Bile-salt stimulated lipase polymorphisms do not associate with HCV susceptibility

Area of Science:

• Immunology
• Genetics
• Virology

Background:

• Bile-salt stimulate lipase (BSSL) is a glycoprotein that binds DC-SIGN.
• BSSL gene polymorphisms, specifically the number of O-linked glycosylated repeats in exon 11, are linked to HIV-1 transmission and disease progression.
• DC-SIGN gene single nucleotide polymorphisms (SNPs) are associated with HCV sexual transmission risk.

Purpose of the Study:

• To investigate whether BSSL gene polymorphisms are associated with Hepatitis C Virus (HCV) susceptibility.
• To determine if BSSL polymorphisms affect HCV risk through differential binding to DC-SIGN.

Main Methods:

• DNA was isolated from two cohorts: the MOSAIC cohort (HIV-1 infected MSM) and the Amsterdam cohort studies (ACS) (intravenous drug users).
• Participants included Hepatitis C Virus multiple exposed uninfected (MEU) and multiple exposed infected (MEI) individuals.
• The number of repeats in BSSL exon 11 was quantified using PCR, and repeat distributions were compared between MEI and MEU groups.

Main Results:

• No statistically significant difference was observed in the copy number of exon 11 repeats in the BSSL gene when comparing HCV infected individuals (MEI) with uninfected individuals (MEU).
• This finding held true for individual repeat numbers and combinations of repeats.
• BSSL polymorphisms, specifically exon 11 repeat copy number, do not appear to influence HCV susceptibility.

Conclusions:

• The copy number of exon 11 repeats in the Bile-salt stimulate lipase (BSSL) gene does not affect an individual's susceptibility to Hepatitis C Virus (HCV) infection.
• Unlike its association with HIV-1, BSSL polymorphisms do not appear to play a role in HCV risk.
• Further research may be needed to explore other potential genetic factors influencing HCV susceptibility.