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November 2007 HCV Advocate

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Genotype 1b and HCC
Alan Franciscus, Editor-in-Chief

Annual Flu Shots
Alan Franciscus, Editor-in-Chief

Treating HCV Patients with Psychiatric Disorders
Alan Franciscus, Editor-in-Chief

Non-Invasive Markers of Liver Fibrosis
Alan Franciscus, Editor-in-Chief

HealthWise: Viruses - A Good Offense is the Best Defense
Lucinda K. Porter, RN, CCRC

Disability & Benefits: SSI and SSDI: How Much Difference Can a Letter Make?
Jacques Chambers, CLU

Review of The Invisible Enemy: A Natural History of Viruses
Alan Franciscus, Editor-in-Chief


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Genotype 1b and HCC
Alan Franciscus, Editor-in-Chief

In general, hepatitis C is a slowly progressive disease that can take many years before it produces severe liver damage.  In the past, genotype 1 was believed to lead to more severe disease progression than the other genotypes.  But that view fell out of favor because the clinical data at the time did not support it.  However, a couple of smaller studies and now this larger long term 17-year study show that genotype 1b is a more aggressive form of HCV infection, at least when it comes to the development of hepatocellular carcinoma (HCC, or liver cancer) especially after the development of cirrhosis.  

S. Bruno and colleagues published a study in Hepatology, “Hepatitis C virus genotype 1b as a major risk factor associated with hepatocellular carcinoma in patients with cirrhosis:  A seventeen-year prospective cohort study.”  In this study, 163 consecutive HCV-patients with cirrhosis were enrolled between January 1989 and December 1990.  Consecutive patients are people who were seen at clinics and were not specifically recruited for the study.  The patient characteristics of the study participants were: males (51%), genotype 1b (64%), Genotype 2 a/c (32%), other genotypes (4%).  The median age was 58.7 years in patients infected with HCV genotype 1b and 59.5 in patients with genotype 2a/c.  A higher proportion of patients with genotype 2a/c than patients with genotype 1b had Child-Pugh class B at enrollment (25% vs. 12%).  A sub-analysis was also undertaken in a subset of patients who received interferon or interferon plus ribavirin therapy. 

The patients were given an ultrasound to detect possible liver cancer every six months.  Only 18 patients were lost to follow-up. 

The authors reported that after a mean follow-up period of 10.7 years, 44 of the 104 patients with HCV genotype 1b developed liver cancer compared to 10 of the 52 patients with HCV genotype 2a/c.  The predictors associated with liver cancer development were genotype 1b, esophageal varices,  male gender, and age over 60 years.   This increased rate of liver cancer in genotype 1b compared to HCV genotype 2a/c is worrisome given that people with HCV genotype 2a/c had more advanced disease when they were enrolled in the study.  

Of note, a sub-analysis was done on the patients who were treated with interferon and achieved a sustained virological response (SVR).  The standard of care at that time for HCV treatment was interferon monotherapy (injected 3 times a week).  As expected the SVR rates were very low – only 12 patients.  But what is interesting is that in people with HCV genotype 2a/c the development of liver cancer was similar in the treated and untreated group.  However, the rate of progression to liver cancer was lower in the HCV genotype 1b group who achieved an SVR compared to the untreated group.  In fact no patients with HCV genotype 1b who achieved an SVR developed liver cancer.  However, this information should be used with caution since there were so few people who were able to achieve an SVR, but it certainly warrants further study. 

The authors concluded that “HCV genotype 1b is associated with a statistically significant higher risk of developing HCC.  Patients with cirrhosis that are infected with this genotype require more intensive surveillance for the early detection and aggressive management of neoplasia [cancer].” 

A bit of caution should be used in the interpretation of this data.  The association between the increased risk of liver cancer was found in people with genotype 1b who also had esophageal varices, older age, a low prothrombin time and elevated alfa fetoprotein – which are all indications of advanced liver disease and liver cancer.  To properly answer the question as to  which genotype is more likely to lead to more severe or faster disease progression, a prospective study is needed that begins with the approximate date of infection and follows people over a long period of time.  However, this study does provide important information that should be incorporated into the management and treatment of hepatitis C.

Child-Pugh is a scoring system that classifies as well as projects survival rate.  The classification is based on a point system depending on the severity of liver disease according to the degree of ascites, blood concentrations of bilirubin and albumin, prothrombin time, and degree of encephalopathy. 

Child-Pugh classifications are:
• class A – well-compensated disease
• class B – significant functional compromise
• class C – decompensated disease. 

Reference:
Hepatology, 2007 Aug 6; [Epub ahead of print]

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Annual Flu Shot
Alan Franciscus, Editor-in-Chief

It’s that time of year again when our attention turns to the fall and winter and the potential risk of catching a cold or influenza (flu).  Many people confuse these two conditions – the common cold is mostly inconvenient, annoying and can make everyday life miserable.  However, the flu is a serious condition that can produce considerable  health consequences and even death in some people. The general recommendation is that people with hepatitis C should be vaccinated annually – be sure to talk with your medical provider about the annual vaccine.

The flu or influenza causes about 36,000 deaths each year in the United States.  Prior to the development of vaccines, influenza was one of the leading causes of death worldwide.  For instance, it is estimated that the Spanish flu (H1N1) of 1918 killed between 50 and 100 million people worldwide.  But this was before the development of an annual flu vaccine which has dramatically reduced the illness and death associated with influenza outbreaks. 

Unfortunately, there is no vaccine that will provide life-long protection because the influenza virus constantly mutates and infectious new strains emerge every year.  Due to the constant mutation of the virus a new vaccine must be developed every year that is ‘predicted’ to protect people from the more serious strains that are currently circulating.

In an effort to curb future outbreaks of the flu, the World Health Organization (WHO) set up a surveillance system that included 110 laboratories in 85 countries which constantly monitor flu strains circulating in their areas in an effort to identify new strains that may emerge in the coming year.  This information is fed into three major WHO laboratories that are responsible for monitoring major outbreaks from around the world.

In February of each year, scientists from these laboratories meet in Geneva to review the data and recommend strains that should be included in the annual vaccine.  The production of the vaccine takes about 9 months and it is distributed to health care providers in the northern hemisphere in October.  It is recommended that people get the vaccine in October or November to provide enough time for immunity – it takes about 2 weeks for the body to develop antibodies.  It is estimated that 80% of vaccinated individuals will develop immunity to circulating strains of influenza.  However, even if the strain is not included in the current vaccine, the vaccine will act as a booster to prior vaccinations to help lessen the severity of illness for any strain of the flu.

For more information about influenza and additional steps to prevent getting a cold or the flu please check out our HCSP Wellness Fact Sheets:

• Flu Shots

• Influenza

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Treating HCV Patients with Psychiatric Disorders
Alan Franciscus, Editor-in-Chief

It is estimated that between 6.8% and 8.5% of people with chronic psychiatric disorders are also infected with hepatitis C.  The current treatment for hepatitis C is pegylated interferon plus ribavirin therapy, which is well-known for producing psychological side effects.  The more severe and uncommon side effects of interferon can include moderate to severe depression, mania, psychotic symptoms, delirium syndromes, relapse in alcohol and drug abuse and even suicidal thoughts.   In the past, most medical providers have been reluctant to treat HCV patients with chronic psychiatric disorders with pegylated interferon for fear that the psychiatric disorders may be exacerbated or made worse by interferon.  But it is important to know that in order to stop the spread of HCV, reduce the future disease burden of HCV, and alleviate the pain and suffering of hepatitis C, steps need to be taken to try to understand and treat this high prevalence population.  Unfortunately, there has been too little research into the issues of treating this population.  However, in the small studies that have been conducted so far it has been found that treating people with HCV and psychiatric disorders produces similar sustained virological response rates (SVR) when compared to people without psychiatric disorders.   A new study, “Hepatitis C Treatment in ‘Difficult-to-Treat’ Psychiatric Patients with Pegylated Interferon-Alpha and Ribavirin:  Response and Psychiatric Side Effects,” by M. Schaefer and colleagues, is adding to the growing body of evidence that is showing that it is safe and effective to treat people with psychiatric disorders. 

In their study, M. Schaefer and colleagues treated seventy patients – 17 patients without psychiatric diseases or drug addiction (control group); 22 patients with psychiatric disorders, 18 patients who had received methadone maintenance therapy, and 13 patients who were former drug users.  All patients were treated with pegylated interferon plus ribavirin.  The characteristics of the study participants were:  male (62.9%), median age- 43.9 (± 9.12), genotype 1 (62%), genotype 2 (1.4%), genotype 3 (34.3%), genotype 4 (1.4%) (note:  some patients had more than one genotype),  and median HCV RNA or viral load was 1,011,843 (±2,143,366).  All patients were treated with pegylated interferon (peg once a week) plus ribavirin dosed by body weight (800-1,200 mg/day).  Treatment duration was 24 weeks for people with genotypes 2 and 3 and 48 weeks for people with genotypes 1 and 4.  The results (SVR, adherence, and psychiatric side effects) between the groups was compared.

The authors reported that 58.6% of all patients achieved an SVR. Breaking it down by study group it was found that 58.8% of the control group, 50% of the psychiatric group, 72.2% of the methadone group, and 53.8% of former drug users achieved an SVR.  It was also reported that methadone patients and former drug users had significantly higher drop out rates. 

Of note, the authors did not find a difference in the depressive or psychotic symptoms or side effects between the groups during treatment.  But the control group without pre-existing psychiatric disorders had lower pre-treatment psychiatric scores and a significant higher increase to maximum scores during treatment.  It was also reported that only genotype was associated with SVR.  In other words, the other factors such as psychiatric, methadone, former drug abuse, type of psychiatric diagnosis, depression scores (before and during treatment), gender, or liver enzyme levels did not positively or negatively affect SVR rates. 

The authors concluded that “the data from our prospective, controlled trial provided evidence that treatment of chronic hepatitis C infection with pegylated interferon alpha and ribavirin is possible in different subgroups of ‘difficult-to-treat’ psychiatric patients.”  The authors also strongly recommended an interdisciplinary approach with psychiatric, addiction and hepatitis C medical providers to optimize treatment outcome.   Clearly more studies are needed to further elucidate the most effective methods of treating HCV positive people with psychiatric disorders with current treatment regimes, but even more important is to start now to design and carry out large prospective clinical trials on the new HCV compounds in development before they are approved for treatment of hepatitis C so that this highly prevalent population is not left behind or forgotten.

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Non-Invasive Markers of Liver Fibrosis
Alan Franciscus, Editor-in-Chief

The gold standard of care for assessing the health of the liver is the liver biopsy.  However since the procedure requires that a needle be inserted through the skin (percutaneous) there is a potential for complications even though the incidence of complications is extremely low.  The complications of a liver biopsy can include internal bleeding, and puncturing another organ such as the lungs, stomach, intestines, or any other organs that are close to the liver.  In regards to accuracy of the biopsy the sample liver tissue size is important for correctly staging and grading a liver biopsy.  Another problem is that the tissue taken from one part of the liver may not be 100% representative of the entire liver.  Once the liver tissue sample is collected it is graded and staged by a specialist (pathologist), which could lead to possible human error in interpreting the results.  In addition there is no standardized interpretation protocol so it is difficult to compare the results of different biopsies read by different pathologists.  Price is also an issue since a typical liver biopsy can cost between $1,500 and $2,000.   Given these potential problems it is not surprising that there is a lot of research that is being conducted on the development of non-invasive tests.  The tests that have been developed so far have had mixed results in accuracy when compared to the results of a liver biopsy.  There have been few prospective clinical trials that have compared the results from various non-invasive markers to the results from a liver biopsy.  Until now…..

This year the results from a prospective clinical trial that compared six non-invasive tests was published.  “Prospective comparison of six non-invasive scores for the diagnosis of liver fibrosis in chronic hepatitis C,” by Vincent Leroy and colleagues, was published in the Journal of Hepatology. In this study the following serum marker scores were compared to the results obtained from a liver biopsy:

1.   MP3:  combines PIIIN (a marker of fibrogenesis), and matrix metalloproteinase MMP-1 (involved in fibrolysis)
2.   Fibrotest:  combines serum concentrations of a2 macroglobulin, haptoglobin, gGT, bilirubin, and aplipoprotein A1
3.   Fibrometer: combines hyaluronate, prothrombin time, platelets, AST, a2 macroglobulin, urea, and age, and the formula is adjusted based on the cause of the liver disease.
4.   Hepascore: combines bilirubin, gGT, hyaluronic acid, a2 macroglobulin, age, and gender.
5.   Forns’ score:  combines age, gGT, cholesterol, and platelet count.
6.   APRI:  based on AST activity and platelet count. 

 In this prospective study, 180 consecutive patients underwent a liver biopsy between 2002 and 2004. 

Liver biopsy results
All liver tissue samples were analyzed twice by a single senior pathologist.  Liver fibrosis and necroinflammatory activity were evaluated according to the METAVIR scoring system.  The METAVIR scoring system was specially designed for patients with hepatitis C.  The grade is assigned a number based on the degree of inflammation, which is usually scored from 0-4 with 0 being no activity and 3 or 4 considered severe activity.  The METAVIR system also includes scores for necroinflammatory activity ranging from A0 to A3 (A0= no activity, A1 = minimal activity, A2 = moderate activity, A3 = severe activity.)

The stage score represents the amount of fibrosis:

• Stage F0 = no fibrosis
• Stage F1 = mild fibrosis
• Stage F2 = moderate fibrosis
• Stage F3 = bridging fibrosis
• Stage F4 = cirrhosis

Additionally, sinusoidal fibrosis was staged: 0=no fibrosis, 2=moderate to severe fibrosis. 

The overall results found that that 89 (49.4%) patients had no/mild fibrosis (F0/F1), and 51 (28.3%) had extensive fibrosis or cirrhosis (F3/F4).  It was also found that the METAVIR fibrosis stage was significantly correlated to sinusoidal fibrosis stage (p<0.001).

Note: The statistical measurement used to establish the overall performance of the serum markers that correlated with the liver biopsies was the AUROC – Area Under the Receiver Operating Characteristic (curve). 

The overall diagnostic performance ranged from 0.86 for Fibrometer to 0.78 for Forns’ score (p=ns) for discriminating F0/F1 vs. F2/F3/F4.  For discriminating F0/F1/F2 vs. F3/F4, AUROCs ranged from 0.91 for Fibrometer to 0.78 for Forns’ score (p<0.02).  Significant or extensive fibrosis was predicted in 10-86% of patients with positive predictive value (PPV) ranging from 55% to 94%.  Using a variety of statistical methods the authors stated that “The best combinations could select one-third of patients for whom either absence of significant fibrosis or presence of extensive fibrosis could be predicted with more that 90% of certainty.”  This study has confirmed what other smaller studies found: that non-invasive markers are good for detecting either no fibrosis or extensive fibrosis.  Unfortunately, the grade and stage in between is more challenging, at least in the setting of a non-invasive tests. 

The authors also looked at combining various non-invasive tests to increase the accuracy of single marker tests.  In this setting the authors found that combining various tests and using cut-off points for determining the likelihood of accurate readings was the best approach.  Based on their findings the authors developed an algorithm for detection of fibrosis in hepatitis C patients with elevated transaminases (see below).

 

 

Reference:
J Hepatology, 2007 May; 46(5): 775-82. Epub 2007 Jan 26

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HealthWise: A Good Offense is the Best Defense (Third in a four part series)
Lucinda K. Porter, RN

The first article in this series focused on basic viral information. Last month’s Healthwise concentrated on the immune system. This month, we will discuss a powerful anti-viral weapon – prevention.

Prevention is a multifaceted tool. It is more than good hygiene and practicing safer sex. It includes immunization and taking care of our health. Prevention is knowing how to navigate in a world of germs.

Prevention is a two way street. Taking steps to avoid viruses is crucial. However, once a virus moves into the body, then the task is to avoid passing it on. To dodge getting a virus or giving one, use the same precautions.

Learn how germs are passed and what you can do to minimize this happening. Transmission prevention ranges from safer sex to avoiding mosquito bites, from not sharing your drinking glass when you have a cold to washing your hands before you prepare food. Spend some time learning techniques to prevent the spread of infectious diseases. The Mayo Clinic provides good advice at www.mayoclinic.com/health/infectious-disease/ID00004. For information specific to the hepatitis C virus (HCV), visit www.hcvadvocate.org/hepatitis/factsheets.asp.

Many viruses are transported from our hands to our eyes, nose, or mouth. Good hand washing is the enemy of viruses. Most of us do not wash our hands properly or nearly enough or for long enough. Alcohol-based hand sanitizers are effective if used correctly. For tips on hand hygiene, visit the Mayo Clinic’s website at www.mayoclinic.com/health/hand-washing/HQ00407.

Unless we live in a glass bubble, it is virtually impossible to avoid all viruses. Fortunately, we have the capacity to build immunity to some viruses. This occurs if we have antibodies to a virus. Mentioned last month, antibodies specialize in finding and neutralizing specific invading microbes, called antigens. When these two pair up, it sets off an antigen-antibody reaction, which is one of the immune system’s strongest weapons.

Newborns are born with some immunity. Mothers pass antibodies to the developing fetus and later through their breast milk. Over time, infants lose these and need to make their own antibodies. The process of manufacturing antibodies is called acquired immunity.

We acquire immunity in three basic ways:

  1. get the virus and manufacture our own antibodies,
  2. get the vaccine and make our own antibodies, and
  3. temporarily use someone else’s antibodies.

Let’s start with the first and most common way. Those of you who are “more mature” may remember measles, mumps, and German measles. These diseases are caused by viruses. If you got the disease, you never got it again.  That’s because your body manufactured measles antibodies, mumps antibodies, and so on. This is naturally acquired immunity.

Although many of us get colds every year, we actually don’t get the same cold each time. Colds are caused by viruses. According to the National Institute of Allergy and Infectious Disease, more than 200 viruses can cause a cold. Theoretically, if you caught all of these viruses, your body would produce antibodies for each and you would not get any more colds. An interesting side note – when we catch a cold, the symptoms we feel are mostly from our immune system’s response to the virus rather than from the virus itself.

Immunization is the second way to acquire immunity. Our children may never have had measles, mumps or German measles, but they have antibodies against these viruses. That’s because they were vaccinated or immunized. For the same reason, our grandchildren aren’t getting chicken pox since that vaccine became available.

Vaccines stimulate antibody production. A vaccine may be a modified form of a virus. When we are vaccinated, we don’t actually get the virus or the disease. Instead, the immune system produces antibodies against that disease. Some people are afraid that they will get sick if they are immunized. In rare cases, some will have an allergic reaction. Most people feel fine after immunization. Some may feel a little achy or sore at the injection site. These reactions are not from the vaccine but from the immune system’s response to the vaccine.

Immunization is one of the greatest advances in medicine.  Polio was eradicated in the U.S.; smallpox from the world. Vaccines can protect us from tetanus, diphtheria, whooping cough and hepatitis B. We can protect ourselves from influenza, pneumonia, and hepatitis A.  Vaccines are now available to protect against shingles and cervical cancer.

Occasionally some controversy arises about immunization, particularly from outside of mainstream western medicine. Vaccines are well tested. The most well-known expert in Complementary and Alternative Medicine, Andrew Weil, M.D., publicly supports the use of vaccines. He reports that he and his teenaged daughter stay current with a flu shot and other immunizations.

The main types of acquired immunity are active and passive. Active is what I described earlier – a modified form of the virus stimulates antibodies. The process of manufacturing antibodies is active, either by getting the disease or the vaccine. Passive immunity is the third way to acquire antibodies. The body does not make antibodies – it borrows them from another human or animal.

Imagine you have a family member who has hepatitis A (HAV) and you have never had HAV or its vaccine.  Your medical provider may inject you with a preparation filled with antibodies collected from the blood of huge numbers of people. This preparation is called gamma globulin or immune serum globulin. It gives you a temporary reserve of antibodies that will fend off HAV. This passively acquired immunity usually lasts a few weeks or months.

Unfortunately, everything has exceptions. Medicine is like the rest of life and nothing is black or white. For instance, some immunizations may give life-long protection, while some give shorter protection. Some people have had diseases more than once – probably because they had a mild form the first time and they didn’t make enough antibodies. Moreover, there are some viruses against which we can make antibodies but the virus sticks around, such as HIV and HCV.

The hepatitis viruses are particularly inconsistent. This makes sense because the hepatitis viruses are not all in the same family. Hepatitis A (HAV) acts like a typical virus. Get HAV once and you never get it again. Get the HAV immunization and you are protected, although you may need a booster in about 25 years.

Hepatitis B (HBV) breaks the most rules. The majority of people who have a natural exposure will get well and have protective antibodies. However, a small percentage will develop chronic HBV and will be carriers. HBV frequently becomes a chronic condition if the exposure occurred during infancy or fetal development.

The HBV vaccine is effective and may last a lifetime. People who were immunized seem to be protected from HBV even if their antibody level is below detection. HAV and HBV immunizations are advised for people living with HCV who have not had either of these diseases.

This brings us to HCV. The majority of cases are chronic. Approximately 20% who are exposed to this virus will develop antibodies but not a chronic infection. No one knows if HCV antibodies protect against future infection.  There is no HCV vaccine.

We started this series with basic virus information and then proceeded to the immune system. This month we highlighted the gateway to health – prevention.  Immunization and good habits can protect us as well as others. Next month’s Healthwise will discuss how to help your immune system to do its job.

Reference
Centers for Disease Control www.cdc.gov

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Disability & Benefits: SSI and SSDI: How Much Difference Can a Letter Make?
Jacques Chambers, CLU

It’s complicating enough that Social Security operates two entirely separate disability benefit plans, and having their initials only one letter apart practically guarantees confusion. Yet one letter can be very important as there is a world of difference between the two plans. The two plans are SSI (Supplemental Security Income) and SSDI (Social Security Disability Insurance). Perhaps the best way to clear the confusion is to look at them together.

NOTE: This is an overview only to clarify the distinctions between SSI and SSDI. This is not intended to provide a comprehensive description of either plan.

First, the concept and goal of each plan shows why there are major differences:

SSI is a “needs-based” benefit. In addition to providing benefits to persons who are disabled of any age including children, it also pays monthly benefits to people over age 65 who qualify financially whether or not they are disabled. The key to SSI benefits is “financial need.” The “Financial Eligibility,” discussed below, is based on the person’s lack of personal resources and income to meet necessities of life.

SSDI is also called SSD. Social Security calls it just “Disability” and refers to the DIB, or the Disability Insurance Benefit. Whatever it’s called (we’ll use SSDI), the program was created so workers who become disabled and unable to work to their normal retirement age will be able to access their Social Security retirement benefit early. Private pension plans would call this a “disability ‘retirement’ benefit.” Financial eligibility, discussed below, is solely based on the length of time and amount paid in F.I.C.A. payroll taxes.

There are some similarities between the plans:

Both SSI and SSDI:

  • Are administered by the federal Social Security Administration.
  • Will pay a monthly benefit to totally disabled persons who qualify.
  • Require the very same level of medical disability to qualify for benefits, and follow the same procedure in determining whether or not an applicant is disabled (See “Getting Disability Benefits under Social Security with HCV” in the Benefits Section of the HCV Advocate Website; it applies to both SSI and SSDI).
  • That’s about it for similarities.

Now, the major differences:

Amount of Monthly Benefit
SSI pays a set amount each month. The amount will vary some depending on whether the beneficiary lives independently, lives in a board and care facility, has cooking facilities, lives rent-free, is blind, and several other factors.

A disabled person living alone in his/her own apartment with cooking facilities is eligible to receive up to $623 per month during 2007 from the federal government. The amount is raised each year with a Cost of Living Increase. However, SSI functions as a safety net, or a floor of income; any other income received is deducted from that SSI base amount, although they will ignore the first $20 per month received from another source.

SSP - Some states supplement the federal SSI payment with an additional payment raising the total monthly payment. California’s contribution, for example, increases the $623 to about $850 per month. Check with your local Social Security office to see what your state does.

SSDI pays a monthly benefit based on the amount of F.I.C.A. payroll taxes the person has paid into Social Security over his/her working career. The benefit may be anywhere from one dollar per month to around $2,400 per month.

The calculation attempts to estimate what the retirement benefit would be if the person continued working to retirement and pay that amount as the SSDI monthly benefit.

Each year about three months before each person’s birthday, Social Security sends out a statement summarizing the F.I.C.A. taxes paid and estimated retirement benefits plus what the disability payment would be. Statements can also be requested at the Social Security website, http://www.ssa.gov.

Financial Eligibility
These are the non-medical requirements for the benefits. One is based on what you “don’t have” while the other looks only at the payroll taxes you paid.

SSI benefits are only available to persons who can show that they have very few assets or resources and low income.

Resources/Assets must be less than $2,000 ($3,000 for a married couple). This includes all money in checking, savings, as well as retirement savings accounts. It also includes real estate (except the home you live in), stocks, bonds, mutual funds, and other investments. It does NOT include one car, the residence you live in, most personal property including furniture and clothing, and certain other exempt items.

Income is more complicated since it is related to the amount of SSI benefit you are eligible to receive and that varies. Generally, your income must be less than the amount of benefit you would be eligible to receive, and SSI will only pay the difference between your other income and the amount you would be entitled to receive based on your residence and living situation.

For example, if you would be eligible to receive $623 from SSI but your SSDI pays you $700 per month, you would not be eligible for any SSI benefit. However, if your SSDI payment were only $300, you would be eligible for a partial payment from SSI that would take your total income up to approximately $623 per month.

SSDI financial eligibility is based solely on the Social Security (F.I.C.A.) payroll taxes you paid over your working career. It totally ignores how much money you do or don’t have. To be eligible for SSDI, you must have paid F.I.C.A. taxes in 20 out of the last 40 calendar quarters (five out of the last ten years). If you are under age 31, that number is reduced. If you are over age 42, the minimum number of quarters increases approximately one quarter for each year over age 42.

As long as you can meet the payroll tax payment requirement, you may receive SSDI benefits if you become totally disabled, regardless of what other income or wealth you may have.

When Monthly Payments Start
When monthly benefits start varies between the two plans.

SSI benefits start on the first of the month that you first submit your application, even if it takes several months to get approval.

For example, you submit your SSI application on April 14 and your claim is approved on July 25. Social Security will owe you benefits from April 1, which they will send you in a lump sum payment.

Once you are approved, SSI checks arrive on the first of each month.

SSDI benefits start in a totally different manner. First, you are not eligible to receive any SSDI benefits during the first five calendar months of your disability, regardless of when you apply for benefits.

For example, you stop working due to symptoms of HCV on February 14, 2006. You don’t get around to applying for SSDI benefits until September 3, 2006. On November 10, 2006, Social Security sends you a letter saying that you were approved for SSDI benefits and the Onset Date (the day they consider your total disability to have started) is February 15, 2006, the day after your last day of work. You would be eligible for benefits beginning August 1, 2006 (five calendar months after your Onset Date). You would receive a lump sum check for the benefits from August through November.

The regular monthly checks for SSDI come in the month following the month that you “earn” the benefit. Your SSDI check for April will come during May.

Medical coverage
In most states, medical insurance coverage accompanies SSI and SSDI.

SSI will vary some by state, but in almost all states, you are eligible for Medicaid if you receive even one dollar from SSI. In most states, Medicaid comes automatically with approval for SSI benefits. In some states you must make separate application with your state’s Department of Human Services.

SSDI is accompanied by Medicare, the federal healthcare plan, regardless of what state you live in. However, a person receiving SSDI benefits does not become eligible for Medicare until they have received benefits for twenty-four months (29 months after date of disability counting the five month waiting period for SSDI benefits).

In the SSDI example above, the person who starts receiving SSDI benefits on August 1, 2006 will be eligible for Medicare on August 1, 2008.

Periodic Confirmation of Continued Eligibility for Benefits
Both plans will periodically re-examine your medical records to see if you are still totally disabled. The review to see if you are still disabled is called a Continuing Disability Review. It will occur every three to seven years, depending on the nature of your disability. For persons with HCV, the disability reviews will usually be from five to seven years apart.

SSI will review your financial records every year to see if you still qualify for SSI benefits. If your income or resources exceed their maximums, your benefits will stop.

SSDI has no ongoing review of financial eligibility. SSDI beneficiaries only have the Continuing Disability Reviews.

If you apply to Social Security for disability benefits, they are supposed to screen you for both SSI and SSDI. Just to be sure, if you find your SSDI is less than $900 per month, ask the representative about SSI to see if you might be eligible.

When you apply for SSI, in addition to medical records, Social Security will want to see financial records, including bank statements, lease and mortgage agreements, savings and other documentation of your financial status.

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Review of The Invisible Enemy: A Natural History of Viruses, by Dorothy H. Crawford
Alan Franciscus, Editor-in-Chief

The Invisible Enemy is a very good overview of the world of viruses.  Virologist Dorothy H. Crawford has written a book that is scientific, but it is also interesting, enjoyable, and very readable.  In fact, I became so immersed while reading the book that I felt that I was reading a historical novel and not a book on the science of viruses.  But that is what is so enjoyable about this book – Ms. Crawford weaves together interesting tales, scientific data and her thoughts on viruses in a way that helped me to understand these primitive proteins and their impact on the history and evolution of the human race.  

Throughout the book there is information about the history of a variety of viruses:

 • Yellow fever: how it is spread by mosquitos, the pandemics it has caused throughout history, the spread of yellow fever in the U.S., how the transmission routes were first identified, and more importantly how the spread of yellow fever was stopped in this country.

 • Polio: the impact of this disease on the U.S., how it is spread and the development of a vaccine that has helped to eradicate it from the U.S. and around the world.

 • HIV: a good overview of the history of HIV, how HIV replicates, and the efforts to manage HIV and stop its transmission. 

 • Hepatitis viruses: There is a brief overview of hepatitis A, B, and C.

There is also an overview of the emerging viruses that have the potential to cause future pandemics:

 • Ebola: The emergence of this virus from central Africa and the effects of the virus on the human body.

 • Hanta virus: a virus that caused small but widespread infection in the Western U. S. that by the end of 1995 caused 58 deaths—out of a total of 119 people who became infected.  

 • Bird flu: a brief overview of bird flu and how viruses can jump between species, what is being done to curb a potential pandemic and some realistic data that should help to alleviate some of the fear that has been generated about bird flu in the media.

What is remarkable is that after reading the book I came away with a better understanding of viruses and less fear of potential outbreaks that the media has sensationalized in the last couple of years.

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