Hepatitis C is a
liver disease. Hepatitis (HEP-ah-TY-tis)
makes your liver swell and stops it from working right.
Hepatitis C is a virus that often silently attacks your liver.
Most people infected with the hepatitis C virus (HCV) have no
symptoms at all. In fact, most people don't know they have the
disease until liver damage shows up, decades later, during
routine medical tests.
is one of six identified hepatitis viruses the others are A, B,
D, E and G. All cause the liver to become inflamed, which
interferes with its ability to function. Hepatitis C is
generally considered to be among the most serious of these
if you have a hepatitis C infection, it can lead to liver
cancer, liver failure or cirrhosis irreversible and potentially
fatal scarring of the liver. Unlike HIV, the virus that causes
AIDS, the hepatitis C virus usually isn't transmitted through
sexual contact. Instead, you're more at risk if you're exposed
to contaminated blood through needles shared during drug use or
through blood transfusions.
vaccines exist for hepatitis A and B, no vaccine for hepatitis C
has been developed. Researchers hope to find a medication that
will slow or stop the growth of the virus and prevent long-term
complications, such as cirrhosis and cancer, from developing.
What causes hepatitis C?
Hepatitis C is caused by a virus.
A virus is a germ that causes sickness. (For
example, the flu is caused by a virus.) People can pass viruses
to each other. The virus that causes hepatitis C is called the
hepatitis C virus.
Hepatitis C Causes:
HCV is not related to the
other viruses that cause hepatitis. Like the other hepatitis
viruses, however, it is contagious. The hepatitis C virus is
transmitted mainly by contact with blood or blood products.
Sharing of contaminated
needles among IV drug users is the most common mode of
transmission. Using a needle to inject recreational drugs,
even once several years ago, is a risk factor for hepatitis
Transfusion with infected
blood or blood products, hemodialysis, or transplantation of
organs from infected donors was once a common mode of
transmission but is now rare.
In 1992, a test became
available for checking blood for HCV. Blood and blood
products are now tested to ensure that they are not
contaminated. As a result, cases of hepatitis C related to
transfusion, hemodialysis, or transplantation have dropped
to almost zero since then. Transfusion of blood or blood
products before 1992 is a risk factor for hepatitis C.
Less common causes of HCV
transmission include the following.
From mother to infant at the
time of childbirth
Through sexual intercourse
with an infected person: Having multiple sex partners is a
Needle sticks with HCV-contaminated
blood: This is mostly seen in health care workers. The risk
of developing HCV infection after a needle stick is about
You cannot get hepatitis C by
living with, being near, or touching someone with the
disease. You can get the disease by sharing a razor, nail
clippers, or other such items with an infected person.
The source of transmission is
unknown in about 10% of people with acute hepatitis C and in
about 30% of people with chronic hepatitis C.
could I get hepatitis C?
You could get hepatitis C by:
is spread by contact with an infected person's blood.
You could get
hepatitis C by haring drug needles.
getting pricked with a needle that has
infected blood on it (hospital workers can get hepatitis C
Having sex with an infected person,
especially if you or your partner has other sexually
Being born to a mother with hepatitis C.
In rare cases, you could get hepatitis C by
getting a tattoo or body piercing with un sterilized, dirty
You can NOT get hepatitis C by:
shaking hands with an infected
hugging an infected person.
kissing an infected person.
sitting next to an infected person.
get hepatitis C from a blood transfusion?
had a blood transfusion or organ transplant before 1992, you
might have hepatitis C. Before 1992, doctors could not check
blood for hepatitis C, and some people received infected blood.
If you had a blood transfusion or organ transplant before 1992,
ask a doctor to test you for hepatitis C. (See "What are the
tests for hepatitis C?")
A doctor can test
you for hepatitis C.
What are the symptoms?
Although hepatitis C damages the liver, 80% of
people with the disease do not have symptoms. In those who do,
symptoms may not appear for 10-20 years, or even longer. Even
then, the symptoms usually come and go and are mild and vague.
Unfortunately, by the time symptoms appear, the damage may be
A minority of people have symptoms during
the early acute phase of the infection. These symptoms
typically develop 5-12 weeks after exposure to HCV. Some
people describe the symptoms as being flu like. The symptoms
may last a few weeks or months.
Loss of appetite
Pain over the liver (on the right side of
the abdomen, just under the rib cage)
Jaundice - A condition in which the skin
and the whites of the eyes turn yellow
Dark-colored urine (may look like cola or
Stools become pale in color (grayish or
Prolonged nausea and vomiting can cause
dehydration. If you have been vomiting repeatedly, you may
notice the following symptoms:
Fatigue or weakness
Confusion or difficulty concentrating
Chronic hepatitis C can lead to cirrhosis
of the liver in many people, a condition traditionally
associated with alcoholism. Cirrhosis is a condition in
which healthy liver tissue is replaced by fibrous tissue,
followed by scarlike hardening. As this happens, the liver
gradually begins to fail, or lose its ability to carry out
its normal functions. Eventually, symptoms develop. Symptoms
of cirrhosis include the following:
Fluid retention causing swelling of the
belly (ascites), legs, or whole body
Disturbances in sleeping
Loss of appetite, weight loss, wasting
Vomiting with blood in the vomit
Mental disturbances such as confusion, lethargy, extreme
sleepiness, or hallucinations (hepatic encephalopathy).
hepatitis C treated?
Hepatitis C is
treated through shots of medicine.
Hepatitis C is treated with a drug called
peginterferon, usually in combination with the drug ribavirin.
You may need surgery if you have hepatitis C for many years.
Over time, hepatitis C can cause your liver to stop working. If
that happens, you will need a new liver. The surgery is called a
liver transplant. It involves taking out the old, damaged liver
and putting in a new, healthy one from a donor.
How can I protect myself?
You can protect yourself and others from hepatitis C.
If you inject drugs, use your own needles.
There is no vaccine to prevent
hepatitis C, but you can reduce your risk of becoming infected
You do not share needles to
inject drugs. If you are injecting drugs, the best way to
protect yourself is by not sharing needles or other
equipment (such as cotton, spoons, and water) with others.
Many cities have needle exchange programs that provide free,
sterile needles so that you do not have to share needles. If
you want to stop using drugs, ask your doctor or someone you
trust to help you find out about drug treatment programs.
You work in a health care
setting and you follow your institution's safety guidelines.
You wear protective gloves and clothing and dispose of
needles and other contaminated sharp objects properly.
You make sure the practitioner
sterilizes the instruments and supplies if you get a tattoo,
have your body pierced, or have acupuncture.
If you have hepatitis C, you
can help prevent spreading it to others if.
You do not share needles or
other equipment such as cotton, spoons, and water if you
continue to use needles to inject drugs.
You keep cuts, scrapes, and
blisters covered to prevent others from coming in contact
with your blood and other body fluids. You also throw out
any blood-soaked items such as used Band-Aids.
You do not donate blood or
You wash your hands and any
object that has come in contact with your blood-thoroughly
with water and soap.
You do not share your
toothbrush, razor, nail clippers, diabetes supplies, or
anything else that might have your blood on it.
Breast-feeding mothers who have hepatitis C can continue to
breast-feed their babies because hepatitis C cannot be spread
through breast milk. If you are breast-feeding, you should try
to avoid having cracked nipples, which might pose a risk of
spreading the virus to your baby.
In America, since HBsAg screening was introduced, the incidence
of post-transfusion hepatitis has a declined, but a significant
number of cases remained. At least 95% of post-transfusion
hepatitis was caused by non-A non-B. Worldwide, there are
thought to be 100 million carriers of hepatitis C. It is
particularly prevalent in Japan, where it is thought to be
responsible for the majority of cases of hepatocellular
carcinoma. There are 175,000 new cases of hepatitis C in the US
per year. In the US, NANBH infection is more common than HBV
infection amongst IVDA and those given blood transfusions. NANBH
is usually transmitted parenterally. Sexual transmission can
occur albeit considerable less efficient for HBV. There were
recent reports of vertical infection.
Risk Groups for hepatitis C in the U.S.A.
Blood transfusion 5%
Household contacts 8%
Health care workers 20%
Unidentified sources 43%
The highest HCV antibody
prevalence is found in haemophiliac patients who have received
untreated blood or blood products where up to 85% of such
patients in the UK have antibodies. A large proportion of cases
occur in people with no known risk factors. The evidence for and
against sexual spread is confusing. It is noteworthy though that
20% of non-drug using female partners of IV drug users with
hepatitis C are positive for anti-HCV. In general, the mode of
HCV transmission is similar to HBV.
workers experiencing needlestick injuries are also at risk of
acquiring HCV infection. In one study, 3% of health workers with
a needlestick exposure in which the source patient was anti-HCV
positive converted to anti-HCV. Accumulating evidence indicates
that HCV is transmitted from mother to infant; however the
actual risk is unknown. Anti-HCV seroconversion has only been
rarely documented among infants born to anti-HCV positive
mothers unless their mothers were also infected with HIV.
However, in studies using PCR, HCV transmission apparently
occurred without anti-HCV seroconversion.
In common with other RNA viruses, wide genetic
variation of hepatitis C exist in nature. On the basis of
phylogenetic analysis, HCV has been classified into six major
genotypes (types 1 to 6) of which four (types 1 to 4) contain
several more closely related subtypes (e.g. a, b and c). In
West-ern Europe and the USA, the predominant geno-types are la,
lb, 2b and 3a, with some variation in frequency. In Japan and
Taiwan types lb, 2a and 2b are seen most frequently. Elsewhere
in Asia, genotype 3 is the most common, and genotype 4 is found
frequently in the Middle East and Africa. Type 5 is mainly found
in Southern Africa and type 6 in SE Asia. There is increasing
evidence demonstrating a link between HCV genotype and disease
severity and re-sponsiveness to interferon therapy. Genotype lb
was found significantly more often in cases of severe liver
disease such as cirrhosis and hepatocellular carcinoma. It was
also associated with a longer disease duration and a higher
level of viraemia than other genotypes. Individuals infected
with genotype 1b are less likely to respond to interferon
What are the tests for hepatitis C?
The doctor will take some blood to check for hepatitis C.
To check for hepatitis C, the
doctor will test your blood.
These tests show if you have
hepatitis C and how serious it is.
The doctor may also do a liver
biopsy (BYE-op-see) is a simple test. The doctor removes a tiny
piece of your liver through a needle. The doctor checks the
piece of liver for signs of hepatitis C and liver damage.
the first generation ELISA kits relied on a fusion protein
antigen produced from a original 5-1-1 clone with a few
adjoining clones. The antigen was denoted as the C100 antigen.
The problem with the first generation kits was that the antigen
used was non-structural and thus may not pick up all cases of
HCV. Furthermore, antibodies against this antigen could not be
detected until 15 weeks after the onset of hepatitis. Therefore,
HCV infection cannot be excluded in those whose serum is
antibody-negative up to 6 months after the onset of symptoms.
The first generation kits had also been demonstrated to have a
poor specificity. Second and third generation assays are now
used for serological diagnosis. Second generation assays
incorporate C22 core antigen as well as NS4 (C-100-3) and NS3
antigens. The newer third generation assays incorporate NS5 as
an additional antigen. However this increase in sensitivity is
offset by a slight decrease in specificity. They reduce the
"diagnostic window" down to 4 weeks after initial infection.
Recombinant Immunoblot assays (RIBA)
were developed by Ortho whereby nitrocellulose strips were
coated with discrete bands of E. coli and yeast cloned
antigens. It is thought that this test carried a much higher
specificity with equal sensitivity. Another method to increase
sensitivity was to use "blocking tests". Sera positive for anti-HCV
were blocked by C-100-3 antigen. Inability to be blocked is
interpreted as non-specificity. Recombinant antigens are being
developed based on structural proteins which should lead to
serological tests with higher sensitivities. Also it is feasible
that antibodies to these antigens may appear earlier and thus
diagnosis of acute infection may become possible.
2. Polymerase Chain Reaction:
A PCR test had been developed where the level of HCV viraemia is
roughly quantified and thus infectivity of the blood. A 5'
conserved non-coding region had been identified. PCR has
enormous potential value in support of the anti-HCV ELISA and in
the study of HCV. It can be used to diagnose acute infection as
HCV viraemia occurs well before the development of anti-HCV
antibodies. Evidence provided by PCR for fluctuated level of
infectivity in certain individuals may play an important role in
the consideration of infectivity of seropositive donors. RIBA-2
positivity appears to correlate well with PCR positivity. A
branched DNA assay has also been developed for the detection of
3. Hepatitis C Antigen:
Recent reports described the identification of hepatitis C
antigen (HCAg) in hepatocytes of patients suffering from chronic
HCV infection using a FITC polyclonal IgG obtained from patients
with hepatitis C. A test for hepatitis C antigen in serum is
being developed for the detection of HCV viraemia, rather like
Immunsystem und Hepatitis-C
Each clinical form of viral
hepatitis with HBV can also occur with HCV. Acute disease may
lead to recovery, fulminant hepatitis, relapsing hepatitis with
intervening periods of normal liver function, inapparent chronic
infection, chronic active hepatitis and cirrhosis have been
documented. The incubation period lies between that of HAV and
HBV. HCV infection is particularly associated with high ALT
levels and it was suggested that ALT levels could be used as
surrogate marker for the screening of NANBH before the
availability of a test for anti-HCV.
It is thought chronic infection occurs in 50- 75% of all
patients infected with HCV, in contrast to 10% for adults
infected with HBV. In a cohort study where patients with HCV
chronic disease had been followed up for 10 years, 20% have
cirrhosis, 30% made improvements, 45% remained stable, 25% have
shown progression (including the development of cirrhosis).
Several recent studies
have established a strong association between HCV and
hepatocellular carcinoma. anti-HCV antibodies, in the absence of
HBV markers, were detected in 44.5% of HCC patients in Spain,
43% in Japan, 16% in Italy, 7% in South Africa. Since HBV
carriers often have chronic HCV infection, it is conceivable
that the 2 viruses may act together to cause HCC and
epidemiological data linking HBV to HCC may require reassessment
in terms of the magnitude of the risk involved with the
availability of testing for chronic HCV infection. HCV may prove
to be as important as HBV in the causation of hepatocellular
carcinoma worldwide. It has recently been suggested that the
risk of developing HCC is approximately 5% year in cirrhotic
patients with chronic hepatitis C; this is greater than the risk
from hepatitis B.
In chimpanzees and to a lesser
extent in humans, cytoplasmic tubules (cylindrical confronting
cisternae) are regularly seen under EM. The nature of these
structures are unknown in particular to the part they may play
in HCV replication. In HCV hepatitis, direct cytopathic damage
to the hepatocytes is thought to be the mechanism of
pathogenesis, in contrast to the immunopathological mechanisms
Hepatocyte injury CMI direct CPE.
In general, hepatitis C is a slower disease than hepatitis B. It
takes 10 years to develop chronic hepatitis, 20 years to develop
cirrhosis, and 30 years to develop hepatocellular carcinoma.
There are certain nonhepatic disorders which are sometimes
associated with chronic hepatitis C infection. eg. mixed
cryoglobulinaemia, membranoproliferative glomerulonephritis,
Sjogren's syndrome, sporadic porphyria cutanea tarda, and lichen
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