At Last! New Treatment Options for HepC
Horizons in Hemophilia, September 2015
By Francie Lasseter, RN, Emory University Hospital Midtown
Less than a year ago, treatment of the most common type of the Hepatitis C (HepC) virus took a huge step forward, resulting in many people now being able to treat HepC by taking one pill, once a day, for three months. Adding to that good news, studies have shown that this all-oral treatment has a success rate of 90-98%.1 This change came about on October 14, 2014, when the Food and Drug Administration (FDA) approved the medication Harvoni, the first all-oral treatment for HepC genotype 1.
For those who are familiar with the interferon-containing regimens previously used for HepC treatment – a treatment that was used for over 20 years—this change has been incredible. Following is a recap of the history of the HepC virus and the evolution of knowledge and treatment that has brought us to where we are today.
A Brief History of HepC Infection
The HepC virus was first identified as a distinct pathogen in 1989. Prior to that time, it was known as “non-A non-B” hepatitis and believed to be benign (not harmful). Unfortunately, this has proven to be incorrect. According to the CDC, chronic infection with HepC is currently the leading cause of cirrhosis and liver cancer (hepatocellular carcinoma, aka HCC) in the United States. 2
Up until the time of identification and elimination of HepC from donated blood and plasma in the U.S., it’s estimated that more than 90% of people with hemophilia treated with factor concentrate, plasma and/or blood products, were infected with the virus.3 The period of this contamination with HepC was during the 1970s and 1980s. It was also during this time that contamination with the Human Immunodeficiency Virus (HIV) occurred, along with its terrible consequences. Many people with hemophilia and other bleeding disorders were infected and died. We will always remember them.
HepC is a virus that infects the liver, causing inflammation, and the infection can be insidious – both subtle and serious. An infected person may not “feel” symptoms for years, routine blood tests can be misleading, and doctors and scientists are often unable to predict which patients are most likely to develop advanced liver disease. In 80% of people exposed to the virus, HepC infection becomes a chronic disease. In approximately 5-20% of those people, the liver can become so damaged by the virus that it develops cirrhosis (scarring), and in 1-5% of these people, disease progression can be fatal.4
The HepC virus is identified by different genotypes; these can be thought of as different “strains” of HepC and represent genetic differences in the virus itself. Genotype is important when it comes to treating HepC as the genotypes respond differently to different medications. The majority of infections in the U.S. are with HepC genotype 1 (75%), followed by genotypes 2 and 3 (20-25% of infections), and then smaller numbers of people are infected with genotypes 4, 5, and 6.
A Brief History Treatment
For those chronically infected with HepC, the hope of eliminating the virus and preventing further and/or serious liver damage lies in treatment. Up until the last few years, the backbone of that treatment was the injectable medication, interferon. Initially used as a single agent three times a week, the success rate was approximately 6%. In 1998, the FDA approved another medication, Ribavirin, for use along with interferon for treatment of HepC. Dosing of Ribavirin required a person to take multiple pills twice a day; this combination raised the success rate to approximately 40%. In 2001, a long-acting form of interferon, known as Pegylated interferon (PEGinterferon), was approved by the FDA. When used with Ribavirin, this medication increased the success of treatment to approximately 65% (in people with genotypes 1 and 4 the virus cleared in 50% of cases; in genotypes 2 and 3, it was 80%). Most HepC treatment with interferon lasted 48 weeks.
For ten years, this was the only treatment available for HepC. As anyone who has been treated with, or worked with, interferon knows, the medication can bring with it a host of unpleasant side effects. It can cause the “flu-like” symptoms of nausea, body aches, fevers and fatigue, along with depression and mood changes. In some patients, and along with Ribavirin, it would also destroy blood cells, causing deficiencies in a number of important blood counts, requiring frequent monitoring and further interventions (treatments).
In spite of this, many people treated their HepC with a combination of interferon and Ribavirin. Some were unable to tolerate the side effects and did not complete treatment. Others decided to delay treatment until something better came along. Researchers and scientists have worked hard throughout those years to better understand the virus and develop more effective treatments.
Then, in 2011, a new and exciting turn of events came about when the first direct acting antivirals (DAAs) were approved by the FDA for use in the treatment of HepC. For people with HepC genotype 1, one of two DAAs (boceprevir and telaprevir) could be used along with PEGinterferon and Ribavirin, resulting in both a shorter length of treatment for most patients (24 weeks), as well as a significant increase in success to approximately 80%. Though the prospect of success became much better for people with HepC genotype 1, the potential for side effects associated with interferon and Ribavirin continued.
The discovery and approval of these new medications, however, ushered in the advent of a new era in HepC treatment. Other drugs in this class of medications (DAAs) were being studied and appeared to bring the promise of all-oral treatments for HepC.
2013 & 2014: All-Oral Treatment for HepC
For people with genotypes 2 and 3, that promise was realized at the end of 2013 when the FDA approved two newer DAAs, Olysio (simeprevir) and Sovaldi (sofosbuvir), for use with Ribavirin. For this group, interferon was no longer needed and HepC treatment became all-oral.
Then, 25 years after the virus was first identified as HepC in 1989, the first all-oral treatment for HepC genotype 1 was approved by the FDA (October 2014). This medication, Harvoni, is a combination of three DAAs. With this advance, HepC treatment for many now consists of taking one pill, once a day, for 12 weeks—a far cry from the days of injecting interferon, taking multiple pills, and experiencing the side effects and low response rates that went along with HepC treatment in the past. Harvoni is generally well tolerated though, like any medication, it brings with it some potential side effects and cautions. In some patients, the length of treatment can be further decreased to just eight weeks.
Later in 2014, another all-oral treatment for HepC genotype 1 was approved, Viekira Pak. Treatment success rates with either of these new, all-oral treatments have risen to greater than 90% for most people and can be as high as 98%, depending on individual factors related to liver health and previous treatment. Other medications for oral HepC treatment continue to be studied and submitted to the FDA. The most recent FDA approval of a DAA was in July 2015 for a medication to treat HepC genotype 3, making it possible to now treat this genotype without Ribavirin.
Something to Think About
The main reason to treat HepC is to prevent progression to serious liver damage. As mentioned previously, 5-20% of people chronically infected with HepC will develop cirrhosis, and a subgroup of these people is at risk for liver cancer and death. Even if it’s not currently life-threatening, liver damage related to HepC can cause fatigue and a general sense of not being entirely well. People who have cleared the virus have commented that they didn’t know the effect that HepC had on their health until after the virus was gone and their overall sense of wellbeing improved; they felt better.
Based on the years in which HepC was transmitted to clients seen at the HTCs, we know that chronic HepC infection has been present for at least 30 years in those who still have the active virus. With vastly improved treatment success and better tolerated medications available, those who have either delayed or failed treatment in the past are encouraged to consider treating their HepC now. The time has never been better.
- Dr. Rachel Friedman-Moraco, a physician with Emory’s Infectious Disease (ID) Division, attends most of Emory’s Hemophilia Clinics and is available to meet with clients there to discuss HepC treatment as well as their individual case. For more information, clients may also contact Emory’s ID Clinic at (404) 686-2349.