VA: Vets last year, 31% were positive for HCV

[Guest guest]

Dear Philly Firefighters,

Note: US Veteran Population is 26 Million today, and growing.....

" The present veteran population is estimated at 25.6 million, as of July 1,

1997. " http://www.va.gov/organization/Vavdva.htm

31% HCV infection rate, times 26 million = 8.06 million US Veterans that

might have HCV today.

Where's the outrage?

The CDC has told America that HCV is from IV Drug use. The WWII and Korean

War vets with HCV are not junkies and their families are not pleased to find

this Government in a process of yet another cover-up. This time concerning

million, if not tens of millions, of US Citizens.

The Veterans have tried to carry the message for 2 years now but many are

gone and most are very ill. We need for you to speak now strongly on this

matter and have this government explain why children are mandated to receive

HBV vaccines. Simply put, this Government is now misleading millions of

Citizens to the

point of our demise.

This Government may claim that all the US Veterans that have died from

hepatitis in the past 58 years, from a vaccination that began at the

Rockefeller Foundation [Yellow Fever and HBV] and was given to US Military,

is a National Security issue. But, the death of your fireman should not be

covered up as well.

I hope that your brave fireman are not labeled in the same manner that three

generations of proud US Veterans and their families have been.

Almost every veteran has a prior HBV, but America is not to know that HBV

transduces to HCV. Ask National Security why.

Donnelly

Captain, USAR

``In 95,447 tests for hepatitis C conducted among veterans last year, 31

percent were positive for the hepatitis C antibody.''

Friday April 16, 3:38 pm Eastern Time

Company Press Release

SOURCE: House Committee on Veterans' Affairs

Briefing Unveils Hepatitis C Virus as Emerging Health Threat to U.S.

Veterans

WASHINGTON, April 16 /PRNewswire/ -- Congressman Vic Snyder (D-AR) joined

with health policy experts today to brief Congressional staff on the impact

of the hepatitis C virus on U.S. veterans and the need to ensure that

infected servicemen can receive the treatment they need through Department

of Veterans' Administration (VA) facilities.

Symptoms of hepatitis C may not appear for 10 to 30 years after infection.

As a result, veterans infected with the virus during military service can

have difficulty establishing a service-to-disease connection. Without proof

of a service-related infection, most of these veterans have difficulty

obtaining treatment for this disease in VA facilities.

Hepatitis C is the most common blood-borne infection in the United States.

About 1.8 percent of Americans are infected. In comparison, infection rates

among American veterans are estimated to be considerably higher.

``The number of hepatitis C cases reported among veterans has increased in

the last decade,'' said panel member Dr. Roselle, VA Medical Center,

Cincinnati. ``In 95,447 tests for hepatitis C conducted among veterans last

year, 31 percent were positive for the hepatitis C antibody.''

On March 4, 1999, Congressman Vic Snyder and Senator Olympia Snowe (R-ME)

introduced legislation (H.R. 1020 and S. 71, respectively) which would

establish a presumption of service connection for veterans with hepatitis C.

Both bills have been referred to the appropriate House and Senate VA

committees for review.

``Because of exposure to risk factors, veterans appear to have a much higher

incidence of hepatitis C than in the general population,'' Snyder said.

``Establishing service connection can be difficult under current law for

many veterans.''

``Service connection will enable veterans infected with hepatitis C to

receive potentially life-saving treatments without experiencing the delays

they often face now,'' said panelist Bill Russo, Director of Benefits,

Vietnam Veterans of America.

``The expense of treatment now will be nearly recouped by preventing

expensive procedures, like liver transplantation, in the future,'' said

panelist B. Wong, MD, New England Medical Center, Tufts University

School of Medicine, Boston. Hepatitis C is now the leading cause of liver

transplantation in the United States and accounts for about half of liver

transplants conducted at VA facilities.

Hepatitis C is spread primarily by direct contact with contaminated blood.

The Centers for Disease Control and Prevention (CDC) estimates that nearly 4

million Americans have been infected with the virus. Left untreated,

hepatitis C can lead to chronic hepatitis, cirrhosis (scarring of the

liver), liver cancer, and death.

Other panelists included, Miriam Alter, Ph.D, Hepatitis Branch, Centers for

Disease Control and Prevention; Terry Baker, Veterans Service Officer,

Delaware VA, hepatitis C patient; and Doug Wallin, Assistant Director,

Compensation and Pension Services, Department of Veterans' Affairs.

SOURCE: House Committee on Veterans' Affairs

----------------------------------------------------------------------------

http://biz./prnews/990416/dc_congres_1.html

Hep C Bill Would Aid Firefighters

http://www.phillynews.com/daily_news/2000/Feb/16/local/HEPC16.htm

by Knipe Brown

Daily News Staff Writer

The plight of Philadelphia firefighters struggling with the deadly

hepatitis

C virus has led to a proposed federal law that may help save the lives of

firefighters and paramedics across the country.

U.S. Rep. Bob Brady of Philadelphia yesterday introduced a bill to provide

more than $10 million nationwide for hepatitis C treatment, testing and

education for firefighters and other emergency response workers.

" This is just the beginning, " Brady said. " We want to get it known that this

is a national problem affecting people who put their lives on the line every

single moment, never knowing whether they're going to come home at the end

of

the day or night. "

Philadelphia is the first major city in the nation to test its firefighters

for hepatitis C, a blood-borne disease that attacks the liver.

In November, 130 city firefighters, or 6 percent of the 2,100 tested, were

diagnosed with the hepatitis C virus. At least two firefighters have died of

the disease and others are seriously ill.

The rate, health experts say, is three times the national average of 1.8

percent.

Since Philadelphia's epidemic became public, Casey, president of the

city Firefighters' Union, has fielded dozens of calls from fire departments

across the nation concerned about the disease.

" This is not just a Philadelphia problem, " Casey said yesterday. " I have

taken calls from Chicago, Miami and Las Vegas indicating that this is

something affecting firefighters across the country. "

Legions of firefighters are expected to descend on Washington in March to

push for passage of the bill as part of their annual legislative lobbying

effort, he said.

" We believe we should be taken care of by our municipalities and our federal

government, " Casey said.

Federal, state and local action is necessary because, while there is no

vaccine or cure, the disease can be controlled with early diagnosis and

treatment, Casey said.

Firefighters also are pushing for changes in the Pennsylvania Workers

Compensation Act which would designate hepatitis C as an occupational

illness.

In support of changes in the act, state Rep. Curtis of Philadelphia

has introduced a bill calling for an investigation to determine whether a

statewide epidemic exists among firefighters and paramedics.

Philadelphia firefighters and their doctors believe they were infected in

the

line of duty through contact with the blood and body fluids of sick patients

and fire and accident victims.

Brady's bill comes little more than a month after a special Daily News

report

detailing the epidemic among city firefighters, and how the city had refused

to recognize the problem.

Shortly thereafter, Mayor Street pledged to allocate up to $3 million a year

to help cover the costs of treatment for stricken firefighters and

paramedics.

Volunteer firefighters also are included in Brady's bill.

The legislation has been sent to a House committee, which will review it and

determine whether to hold public hearings on the issue. Brady said he plans

to fight to ensure the bill doesn't languish in committee for eternity.

Brady, a Democrat, said his bill has bipartisan support, with Rep. Curt

Weldon, R-Pa., of Delaware County, a volunteer firefighter, co-sponsoring

the

measure.

" I don't know anybody who could be against it, " Brady said. " How can anybody

be against taking care of firefighters? "

-----------------------------------------------------------------------

Send e-mail to knipej@...

Mortality of Korean War Veterans Infected with Hepatitis C Virus

A cohort of approximately 100 veterans have been identified as Hepatitis C

Virus (HCV) infected by testing a collection of serum specimens collected

from approximately 9,500 military recruits during the period 1949 to 1954.

Along with a control cohort of 400 HCV negative recruits, these individuals

will be followed up for all-cause and cause-specific mortality endpoints in

order to describe the long-term natural history of HCV infection. These

veterans represent an excellent surrogate population for the thousands of

infected blood donors now being identified as the result of the discovery of

HCV and the development of highly specific tests.

Study Director

, M.D., M.P.H.

Institute of Medicine

Email: rmiller@...

http://www2.nas.edu/mfua/2172.html

------------------------------------

TITLES

------------------------------------

Intro:

1999 Jul

Natural and iatrogenic variation in hepatitis B virus.

1999 Aug

A likelihood-based method of identifying contaminated lots of blood product.

1998 - May

Incidence of hepatitis C in patients receiving different preparations of

hepatitis B immunoglobulins after liver transplantation.

1987 Apr

A serologic follow-up of the 1942 epidemic of post-vaccination hepatitis in

the United States Army.

1986

Transmission of AIDS virus by transfusion and blood products. Risks and

preventive strategies].

1984 Dec

Antibody to the hepatitis B virus-associated delta-agent in immune serum

globulins.

1980 Jan-Feb

Levels of anti-A and anti-B in commercial immune globulins.

1976 Mar-Apr

Hepatitis B virus and hepatitis B surface antigen in human albumin products.

1975 Sep-Oct

Antibody to the hepatitis B surface antigen in immune serum globulin.

1972 Nov

Posttransfusion hepatitis after exclusion of commercial and hepatitis-B

antigen-positive donors.

------------------------------------

ABSTRACTS

------------------------------------

Rev Med Virol 1999 Jul;9(3):183-209

Natural and iatrogenic variation in hepatitis B virus.

Ngui SL, Hallet R, Teo CG

Section of Hepatology, Rush-Presbyterian-St. Luke's Medical Centre, 1725

West on, Chicago, Illinois 60612, U S A.

The existence of HBV as quasispecies is thought to be favoured by the

infidelity of HBV RT, which would account for the emergence of the many

natural mutants with point substitutions.

RT infidelity may also underlie the hypermutation phenomenon.

Indeed, the oft-reported point mutation in the preC gene that leads to

failure of HBeAg synthesis may be driven by a hypermutation-related

mechanism.

The presence of mutants with deletions and insertions involving single

nucleotides and oligonucleotides at specific positions in the genome, and of

mutants with deletions of even longer stretches particularly in the C gene,

suggests that other mutagenic mechanisms operate.

Candidates include

slippage during mispairing between template and progeny DNA strand,

the action of cellular topoisomerase I, and

gene splicing using alternative donor and acceptor sites.

Natural substitutions, deletions or insertions involving the Cp/ENII locus

in the X gene can significantly alter the extent of viral replicative

activity.

Similar mutations occurring at other locations of Cp/ENII, and at B-cell

epitope sites of the S gene are associated with failure to detect

serological markers of HBV infection.

HBV variation can also arise from recombination between coinfecting strains.

S gene mutations that become evident following HBIG [HB Immune Globulin]

administration and HBV vaccination are all point substitutions, as are

mutations in functional RT domains of the P gene after treatment with viral

RT-inhibitory drugs.

Widespread and long-term use of prophylactic and therapeutic agents may

potentially generate serologically occult HBV variants that might become

difficult to eradicate.

Copyright 1999 Wiley & Sons, Ltd.

PMID: 10479779

[NOTE: in short - HBV Immune globulin [HBIG] mutates the same way HBV does

when exposed internally to radiation therapy........ that leads to the next

question, were there any contamiated lots of HB Immune Globulin? See

below.....]

Int J Epidemiol 1999 Aug;28(4):787-92

A likelihood-based method of identifying contaminated lots of blood product.

Reilly M, Lawlor E

Department of Statistics, University College Dublin, Ireland.

BACKGROUND:

In 1994 a small cluster of hepatitis-C cases in Rhesus-negative women in

Ireland prompted a nationwide screening programme for hepatitis-C antibodies

in all anti-D recipients.

A total of 55 386 women presented for screening and a history of exposure to

anti-D was sought from all those testing positive and a sample of those

testing negative.

The resulting data comprised 620 antibody-positive and 1708

antibody-negative women with known exposure history, and interest was

focused on using these data to estimate the infectivity of anti-D in the

period 1970-1993.

METHODS:

Any exposure to anti-D provides an opportunity for infection, but the

infection status at each exposure time is not observed. Instead, the

available data from antibody testing only indicate whether at least one of

the exposures resulted in infection. Using a simple Bernoulli model to

describe the risk of infection in each year, the absence of information

regarding which exposure(s) led to infection fits neatly into the framework

of 'incomplete data'.

Hence the expectation-maximization (EM) algorithm provides estimates of the

infectiousness of anti-D in each of the 24 years studied.

RESULTS:

The analysis highlighted the 1977 anti-D as a source of infection, a fact

which was confirmed by laboratory investigation.

Other suspect batches were also identified, helping to direct the efforts of

laboratory investigators.

CONCLUSIONS:

We have presented a method to estimate the risk of infection at each

exposure time from multiple exposure data.

The method can also be used to estimate transmission rates and the risk

associated with different sources of infection in a range of infectious

disease applications.

PMID: 10480712, UI: 99408589

Ann Intern Med 1998 May 15;128(10):810-6

Incidence of hepatitis C in patients receiving different preparations of

hepatitis B immunoglobulins after liver transplantation.

Feray C, Gigou M, D, Ducot B, Maisonneuve P, Reynes M, Bismuth A,

Bismuth H

Centre Hepato-Biliare, Laboratoire d'Anatomo-Pathologie et Transfusion

Sanguine, Hopital Brousse, and Universite Paris-Sud, Villejuif, France.

BACKGROUND: Recurrence of hepatitis B virus (HBV) or hepatitis C virus (HCV)

infection after liver transplantation is a clinical problem. Polyclonal

immunoglobulins against hepatitis B surface antigen (HBIGs) prevent the

recurrence of HBV infection, but no effective prophylaxis is available for

HCV infection.

Before screening of blood donors was introduced in France, HBIGs may have

contained antibody to HCV (anti-HCV).

OBJECTIVE: To determine the influence of HBIG on the occurrence of hepatitis

C after liver transplantation before and after 1990. DESIGN: Retrospective

cohort study. SETTING: Liver transplantation unit of a university hospital.

PATIENTS: 428 consecutive patients who had liver transplantation because of

cirrhosis between 1984 and 1994. MEASUREMENTS: Detection of serum HCV RNA

before and 1 year after transplantation and findings on liver graft biopsy.

RESULTS: Among the 218 patients who had HCV infection before

transplantation, the incidence of HCV viremia after transplantation was

lower in those receiving HBIG than in those not receiving HBIG (25 of 46

patients [54%] compared with 162 of 172 patients [94%]; P < 0.001). In

patients receiving HBIG, the incidence of HCV viremia after transplantation

was lower among those who had transplantation before March 1990 than among

those who had transplantation after this date (15 of 33 patients [45%]

compared with 10 of 13 patients [77%]; P = 0.05). Among the 210 patients

without HCV infection before transplantation, acquired infection was

significantly less frequent in those receiving HBIG than in those not

receiving HBIG (18 of 68 patients [26%] compared with 40 of 86 patients

[47%]; P < 0.001). Passively transmitted anti-HCV was transiently detected

in patients receiving HBIG before March 1990. Multivariate analysis in

patients with HCV infection before transplantation showed that the absence

of HBIG and transplantation after March 1990 were independent significant

risk factors for chronic hepatitis C after transplantation. CONCLUSIONS:

Polyclonal immunoglobulins that are treated for viral decontamination and

contain anti-HCV could prevent HCV infection.

PMID: 9599192, UI: 98243005

N Engl J Med 1987 Apr 16;316(16):965-970

A serologic follow-up of the 1942 epidemic of post-vaccination hepatitis in

the United States Army.

Seeff LB, Beebe GW, Hoofnagle JH, Norman JE, Buskell-Bales Z, Waggoner JG,

Kaplowitz N, Koff RS, Petrini JL Jr, Schiff ER, et al

An epidemic of icteric hepatitis in 1942 affected approximately 50,000 U.S.

Army personnel.

This outbreak was linked to specific lots of yellow-fever vaccine stabilized

with human serum.

To identify the responsible virus and the consequences of the epidemic,

during 1985 we interviewed and serologically screened 597 veterans who had

been in the army in 1942.

These subjects were selected from three groups.

Group I consisted of patients who had received the implicated vaccine and

had jaundice;

Group II had received the implicated vaccine but remained well;

Group III had received a new, serum-free vaccine, with no subsequent

jaundice.

Ninety-seven percent of Group I,

76 percent of Group II, and

13 percent of Group III

were positive for antibodies to hepatitis B virus.

Only one subject had hepatitis B surface antigen, for a carrier rate of 0.26

percent among recipients of the implicated vaccine.

The prevalence of hepatitis A antibody was similar in all three groups, and

no subject had antibody to hepatitis delta virus.

We conclude that hepatitis B caused the outbreak, that about 330,000 persons

may have been infected, that the hepatitis B virus carrier state was a rare

consequence, and that the outbreak induced hepatitis B antibodies that

appear to persist for life.

PMID: 2436048, UI: 87172914

Gastroenterology 1984 Dec;87(6):1213-6

Antibody to the hepatitis B virus-associated delta-agent in immune serum

globulins.

Ponzetto A, Hoofnagle JH, Seeff LB

Fifty lots of immune serum globulin prepared by four United States

manufacturers between 1944 and 1977 were tested for the presence and titer

of antibody to the hepatitis B virus-associated delta-agent. Anti-delta was

detected in 28 of the 50 lots (56%) of immune serum globulin at titers

ranging from 1:10 to 1:400. Anti-delta was present in 75% (6 of 8) of lots

produced between 1962 and 1965, in 77% (17 of 21) produced between 1967 and

1970, in 45% (5 of 11) produced between 1971 and 1972 and in none (0 of 9)

produced since 1973. A single lot of globulin prepared from plasma that was

collected in 1944 from United States Army soldiers also contained detectable

anti-delta. These data indicate that delta-infection has been occurring

among hepatitis B surface antigen (HBsAg) carriers in the United States

since the 1940s. The decrease in prevalence of anti-delta in immune serum

globulin lots coincided with the start of routine HBsAg screening of blood

and plasma. The elimination of HBsAg-positive units from plasma pools has

reduced levels of HBsAg and anti-delta and should have decreased the risk of

transmission of both type B hepatitis and delta-hepatitis by plasma

products.

PMID: 6092192, UI: 85028257

Transfusion 1980 Jan-Feb;20(1):90-2

Levels of anti-A and anti-B in commercial immune globulins.

Gordon JM, Cohen P, Finlayson JS

Samples from 168 lots of immune serum globulin, tetanus immune globulin, and

Rho (D) immune globulin produced by seven American manufacturers during the

period 1973-1977 were analyzed for anti-A and anti-B content by saline and

antiglobulin titration. There was appreciable variation among manufacturers,

but between 1973 and 1975 all products showed a significant decrease in

alloantibody titer. This trend did not continue during the interval

1975-1977; the titers of most manufacturers' products remained near the 1975

level. The anti-A titer of a given product was approximately one dilution

higher than the anti-B; both titers were usually increased by anti-human

serum, though this occurred more often in the case of anti-B.

PMID: 6986683, UI: 80125049

Transfusion 1976 Mar-Apr;16(2):141-7

Hepatitis B virus and hepatitis B surface antigen in human albumin products.

Hoofnagle JH, Barker LF, Thiel J, Gerety RJ

A collection of 1,985 lots of normal serum albumin (NSA) and 1,361 lots of

plasma protein fraction (PPF) prepared between 1958 and 1974 were tested for

the presence of hepatitis B surface antigen (HBsAg). Twenty-one percent of

NSA lots and 71 per cent of PPF lots were HBsAg-positive by

radioimmunoassay. There was considerable variation in frequency of

HBsAg-positive lots among the 17 different manufacturers of NSA and the six

manufacturers of PPF.In general, those lots prepared from volunteer donor

plasma and placental material demonstrated lower rates of HBsAg-positivity

than those prepared from commercial donor plasma. A striking decrease in the

prevalence of HBsAg-positive lots of both NSA and PPF occurred during the

period 1971 to 1973, coincident with the onset of routine screening of all

plasma for HBsAg. Although NSA and PPF can be HBsAg-positive, they probably

do not transmit type B hepatitis. Serologic tests for HBsAg and antibody to

HBsAg revealed that albumin products prepared from infectious, icterogenic

plasma were infectious prior to pasteurization, but that they no longer

transmitted type B hepatitis after heat treatment at 60 C for ten hours.

PMID: 1258115, UI: 76155108

Transfusion 1975 Sep-Oct;15(5):408-13

Antibody to the hepatitis B surface antigen in immune serum globulin.

Hoffnagle JH, Gerety RJ, Barker LF

A collection of 1,278 lots of immune serum globulin (ISG) prepared by 19

United States manufacturers between 1962 and 1974 were tested for the

hepatitis B surface antigen (HBSAg) and antibody (anti-HBS). Ten lots

(0.8%), all of which were produced between 1962 and 1965 by two different

manufacturers, were weakly positive for HBSAg (by radioimmunoassay). Seven

hundred and seven lots (55.3%) were positive for anti-HBS (by passive

hemagglutination). In general, titers of anti- HBS in lots of ISG were low,

and the prevalence of anti HBS positive lots varied considerably among

different manufacturers. ISG prepared from placental material was more

commonly positive for anti-HBS than was ISG prepared from plasma. There was

a striking overall increase in prevalence and titer of anti-HBS in ISG lots

prepared during 1973 and 1974. This probably reflects the effect of

elimination of strongly HBSAg-positive plasma units with the onset of

routine screening for HBSAg which began in 1972.

PMID: 1198681, UI: 76082214

Ann Intern Med 1972 Nov;77(5):691-9

Alter HJ, Holland PV, Purcell RH, Lander JJ, Feinstone SM, Morrow AG,

Schmidt PJ

Posttransfusion hepatitis after exclusion of commercial and hepatitis-B

antigen-positive donors.

No abstract available

PMID: 4628213, UI: 73028623