"That had never been shown before," said lead researcher Dr. Christopher Power, a neurologist who works in the U of A's Faculty of Medicine and Dentistry. "It gets in there, it infects and it replicates. For a virologist, that's a really core observation. You can see infection of the cells and you can see replication."

To show how the hepatitis C virus infects brain cells, Power pointed to a computer screen in his U of A lab on Tuesday.

On one side of the screen, pictures of two healthy brain cells appeared in red. On the other side, those same cells appeared peppered with green dots. And in this picture, green is bad since it represents a buildup of viral proteins that eventually damage and kill the cell. In a way, Power explained, the virus can cause brain cells to drown in their own garbage.

The discovery is important, Power said for a couple of reasons.

First, he said, there are immediate clinical implications. "It tells us we need to be vigilant for neurological problems for people who have hepatitis C," he said.

That would mean taking such steps as ensuring patients have access to a neurologist or psychologist on their team of physicians as well as a liver specialist.

"The second issue is it underscores the importance of developing new treatment for hepatitis C so we can prevent infection of the brain," said Power, whose research is funded by Alberta Innovates — Health Solutions and the Canadian Institutes of Health Research.

There is now no vaccine to prevent hepatitis C. Researchers have uncovered some treatments that work for a portion of patients infected with hepatitis C, but those also can have serious side effects for some people.

Michael Harmsworth, a hepatitis C sufferer who counts Power among his five doctors, said Tuesday he was extremely interested to learn about the research team's discovery. He said he hadn't realized that hepatitis C had the potential to affect the brain until Power showed him computer images of infected tissue samples.

Harmsworth, who was diagnosed about 13 years ago, said it all points toward progress.

Source:  The Edmonton Journal

Healthwise: Finding Safety in Numbers

Lucinda K. Porter, RN

Over the years I have said, “The majority of those infected with chronic hepatitis C virus (HCV) will die with this virus, not of this virus.”  I balance this statement with other equally important information, such as:

·        We can’t accurately predict who will be the ones who will have more serious damage, leading to cirrhosis, liver cancer, or death.

·        Death is just one of the consequences of HCV.  Living with this chronic illness can be a struggle for some, even in situations in which there has been no significant liver disease.

·        Living with HCV affects us mentally, spiritually, and socially.  Physical death is serious and final, but many patients experience metaphorical deaths as they try to come to terms with what it means to have HCV.

Recently I read a well-written blog (hepatitiscnewdrugs.blogspot.com) by Tina (last name unknown), pointing out that when we say most of us will die with rather than of HCV, we do a huge disservice.  This blogger is concerned that this may be interpreted to mean that HCV isn’t serious, and thus, we don’t need to take action.  She makes an impassioned plea to the HCV community to “understand the magnitude of this disease.”

She’s right, especially because what we know in 2010 is different from what we knew ten or more years ago.  When I was first diagnosed, I was told that I had non-A, non-B hepatitis and that it was nothing to worry about.  When HCV was identified, we began to learn more about it, including that it was a progressive disease that affected the entire body as well as the liver. 

Now there is more evidence to examine.  At the 2009 meeting of the American Association for the Study of Liver Diseases (AASLD), Gary Davis and colleagues¹ forecasted the future for HCV.  There will be a significant increase in HCV-related deaths and complications in the years between 2010 and 2030.  This is because the majority of those with HCV, aging Baby Boomers, will have had this virus for a long time, and typically, HCV causes its greatest damage after 20 or more years.  If HCV is left untreated, advanced liver disease will quadruple in the next 10 years—from 30,000 to 150,000 cases annually.  HCV-related liver cancer will triple from 5,000 to 15,000 annual cases.  In short, if HCV-positive Baby Boomers are not treated, the mortality predictions are bleak. 

A side note: Davis and colleagues also reported that there will be a gradual decline in the prevalence of HCV.  This is because many of us will die, mostly from conditions unrelated to HCV; also, the number of new HCV cases is declining.  Acute HCV, infection that is less than 6 months old, is much easier to treat than chronic HCV.  This, coupled with advances in treatment for chronic HCV, means that future generations will have a very different experience of HCV.

The potential threat of HCV is underscored in the Milliman Report.² Here are a few choice quotes:

·        “Our projections suggest that without improvements to the current low effective treatment rate, the U.S. healthcare system will be burdened with more HCV-infected patients progressing to cirrhosis, decompensated cirrhosis, and hepatocellular carcinoma, and ultimately, more patients requiring liver transplants.

·        As the Baby Boomers age, the consequences of HCV infection will become an important cost issue for commercial payers and an even more important cost issue for Medicare.  Over the next 20 years, total annual medical costs for patients with HCV infection are expected to more than double, from $30 billion to over $85 billion, and remain elevated.  Medicare shows the most dramatic cost change, increasing fivefold from $5 billion to $30 billion.” ³

Given this, I reflected on my reasons for saying, “the majority of those infected with HCV will die with this virus rather than of it.”  There are two reasons, the first being to reassure.  I find it comforting to know that of the 3.2 million people with HCV only a small fraction will succumb to it, albeit succumbing to anything is hardly reassuring.  The second reason is to bring perspective.  While it is understandable that we are concerned about liver disease, we are susceptible to plenty of other medical problems. 

According to the latest data (2006) from the Centers for Disease Control and Prevention there are 2,426,264 annual deaths.⁴ The U.S. Census Bureau estimates that there are more than 309 million people in this country.  The leading causes of death are:

·        Heart disease: 631,636

·        Cancer: 559,888

·        Stroke (cerebrovascular diseases): 137,119

·        Chronic lower respiratory diseases: 124,583

·        Accidents (unintentional injuries): 121,599

·        Diabetes: 72,449

·        Alzheimer’s disease: 72,432

·        Influenza and Pneumonia: 56,326

·        Nephritis, nephrotic syndrome, and nephrosis: 45,344

·        Septicemia: 34,234

What does this have to do with HCV?  Everything.  It means that while we are weighing our options—whether it is considering treatment or reviewing the merits of milk thistle—we need to get annual flu shots, exercise every day, eat a healthy diet, schedule regular cancer screenings, and wear our seat belts.  It is not enough to treat HCV—the entire body needs attention, because health is a package deal. 

While we are taking care of our bodies, consider treatment.  Despite the fact that HCV is treatable, many are reluctant to try.  Can you imagine the reaction if medical science announced that there was a treatment for HIV that took a year, had a 50% success rate and had lots of side effects that would reverse when the medications were stopped? I bet HIV patients would be delighted.  Yet we HCVers hesitate, since on the whole, we aren’t saddled with lots of HCV symptoms and imminent death. 

The fact that we need to take HCV seriously does not mean that we have to live with fear and anxiety.  Worrying doesn’t change the facts and it does nothing to help our health; in fact, worry is more likely to hurt our health than to help it.  What I wish for all of us is that we are free from worry, while still acting responsibly. 

Endnotes:

¹ Aging of Hepatitis C Infected Persons in the United States: A Multiple Cohort Model of HCV Prevalence and Disease Progression

² Consequences of Hepatitis C Virus (HCV): Costs of a Baby Boomer Epidemic of Liver Disease” B. Pyenson; K. Fitch; K. Iwasaki.  The Milliman Report was commissioned by Vertex Pharmaceuticals www.vrtx.com/millimanreport.html

³ ibid

⁴ Centers for Disease Control and Prevention’s National Center for Health Statistics  www.cdc.gov/nchs

Source:  HCV Advocate October Newsletter

REALIZE Top-Line Results

Alan Franciscus, Editor-in-Chief

HCV Advocate October 2010 Newsletter

In the September 2010 HCV Advocate newsletter I wrote about Merck/Schering’s two phase III studies of boceprevir and Vertex’s phase III study of telaprevir.  The new drugs are HCV protease inhibitors that are given in combination with pegylated interferon and ribavirin.  Recently, Vertex released the results from their REALIZE study on the re-treatment of HCV genotype 1 patients who did not achieve a sustained virological response (SVR)* with a previous course of pegylated interferon and ribavirin therapy. 

The study included prior non-SVR patients — 354 relapsers, 124 partial responders, and 184 null response patients.* There was limited data on the patient population, but it is important to know that 89% of the patients had a high HCV RNA viral load (greater than or equal to 800,000 IU/mL) and that 26% of the patients had cirrhosis—both are considered poor predictors of treatment response. All the patients were HCV genotype 1 evenly divided between subtypes 1a and 1b.

Overall, 65% in the telaprevir containing groups achieved an SVR compared to 17% in the groups that received the current standard of care — pegylated interferon and ribavirin — without telaprevir. The SVR rates of the telaprevir containing groups vs. standard of care groups by type of prior Non-SVR are listed below. 

The side effects reported were mild to moderate and the discontinuation rates were similar between all the groups including the groups that did not receive telaprevir.

Vertex has stated that they will complete filing for marketing approval with the Food and Drug Administration (FDA) by the end of 2010.  It is estimated that the FDA will approve the triple combination of telaprevir, pegylated interferon and ribavirin in 2011-

2012. 

Next month we will also publish individual fact sheets on the top-line phase III results for both boceprevir and telaprevir.  Additional information will be released at the 2010 American Association for the Study of Liver Diseases (AASLD) conference and the articles in peer-reviewed journals will most likely be available in 2011.

*Definitions:

Sustained virological response (SVR):  undetectable HCV RNA (viral load) 24 weeks after the last dose of medicine was taken.

Relapser:  a person who was undetectable at the completion of at least 42 weeks of therapy but who became detectable during the 24 week follow-up period.

Partial responder: a person who achieved at least a 2 log10 reduction in HCV RNA (viral load) at week 12, but who was never HCV RNA undetectable by week 24 of treatment.

Null responder: a person who achieved LESS than a 2 log10 reduction in HCV RNA by week 12.

Mayo Announces Nearly 5,000 Hepatitis Tests

JACKSONVILLE, Fla. – September 21, 2010 -- The Mayo Clinic has tested thousands of people for potential hepatitis C infections, and today announced there are thousands more to test.

In late August, the clinic announced that an investigation into an employee diverting narcotics from patients led to the discovery of transmission of the disease to at least three patients.

That employee, Steven Beumel, was arrested. He has only been charged in relation to the narcotics, not the hepatitis transmission, because investigators so far believe he was not aware he had hepatitis.

In a release today, the clinic updated its efforts to not only identify everyone who may have potentially been infected, but also to prevent such incidents from recurring.

As of Sept. 19, according to the release, 2,400 patients have either been tested or scheduled for testing.

Beginning today, the clinic is scheduling 2,100 more for testing. The new patients are primarily those who received care in interventional radiology at St. Luke's Hospital between 2004 and April 11, 2008. At that time, Mayo owned St. Luke's.

While results of the tests will not be released, Mayo said it does have a plan for both positive and negative results.

Mayo Clinic in Florida CEO Dr. William C. Rupp said he feels confident the hospital has already identified the "vast majority" of those at risk for infection.

Rupp added that Mayo will do "whatever is necessary" to support its patients.

Source:  First Coast News 

Hepatitis C Virus Infection Linked to Fat Enzyme in Liver Cells

London, October 11, 2010 (ANI) Scientists have found that an enzyme associated with the storage of fat in the liver is necessary for the infectious activity of the hepatitis C virus (HCV).

This discovery may offer a new strategy for treating the infection.

The study by the researchers at the Gladstone Institute of Virology and Immunology (GIVI) shows that the enzyme DGAT1 is a key factor in HCV infection

With several potential DGAT1 inhibitors already in the drug-development pipeline, a treatment for HCV may be possible in the near future.

"Our results reveal a potential 'Achilles heel' for HCV infection," Nature quoted Melanie Ott, senior author on the study, as saying.

"Several DGAT1 inhibitors are already in early clinical trials to treat obesity-associated diseases. They might also work against HCV," said Ott.

It has been recently shown that fat droplets are critically involved in the HCV lifecycle and DGAT1 helps in their formation.

The Gladstone team discovered that HCV infection and viral particle production are severely impaired in liver cells that lack DGAT1 activity.

"We found that HCV specifically relies on one DGAT enzyme, DGAT1. When we inhibit DGAT1 with a drug, the liver still produces fat droplets through another DGAT enzyme but these droplets cannot be used by HCV," said lead author Eva Herker. They found that DGAT1 interacts with one viral protein, the viral nucleocapsid core protein, required for viral particle assembly.

The core protein normally associates with the surface of fat droplets but cannot do so when DGAT1 is inhibited or missing in infected cells.

The study was published in the journal Nature Medicine.

Source:  OneIndia

End of Newsletter, Support Phone Line

Liverhope has reached the point financially where we are no longer able to afford to continue the monthly Newsletter, Support Phone Line, etc. Over the last 12 years we have funded our activities through generous donations from pharmaceutical companies, our members and various fund raising activities. Our income has fallen below our expenses to the point that we can only fund this last newsletter and the last month of the phone line.  We are in the process of applying for grants, but this is the last newsletter and month of phone support unless and until we get more funding.

If you wish to donate, so that we may continue, please send your contribution to LiverHope, 16807 Canterbury Drive, Minnetonka, MN 55345.  It is tax-deductible.

It is Rich’s intention to continue the monthly meetings.