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June 24, 2005
Hepatitis C Hope
The following article is from Pharmaceutical Business Review. I don't know why, exactly, but I love it when these guys talk about Hepatitis c treatment as a business. Maybe it is because I figure their monetary interest fuels their desire to find better and better treatments for Hepatitis c.
What we can discern from reading between the lines in this industry report is that truly new and exciting treatments may still be 5 or six years off. While it is not tomorrow, it is also not decades away. I find that encouraging.
Hepatitis C: hope on the distant horizon
24 Jun 2005, 17:24 GMT - While progress in the hepatitis C virus market is expected to be slow until 2011, the launch of polymerase and protease inhibitors thereafter is expected to fuel rapid growth. The market is expected to exceed $4 billion by 2012 and this growth may even result in a new treatment paradigm.
Driven by a favorable epidemiology and high unmet medical need, the hepatitis C pipeline is both rich and varied. The chronic hepatitis C (CHC) treatment market is currently dominated by market leaders Roche and Schering-Plough, which market both components of the CHC standard of care - a combination of pegylated interferon (Peg-IFN) alfa and ribavirin (RBV).
Historical growth in the hepatitis C market has been high, with a compound annual growth rate (CAGR) of 28.5% experienced between 1999 and 2003. This was mainly fuelled by the launch of RBV in 1998 and the second-generation interferons, Peg-IFN alfa-2b and -2a in 2000 and 2002, respectively - both of which significantly improved the efficacy of therapy.
However, treatment outcomes following Peg-IFN plus RBV combination therapy are highly heterogeneous and depend on the viral genotype with which a patient is infected. Indeed, sustained viral response (SVR) rates in the 'easy-to-treat' genotypes 2 and 3 can be up to 88% of cases. In contrast, less than half of those who harbor hepatitis C virus (HCV) genotype 1 successfully respond to therapy. Significantly, genotype 1 accounts for between 70 to 75% of the patient pool in the West and, therefore, current therapy meets less than 50% of the CHC medical need.
This has led to the accumulation of patients that have failed first-line therapy with the current standard of care, known as non-responders, and patients who responded to therapy but subsequently relapsed. Moreover, as a result of the slow rate of HCV disease progression, the wave of patients seeking treatment is still gaining momentum and expected to peak from 2014 onwards.
Incremental improvements in short term
The combination of high patient potential and significant medical unmet need have attracted big pharma and small biotech alike, creating a pipeline consisting of 28 drugs in clinical development and a range of potential drug candidates at the preclinical stage. However only 14% of these molecules are currently in phase III, with none of these specifically targeting the HCV particle per se. Instead, they act by enhancing the host antiviral response and therefore, no major paradigm changes are expected to occur in HCV therapy for at least the next five years.
Research by Datamonitor found that among the three drugs that are closest to market, only Valeant's RBV follow-up drug viramidine is perceived as a key addition to HCV therapy. The drug has similar efficacy to its predecessor but differentiates itself based on its more favorable toxicity profile.
The highest hopes for effective future HCV therapy are being pegged on the small molecules able to specifically interfere with HCV replication, in particular the NS3 protease inhibitors. This new paradigm was first highlighted as a realistic goal by Boehringer Ingelheim (BI), whose protease inhibitor BILN 2061 demonstrated an unprecedented drop in viral load after only two days of therapy. However, the enthusiasm was largely dampened when BI was forced to suspend further development of the drug due to cardiac toxicity in animals.
With the most developed protease inhibitor - Vertex/Mitsubishi's VX-950 - still at least seven years from reaching the market, hopes are now centered on the polymerase inhibitors, most notably Idenix/Novartis's NS5B polymerase inhibitor valopicitabine (NM283). However clinical development has also led to general disappointment when early-stage trials showed only moderate reductions in viral load with NM283 monotherapy. This led to subsequent clinical trials being designed for combination therapy with Peg-IFN, with the end goal of potentially replacing RBV with NM283.
Is future therapy without an interferon backbone realistic?
Early results from the NM283 clinical trials raise the question about the future role of Peg-IFN in HCV therapy: will it remain the backbone for several years to come or eventually fade from use? Some people believe that future HCV therapy is more likely to consist of combination therapy, based on Peg-IFN plus one or more specific antivirals. Others take a more optimistic view nurtured by faith in that antivirals could be capable of curing HCV infection on their own.
Given the consequences of untreated HCV infection, which include liver cirrhosis, hepatocellular carcinoma, liver transplant and death, many physicians will require convincing data before replacing a proven therapeutic option with antiviral monotherapy. As such, Peg-IFN is expected to retain a relatively strong market presence, despite the plethora of drugs in the pipeline, resulting in a CAGR of 9.9% for the interferon class between 2004 and 2013.
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June 22, 2005
Shorter HCV Treatment? Yes, for some...
Because genotypes 2 and 3 respond so well to interferon therapy, researchers are studying how little they can give and still have a positive effect.
This is great for 30% of North Americans who have chronic Hepatitis c. But the rest of us are still looking at a year of treatment and maybe a 50% chance of success (at best).
Actually, I look at articles like this as much for secondary information as primary. For instance, I hadn't realized that only 5% of Americans have type 2. Wow! This means the best resonse to interferon can only be acheived by 5% of us.
Shorter Hepatitis C Treatment Works for Some
For Those With Hepatitis Type 2 or 3, 3-Month Treatment May Suffice
By Daniel DeNoon
WebMD Medical News
Reviewed By Michael Smith, MD
on Wednesday, June 22, 2005
June 22, 2005 -- Some people with hepatitis C may get by with only three months of treatment, an Italian study shows.
The findings apply only to people infected with type 2 or type 3 hepatitis C virus. They do not apply to people infected with the more common type 1 virus. In the U.S., about 70% of hepatitis C infections are type 1, about 5% are type 2, and about 20% are type 3.
Treatment for hepatitis C isn't easy. The drugs of choice are a once-a-week form of interferon alpha (peg-interferon) plus ribavirin, an antiviral drug. The side effects -- including flu-like symptoms, fatigue, and depression -- can be very hard to handle.
Current guidelines call for six months of treatment for hepatitis C type 2 and type 3 infections. A year of treatment is needed for type 1 infections.
But Alessandra Mangia, MD, of Casa Sollielo della Sofferenza Hospital, in San Giovanni Rotondo, Italy, and colleagues report that some patients with hepatitis C type 2 or type 3 infections may be able to cut their treatment time in half.
Fast Response, Shorter Treatment?
The goal of hepatitis C treatment is what doctors call a sustained virologic response. That's when the hepatitis C virus can no longer be detected in the blood. Many experts call this a cure; others are more cautious. Whatever it's called, patients with sustained virologic responses to treatment almost never see their hepatitis C infection come back to dangerous levels.
Side effects force some patients to quit treatment early. Usually, that means treatment failure; usually -- but not always.
"We saw that a few patients, who withdrew from therapy before the standard six-month period, had sustained virologic responses anyway despite their short course of treatment," Mangia tells WebMD. "And we saw that some patients show a very fast reduction of hepatitis C virus levels after their first interferon treatment."
Did early response to treatment predict who would do well with short-term therapy? The researchers designed an experiment. They enrolled 283 people with hepatitis type 2 or type 3 infection. Seventy of the patients got the full six months of peg-interferon plus ribavirin. The other 213 patients started with the same treatment. If, after four weeks, their blood levels of hepatitis C virus became undetectable, these "fast responders" got only three months of treatment -- called variable-length treatment.
Mangia and colleagues report their findings in the June 23 issue of The New England Journal of Medicine.
What happened?
The researchers had good news for patients with hepatitis C type 2 or 3 that had no evidence of the virus after four weeks of treatment. "Patients treated for 12 weeks were spared the expense and inconvenience of extended treatment and still had a high response rate."
Too Good to Be True?
The response rates were similar between those treated for three months and those treated for six months. Overall, 76% of patients getting standard treatment and 77% of patients getting the variable-length treatment had a sustained virologic response.
But there were some differences.
At first, early responders -- those who had undetectable levels of hepatitis C virus after four weeks of treatment -- looked the same in both the standard and variable treatment groups. Ninety-three percent of early responders treated for six months and 95% of those treated for three months still had no detectable virus at the end of treatment. Six months later, that percentage dropped from 93% to 91% in those treated for six months. But it dropped from 95% to 85% in those treated for three months.
Although it sounds like the variable-length group have more viral "rebound," Mangia notes that the results were very similar between the two groups. And of the 13 patients who rebounded after three months of treatment, 10 agreed to 24 more weeks of treatment. This second course of treatment was successful for nine of these 10 rebounders.
"Only this small number of persons rebounded, without any major side effects, and without any reduction in the response rate for [further] treatment," Mangia says.
But these numbers worry hepatitis C expert Robert Fontana, MD, associate professor of medicine and medical director for liver transplant at the University of Michigan in Ann Arbor.
"Is this really an efficient way to manage patients? If you are going to go through this therapy, you would rather get rid of the virus," Fontana tells WebMD. "Yes, you have less of the side effects with 12 vs. 24 weeks of treatment. But if someone is tolerating it well, why risk the relapse? Plus there is the whole psychological letdown from learning you've had a rebound. ... If you can get by with less treatment, great. But when you start to have a trend toward rebound, I don't think it's worth the risk."
Mangia says her hospital already is using the variable-treatment strategy for all patients with type 2 or type 3 hepatitis C infection.
Based on the study findings, Fontana doesn't think this is a good idea. He praises the Mangia study. Though he notes that it was carefully done and that it addresses crucial issues in hepatitis C treatment, he says doctors and patients would do better to focus on managing side effects than by trying to shorten treatment.
"During the first 12 weeks, the most severe side effects are flu-like symptoms," Fontana says. "Beyond 12 weeks, the depression, the weakness, and the sort of mental aspect becomes more prominent. That is where a lot of patients going out to 48 weeks just can't hack it. By reducing the dose, by seeing patients more often, by introducing antidepressants, and by helping with sleep, you can get a lot of those patients through."
SOURCES: Mangia, A. The New England Journal of Medicine, June 23, 2005; vol 352: pp 2609-2617. Alessandra Mangia, MD, Casa Sollielo della Sofferenza Hospital, San Giovanni Rotondo, Italy. Robert Fontana, MD, associate professor of medicine and medical director for liver transplant, University of Michigan, Ann Arbor. Zeuzem, S. Annals of Internal Medicine, March 2, 2004; vol 140: pp 370-381. AASLD Practice Guideline: "Diagnosis, Management, and Treatment of Hepatitis C," Strader, D. B. Hepatology, April 2004; vol 39: pp 1147-1171.
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June 20, 2005
Once A Month Interferon
Albuferon is an interferon that can be taken once a month and has less side effects than other interferons. It is closer to approval than other drugs being developed and seems like a better option than existing therapy.
New Approach To Hepatitis C
June 20 (ABC7) — A new drug is offering hope for millions of Hepatitis C patients. As Dr. Dean Edell reports, this drug may help patients stay healthier with fewer side-effects.
Superstar Billy Graham took home the Worldwide Wrestling Federation title in 1977, but what happened in the ring brought him a challenge he never expected.
Superstar Billy Graham, retired professional wrestler: "We cut our foreheads to produce blood to make the match look more authentic."
Graham thinks that may be how he contracted Hepatitis C. The disease is most commonly spread through blood.
Vijayan Balan, M.D., hepatologist: "Hepatitis C is a virus that can infect the liver and cause cirrhosis if it is untreated."
Dr. Vijayan Balan is a liver specialist working on a new treatment.
Dr. Balan, M.D.: "I think there is significant hope in conquering this disease."
Right now, patients must take medication once a week that can induce days of flu-like symptoms. Now a new drug, Albuferon, is only taken once a month and causes fewer side-effects.
Dr. Balan, M.D.: "They get the drug more continuously for a longer period of time."
Albuferon is a combination of Interferon, which helps fight infection and Albumin, which allows the medication to stay in the body longer.
Dr. Balan: "You don't have the peaks and valleys with this new drug."
Studies show the drug is safe. Soon it will be tested in up to 1,000 people across the country.
Graham says a drug that's easier to handle would have had him back in the gym sooner and able to focus on the good times.
The first phase of the study showed Albuferon is safe and well tolerated by patients. Right now, more than 1000 people are taking the drug.
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June 11, 2005
Science Finally Replicates HCV in Lab
This breakthrough will go a long way toward helping develop more effective treatments for HCV (and maybe even a vaccine).
'Test tube' hope for hep C drug
Around 3% of people worldwide are thought to have hepatitis C.
US scientists have been able to create infectious hepatitis C in the lab for the first time, offering renewed hope of drugs to beat the virus.
Hepatitis C is a major cause of chronic and sometimes fatal liver disease, affecting 170 million people worldwide.
The virus, HCV, is carried in and can be passed on via the blood.
Currently, it is treated with a combination of two drugs, but about 40% of patients do not respond to this therapy.
This may help in the development of new drugs for combating HCV
Study author Dr Charles Rice
Like all viruses, hepatitis C cannot replicate by itself. It takes over the machinery of the host cell.
However, much about the life cycle of the virus remains poorly understood because, until now, scientists have been unable to reproduce an infectious form of HCV that they can observe and experiment on in the lab.
"This system lays the foundation for future test tube studies of the virus life cycle and may help in the development of new drugs for combating HCV," said researcher Dr Charles Rice from the Infectious Diseases Unit at Rockefeller University.
Achilles' heel
He told the journal Science how in a separate set of experiments they were able to use the lab-grown virus to confirm that a molecule called CD81, which sits on the surface of human cells, plays a crucial role in the entry of HCV.
They found that CD81 molecules which were not attached to the surface of host cells competed with cell-bound CD81 and blocked the entry of HCV into the cell. Furthermore, cells that did not express CD81 were immune to infection.
Scientists already know that a protein produced by HCV, called E2, binds to CD81. It is believed this interaction is necessary for the virus to bind to host cells.
Chief executive of the Hepatitis C Trust and president of the European Liver Patients Association, Charles Gore, said: "Treatment for hepatitis C has improved dramatically in recent years but there is still considerable room for improvement.
"This is one of the reasons why so few - just one-half to one percent - of those with this unacknowledged virus are getting treated each year.
"Any advances that can contribute to improved therapy, and especially the development of a vaccine, are good news for patients."
Dr Teo, consultant virologist at the Centre for Infections, the Health Protection Agency, said: "The ability to culture HCV is the holy grail of HCV research because this will help with improving testing techniques, allow better understanding about how the virus causes illness and help us to explore better treatments for the disease."
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June 09, 2005
HCV Evasive Strategy Being Decoded
While a bit technical I found this article very interesting and informative.
Public release date: 9-Jun-2005
Contact: David March
dmarch1@jhmi.edu
410-955-1534
Johns Hopkins Medical Institutions
Johns Hopkins team finds 'ancestral' hepatitis-C virus at the root of evolution in infections
Scientists discover how virus evades immune system in acute and chronic infections; new vaccines may result.
Researchers at Johns Hopkins have uncovered how a majority of the genetic changes in the hepatic-C virus, the most common cause of liver disease, allow it to evade the body's immune system during infection. Hepatitis C infection can lead to cirrhosis, cancer and even death. In a series of experiments that describe the virus' transition from an acute to chronic infection, the Hopkins team found that one-half of the virus' changes in its genome are in sites under attack by the body's immune system.
As the virus evolves and these changes weaken the body's immune response, a second set of changes at other sites in the genome are reverting back to an "ancestral" set of amino acids.
"We think this piecemeal exchange is helping the virus evade the body's immune system," says study investigator and infectious disease specialist Stuart Ray, M.D., an associate professor at The Johns Hopkins University School of Medicine. "In a newly infected person, the virus may need to adopt new mutations to escape recognition by the immune system's T cells, which fight infection, but it may need to lose the mutations that had protected it in someone else. Despite pressure to change, the virus is always is restoring its shape."
The Hopkins findings, published in a pair of studies in the Journal of Experimental Medicine this week, are believed to be the first description of the precise genetic changes taking place in the virus during the acute phase of infection, when hepatitis C initially escapes the body's defenses and establishes itself in the body. As the infection moves into the chronic stage, the immune response becomes weak and less effective, but until now, no one could explain exactly why.
A second, related experiment produced similar findings when the Hopkins team partnered with researchers in Ireland to perform what is believed to be the first comparison of genetic changes across multiple genes in strains from chronically infected people to the original strain that infected them.
Ray, who served as senior investigator on the first study and led the second, believes the newly identified ancestral component of the viral genome, called a consensus sequence, could serve as the basis for development of a vaccine that is effective against both acute and chronic infections, thereby stemming the epidemic that currently afflicts more than 170 million people worldwide, including 3 million Americans.
"Hepatitis C is extremely difficult to treat if it becomes chronic," says infectious disease specialist Andrea Cox, M.D., Ph.D., an assistant professor at Hopkins who was lead author of the first study. "While approximately 30 percent of patients have a strong enough immune response to rid themselves of the virus during the acute phase, and current treatments are 90 percent effective at treating any remaining acute infections, these treatments are only 50 percent effective against chronic infections, which otherwise persist for life and can cause death."
According to Cox, the hepatitis C virus naturally mutates, or alters its genome, very rapidly. Its strains have two to three times more genetic variability, for example, than HIV, the virus that causes AIDS, and hepatitis C reproduces more than 100 billion times per day, 100 times faster than HIV. Compounding the problem, the infection is asymptomatic in the acute stage, making it less likely that diagnosis will be made early, when it is easiest to treat.
Conventional wisdom, the researchers say, was that the large numbers of mutations were simply random in the virus' ever-changing genome, but the new study suggests that Darwinian genetic selection is at play. That is, the virus' genome changes in ways that make it more reproductively "fit" in the face of each immune system it encounters, changing what is must to evade the immune system in one host, then restoring itself when the pressure is off.
What Ray's team found when the immune response weakens was that the virus naturally mutates toward a set of 3,000 common amino acids, what the researchers considered the virus' most preferred state. During the acute phase, Ray says, the virus is under severe pressure from the immune response and forced to drift away from the consensus sequence, using mutations to evade the immune response. However, the drift was reversible and, once the virus successfully evaded a particular immune cell, its amino acids reverted back to the consensus set.
To assess the genetic changes in the early stages of infection, the researchers decoded, or sequenced, the virus' genome, made up of RNA, which is very similar to the more widely known DNA that makes up the genome of most organisms. The RNA was gathered from eight newly infected patients in Baltimore, Md., all of whom were offered treatment and were participants in a larger study of infectious diseases in intravenous drug users. The sample group was unusual, allowing analyses before and during the early stages of infection. One patient self-recovered, while the rest proceeded to chronic infection.
Using advanced blood-sorting techniques, the Hopkins team extracted millions of immune system cells, including the systems' principal fighters, called T cells, from blood samples taken between 30 days and six months after infection, when the body's initial immune response kicks in and subsequently peaks.
Immune responses were mapped using a series of more than 500 overlapping synthetic peptides, or strings of amino acids whose code was already known. This allowed the researchers to compare changes observed in the RNA sequence to corresponding shifts in the body's immune response to the infection.
When specifically recognized by T cells, the peptides trigger production of interferon gamma, a protein that acts as a signal to many other immune cells to respond to a new infection. Reductions in the production of interferon gamma would indicate, the scientists say, that the immune system was weakening in its response to the virus' mutations.
After analyzing the genetic changes in the sites, called epitopes, where the T cells specifically bind to the virus, the researchers found no changes had occurred during the one year of follow-up in the one patient who self-recovered. However, in the remaining seven patients, there were changes in 69 percent of T-cell epitopes, showing that the virus had mutated at key locations necessary for chronic infection to proceed.
Additional analysis showed that changes in T-cell epitopes were 13 times more frequent than changes in the remaining genome of the virus. The researchers examined the binding ability of T cells obtained early in infection to recognize 10 viral peptides known to have changed during the first six months of infection. Eight showed severely reduced capacity to stimulate production of interferon gamma, offering confirmation that the virus was mutating to evade the immune system.
Analysis of the viral RNA in the blood of seven patients with chronic infections revealed that eight of 16 changes in genome matched to the consensus sequence, confirming the presence of selective evolutionary pressure toward restoration of an ancestral form of the virus.
In the second study, using blood samples collected in Cork, Ireland, the researchers compared the genetic makeup of the virus in 22 chronically infected women to the original strain that had infected them more than 20 years before. The women were among hundreds accidentally infected in 1977 by a blood product tainted with hepatitis C, providing the researchers with unique access to the source of the infection, which came from a single donor unaware of having the illness.
Using computer analysis techniques developed at Hopkins, the scientists mapped these changes against the genetic makeup of the women's immune response. The researchers found that when viral mutations were clustered in epitopes specific to each woman's immune system, the changes were directed away from the consensus sequence, suggesting immune escape. However, when mutations were clustered in epitopes that were not specific, the mutations were reversions back to the consensus sequence.
When the individual genome changes in each woman were mapped on a grid, each woman formed a unique cluster indicating individual, evolutionary selection. However, some of the changes were shared, suggesting convergence, which would not have occurred had the virus simply mutated at random.
"Our results raise the possibility that a hepatitis-C consensus sequence could be the best practical option for a vaccine," says infectious disease specialist David Thomas, M.D., a professor of medicine at Hopkins who served as senior author of the study of Irish women. "If we can focus vaccine development on the common genetic element in chronically infected patients, then we may be able to make a more effective vaccine."
Funding for these studies, which took place from January 2002 to January 2005, was provided by the National Institutes of Health, including the National Institute for Allergy and Infectious Disease, and the National Institute on Drug Abuse.
Other Hopkins investigators in this research were Timothy Mosbruger; Qing Mao, M.D., Ph.D.; Zhi Liu, M.D.; Xiao-Hong Wang, M.D.; Hung-Chih Yang; Xiao-Hang Wang, Ph.D., Dale Netski, Ph.D.; and Drew Pardoll, M.D. Co-investigators in the first study also included John Sidney, Ph.D., and Alessandro Sette, Ph.D., from the La Jolla Institute for Allergy and Immunology, in San Diego, Calif. Collaborators in the second study, conducted at Hopkins and at Cork University Hospital in Ireland, were Liam Fanning, Ph.D., and Kelizaeth Kenny-Walsh, M.D.
Hepatitis C is the leading cause of liver disease in the United States, causing an estimated 10,000 to 12,000 deaths each year. Hepatitis C is transmitted when blood and possibly other body fluids of an infected person enter another person, primarily through injection drug use, exposures in health care settings, from an infected mother to her baby during birth, and occasionally through sexual exposure. Symptoms of hepatitis C may not appear for years after infection, and diagnosis must be confirmed by blood tests. However, in addition to liver inflammation and tumors, earlier signs of infection are persistent flulike symptoms, including any combination of body aches, headaches, night sweats, loss of appetite, diarrhea, fatigue, rash, nausea and mild abdominal pain. Current treatments for hepatitis C involve weekly injections of pegylated interferon for one year, plus twice daily doses of oral ribavirin. While some patients recover on their own, with their immune system attacking the virus and clearing it from the body, most do not. Scientists have not yet determined why this happens in some patients and not in others.
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June 03, 2005
HCV and Bewitched
We have a long way to go before HCV gets the kind of acknowledgement as other infectious diseases. Part of the reason there is so much misunderstanding is that people are hesitant to speak out. No one really wants to be the poster child. Yet.
To get more funding and acknowledgement from the government you can go to hepatitisactivist.org and automatically send a message to your representatives in congress.
Given this kind of story, it seems like the least you can do.
Many angry at hepatitis joke in movie:-
NEW YORK | July 03, 2005 8:11:21 AM IST
Many with hepatitis C are angry at what they call an insensitive joke about the disease in the U.S. movie Bewitched, said the American Liver Foundation.
In the film, one character discourages romantic advances from another character, saying she has hepatitis C.
Tragically, this remarkably tasteless comment plays into the stigma that many people with hepatitis C have to cope with every single day, Frederick G. Thompson, president and chief executive officer of the American Liver Foundation, said in a statement.
I can't imagine anyone in Hollywood making a joke about HIV infection, for example, said Thompson, but because the public is so uneducated about hepatitis C, it apparently seems acceptable to trivialize the disease in a comedic context, at the expense of millions of hepatitis sufferers.
The New York-based American Liver Foundation said it has received hundreds of calls and e-mails from moviegoers expressing outrage and dismay, according to Thompson.
Some 4 million people in the United States have been infected with hepatitis C, and 2.7 million of them are chronically infected.
About 10,000 people die each year from complications of hepatitis C.
(UPI)
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HCV Deaths to Triple in 10 Years
This report references the latest numbers from the Centers for Disease Control and the Wall Street Journal.
The numbers are sobering and give good reason to protect and support your liver as effectively as possible.
June 03, 2005
Hepatitis C deaths expected to triple in next 10 years in U.S.
The number of hepatitis C-related deaths in the United States will triple during the next 10 years, with as many as 30,000 Americans dying annually from problems caused by the disease, says the Centers for Disease Control and Prevention. The Wall Street Journal reports that about 8,000 to 10,000 Americans already die each year from the disease. CDC officials say that many of the people dying from hepatitis C-related complications contracted the virus between the 1960s and the 1980s. Because the virus typically lies dormant in the body for many years, those infected with HCV in the 1990s or later will begin to experience symptoms in the next decade.
HCV, a blood-borne virus, is transmitted through shared needles and blood transfusions, and less commonly through unprotected sex. HCV is a common coinfection among HIV-positive people, with as many as 25% of all HIV patients also infected with hepatitis. As many as 5 million Americans are currently infected with HCV; worldwide, there are an estimated 200 million people with hepatitis C. There is no vaccine to prevent HCV infections, and current treatments are effective for only about half of those patients who take them. New treatments currently in clinical trials might offer better results, experts say, but those drugs are still years away from Food and Drug Administration review and approval.
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