# Association between LDL-R (exon 8 C.1171 G > A) polymorphisms and response to antiviral therapy in hepatitis C virus infection

**Authors:** Mohey Eldin Hassan Shikhoun, Hesham A. M. Ibrahim, Ahmed Abdou O. Abeed

PMC · DOI: 10.1038/s41598-026-38468-w · Scientific Reports · 2026-02-21

## TL;DR

This study found that a specific LDL-R gene variation is linked to how well patients with hepatitis C respond to antiviral treatment.

## Contribution

The study identifies a novel association between LDL-R exon 8 polymorphism and antiviral therapy response in HCV patients.

## Key findings

- The A/A genotype of LDL-R was more common in patients who responded to treatment.
- The G/G genotype was more prevalent in non-responders to antiviral therapy.
- HCV genotype 4 was the most common in both responders and non-responders.

## Abstract

The entry of the hepatitis C virus (HCV) into liver cells is closely associated with its interaction with the low-density lipoprotein receptor (LDL-R), which plays a crucial role in facilitating viral uptake. This study aimed to investigate the association between the LDL-R (exon 8 C.1171 G/A) gene polymorphism and response to antiviral therapy in patients infected with HCV. Participants were divided into three groups. Group I included 30 patients positive for both anti-HCV antibodies and HCV-RNA who did not respond to antiviral therapy. Group II consisted of 60 patients positive for anti-HCV but negative for HCV-RNA, indicating successful treatment response. and Group III comprised 50 healthy individuals negative for both anti-HCV antibodies and HCV-RNA, serving as controls. Diagnostic assessments included reverse transcriptase-polymerase chain reaction (RT-PCR), enzyme-linked immunosorbent assay (ELISA), and standard biochemical tests. Genotyping for LDL-R (exon 8 C.1171 G/A) polymorphisms was conducted using allele-specific PCR on patients from both the responder and non-responder groups. Of the 376 infected patients receiving antiviral therapy, 345 (91.8%) exhibited a positive response to treatment, whereas 31 (8.2%) did not. A total of 90 patients (60 responders and 30 non-responders) were included for genotypic analysis. Among responders, the A/A genotype of LDL-R (exon 8 C.1171 G > A) was the most prevalent (61.7%), whereas the G/G genotype was predominant among non-responders (76.7%). Genotyping analysis demonstrated that hepatitis C virus genotype 4 was the most common, being detected in all 20 responders and in 10 of 20 non-responders. These findings indicate a significant association between LDL-R (exon 8 C.1171 G/A) genetic variants and the response to antiviral therapy in Egyptian patients with chronic hepatitis C.

## Linked entities

- **Genes:** LDLR (low density lipoprotein receptor) [NCBI Gene 3949]
- **Diseases:** hepatitis C virus infection (MONDO:0005231)

## Full-text entities

- **Genes:** LDLR (low density lipoprotein receptor) [NCBI Gene 3949] {aka LDLCQ2}, CD209 (CD209 molecule) [NCBI Gene 30835] {aka CDSIGN, CLEC4L, DC-SIGN, DC-SIGN1, hDC-SIGN}, GGTLC5P (gamma-glutamyltransferase light chain 5 pseudogene) [NCBI Gene 653590] {aka GGT}, ATHS (atherosclerosis susceptibility (lipoprotein associated)) [NCBI Gene 470] {aka ALP}, CD81 (CD81 molecule) [NCBI Gene 975] {aka CVID6, S5.7, TAPA1, TSPAN28}, RAF1 (Raf-1 proto-oncogene, serine/threonine kinase) [NCBI Gene 5894] {aka CMD1NN, CRAF, NS5, Raf-1, c-Raf}, SOS1 (SOS Ras/Rac guanine nucleotide exchange factor 1) [NCBI Gene 6654] {aka GF1, GGF1, GINGF, HGF, NS4, SOS-1}, IFNL3 (interferon lambda 3) [NCBI Gene 282617] {aka IFN-lambda-3, IFN-lambda-4, IL-28B, IL-28C, IL28B, IL28C}, AFP (alpha fetoprotein) [NCBI Gene 174] {aka AFPD, FETA, HPAFP}, SLC17A5 (solute carrier family 17 member 5) [NCBI Gene 26503] {aka AST, ISSD, NSD, SD, SIALIN, SIASD}, CLEC4M (C-type lectin domain family 4 member M) [NCBI Gene 10332] {aka CD209L, CD209L1, CD299, DC-SIGN2, DC-SIGNR, DCSIGNR}
- **Diseases:** hepatic steatosis (MESH:D005234), obesity (MESH:D009765), advanced liver disease (MESH:D008107), fibrosis (MESH:D005355), dyslipidemia (MESH:D050171), malignancy (MESH:D009369), liver cirrhosis (MESH:D008103), chronic hepatitis C virus (HCV) infection (MESH:D019698), hepatocellular injury (MESH:D056486), liver injury (MESH:D017093), HCC (MESH:D006528), co- (MESH:D060085), HCV infection (MESH:D006526), viral infection (MESH:D014777), atherosclerosis (MESH:D050197), infected (MESH:D007239), familial hypercholesterolemia (MESH:D006938)
- **Chemicals:** Sofosbuvir (MESH:D000069474), water (MESH:D014867), isopropyl alcohol (MESH:D019840), AE (MESH:C538178), cholesterol (MESH:D002784), MgCl2 (MESH:D015636), Ficoll (MESH:D005362), EDTA (MESH:D004492), lipid (MESH:D008055), iodine (MESH:D007455), Hypaque (MESH:D003973), PBS (MESH:D007854), DAA (-), silica (MESH:D012822), formamide (MESH:C031066)
- **Species:** Hepatitis B virus (no rank) [taxon 10407], Human immunodeficiency virus 1 (no rank) [taxon 11676], Hepatitis C Virus [taxon 11103], Human immunodeficiency virus (species) [taxon 12721], Homo sapiens (human, species) [taxon 9606]
- **Mutations:** G/A, rs6511720, rs12979860, rs14158, 1171 G > A
- **Cell lines:** Huh-7 — Homo sapiens (Human), Adult hepatocellular carcinoma, Cancer cell line (CVCL_0336)

## Full text

_Full body text omitted from this summary view._ Fetch the complete paper as Markdown: https://tomesphere.com/paper/PMC12929620/full.md

## Figures

8 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12929620/full.md

## References

11 references — full list in the complete paper: https://tomesphere.com/paper/PMC12929620/full.md

---
Source: https://tomesphere.com/paper/PMC12929620