In 1998, another nurse and I started a hepatitis C support group. One of the members who attended faithfully from the beginning, was a man I’ll call Victor. He had genotype 4 hepatitis C, and over the years he endured three treatments, In those days, the medications had debilitating side effects and treatment was long, usually a year. Victor was finally cured with a combination of pegylated interferon and ribavirin. Victor would cheer us on, saying, “Three times is a charm.” After my third and successful hep C treatment, he said, “I told you that three’s a charm.”
Those days were awful and I am glad to have them behind me. Medication is so much easier to tolerate these days, and the cure rates are quite high. The likelihood of success depends on many factors, such as whether or not there is cirrhosis. Generally, nearly everyone will respond to treatment, but it may take more than one course.
It sucks when treatment doesn’t work. It doesn’t matter if treatment was relatively side effect-free, who wants to do it again? But going through hepatitis C treatment again, and again, until we are cured is what is recommended. Living with hep C is risky. Untreated hepatitis C increases risk of cirrhosis, liver cancer, and early death from all causes. Treatment is the logical path to take.
If you are wondering how hepatitis C is retreated, Hep provides information about this. However, if you have genotype 4 and treatment didn’t work, I would like to mention research that was recently published. This research appeared in the February 2019 issue of Hepatology: ‘Frequent Antiviral Treatment Failures in Patients Infected With Hepatitis C Virus Genotype 4, Subtype 4r’ by Slim Fourati, et al.
Fourati and colleagues studied 537 French patients who were treated with direct-acting antivirals (DAAs) but experienced a virological failure between 2015 and 2018. Of these, 121 (22.5 percent) were infected with genotype 4; 27 of these (22.3 percent) had genotype 4 subtype 4r. In short, subtype 4r was over‐represented when compared to its prevalence in the French general population.
Further investigation found that the patients with subtype 4r who had failed DAA treatment, had two to three dominant NS5A resistance‐associated substitutions (RASs). Basically, they clearly had markers for resistance to DAAs. The researchers recommended that these patients should be identified and receive a triple DAA combination regimen as first‐line treatment.
Perhaps if Victor was just beginning his hepatitis C journey now rather than in 1998, he would have had a different experience. His liver specialist would note Victor’s genotype 4, and perhaps test for resistance. Victor might have responded the first time and not have had to live by the motto, “Three’s a charm.” On the other hand, his triple treatment experience inspired me to keep trying.