Clearing hepatitis C virus does not reverse liver scarring already present, and people cured with advanced fibrosis keep a real cancer risk for years. A study of 943 cured patients found one variant, in TLL1, that predicts who — independent of the fibrosis and clinical factors already used to judge that risk.
Interferon-based therapy — and, more recently, direct-acting antivirals — can clear hepatitis C virus from the blood entirely, a result called a sustained virologic response, the laboratory definition of cured. What does not reverse on the same timeline is fibrosis: the scarring the virus caused in the liver while it was present. People who reach cure after their liver is already significantly scarred or cirrhotic keep a real, elevated risk of hepatocellular carcinoma — liver cancer — for years afterward. That is why patients with advanced fibrosis stay on periodic liver imaging after cure rather than being discharged from care.
Matsuura et al. 2017 ran a genome-wide association study in exactly this population — people who had already cleared HCV with interferon therapy — asking who, among the cured, goes on to develop liver cancer. In a combined cohort of 943 patients (457 in discovery, 486 in replication), they found a genome-wide significant association with rs17047200, an intronic variant in TLL1 (tolloid-like 1) on chromosome 4.
The signal held up under multivariate adjustment — it remained an independent predictor after accounting for the clinical factors already used to judge this risk: male sex, advanced fibrosis, and diabetes. The paper also found elevated TLL1 mRNA in fibrotic liver tissue and in liver injury models, and reports evidence that the risk allele may affect how the gene's transcript is spliced — a plausible route from genotype to the fibrogenesis and carcinogenesis the paper links it to.
A sustained virologic response is a real and important result — it is not the end of monitoring for everyone. Whether ongoing liver imaging is needed after cure is a decision clinicians already make from fibrosis stage and clinical history. This variant does not replace that judgment; the study found it as an additional, independent signal within a population already being watched for exactly this reason.
The variant does not diagnose cancer and does not indicate whether someone's hepatitis C has been cured. It is relevant only to a narrower question, within an already-cured population with real fibrosis: how much residual risk remains, on top of what fibrosis stage and the other established factors already say.
Hepatitis B-related liver cancer has its own page, with its own genetics — the two viral causes of liver cancer are tracked separately because the studies behind them are separate.
What a 23andMe/AncestryDNA export or raw VCF can and can't tell you about Liver Cancer Risk After Hepatitis C Is Cured comes down to these specific, well-studied positions — not a diagnosis.
TLL1 · rs17047200
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If significant liver scarring (fibrosis or cirrhosis) developed before cure, yes — that risk does not reverse on the same timeline as the virus clearing, which is why clinicians keep monitoring people with advanced fibrosis after a sustained virologic response.
No. It is unrelated to virologic response. It was studied specifically within a population that had already been cured, asking who among them faced higher residual cancer risk.
The gene showed elevated activity in fibrotic liver tissue in this study, and the risk variant may affect how its transcript is spliced — a plausible link to the scarring process (fibrogenesis) that precedes liver cancer in this setting. The paper established the statistical association and this mechanistic evidence; it did not fully resolve the pathway.
The study was conducted in people treated with interferon-based therapy, which has largely been replaced by direct-acting antivirals since. Whether the same association holds in that group is an open question this page does not resolve.
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