [
6,
7]. Recently, Yan and colleagues identified sodium taurocholate cotransporting polypeptide (NTCP) as a functional receptor of HBV [
8]. NTCP is a member of the solute carrier family 10 (SLC10), the major bile acid uptake system in human hepatocytes, and localized to the basolateral hepatocyte membrane [
9]. Silencing the NTCP expression in primary
Tupaia hepatocytes, HepaRG or primary human hepatocytes diminished HBV infectivity [
8]. A genetic polymorphism (S267F, c.800G > A, rs2296651) in the solute carrier family 10 member 1 gene (
SLC10A1) completely abolished the HBV receptor function of human NTCP [
10]. In addition, a previous study showed that the S267F mutant of NTCP had normal cell surface expression, but resulted in almost complete loss of bile salt uptake [
11]. Starting from this known functional polymorphism, some case control association studies on HBV infection were conducted among Asian patients. However, the results were not consistent [
12‐
15].