Hepatitis C is spread by contact with an infected person's blood.

You could get hepatitis C by

• sharing drug needles
• getting pricked with a needle that has infected blood on it (hospital workers can get hepatitis C this way)
• having sex with an infected person, especially if you or your partner has other sexually transmitted diseases
• being born to a mother with hepatitis C

In rare cases, you could get hepatitis C by

• getting a tattoo or body piercing with unsterilized, dirty tools

You can NOT get hepatitis C by

• shaking hands with an infected person
• hugging an infected person
• kissing an infected person

There are considerable differences in the genetic structure of hepatitis C virus. Accordingly, hepatitis C virus is categorized into six major genetic types (genotypes) and many more subtypes, based on the sequence (order) of nucleotides in the virus. Although the different genotypes are found throughout the world, there is a distinct distribution of genotypes in certain geographic regions. For instance, the most common genotype in South-East S Asia is genotype 1 (1a and 1b), 2 and 3. The influence of genotype on the long-term prognosis of hepatitis C virus disease is still unclear. However, what is clear is that patients infected with genotypes 2 or 3 are much more likely to respond to interferon therapy. In contrast, patients infected with genotype 1 (particularly 1b) or genotype 4 do not respond very well to interferon therapy.

Only a group of people infected with genotype 1 will respond to therapy which will take 48 weeks of therapy. Those with Type 2 or 3 usually require 24 weeks of therapy to clear the virus.

Cryoglobulinemia

This condition is due to the presence of abnormal antibodies (called cryoglobulins) that come from hepatitis C virus stimulation of lymphocytes (white blood cells).

B-cell non-Hodgkin's lymphoma

a cancer of the lymph tissue, has also been associated with chronic hepatitis C virus. The cause is thought to be the excessive stimulation by the hepatitis C virus of B lymphocytes, which results in the abnormal reproduction of the lymphocytes.

Two skin conditions, lichen planus and porphyria cutanea tarda, have been associated with chronic hepatitis C virus.

Screening tests for Hepatitis C

The enzyme immunosorbent assay (EIA) is the conventional, initial screening test to diagnose hepatitis C infection. The EIA measures specific antibodies to small pieces of the hepatitis C virus proteins (antigens). This test, therefore, is referred to as the anti-hepatitis C virus antibody test.

When there is a low likelihood (risk) of hepatitis C infection, individuals who test positive for hepatitis C by EIA should undergo confirmatory testing using a specialized assay that likewise tests for antibodies against the hepatitis C virus proteins. This assay is called the Recombinant Immunoblot Assay (RIBA).

Both the EIA and RIBA tests, however, do not distinguish among acute, chronic, and resolved hepatitis C virus infections because the anti-hepatitis C virus antibodies are in the blood in all three of these situations. Rather, they only indicate exposure of the patient to the virus.

The two most common systems for measuring hepatitis C virus RNA are the reverse transcription polymerase chain reaction (RT-PCR) assay and the branched chain DNA (bDNA) assay. Recently, a third type of assay, called transcription-mediated amplification (TMA), has been release.

There are two types of RT-PCR, qualitative and quantitative. As the name implies, however, qualitative RT-PCR provides only a positive (presence of hepatitis C virus) or negative (absence of hepatitis C virus) result. By contrast, quantitative RT-PCR measures the amount of virus.

Branched chain DNA (bDNA) is the other quantitative technique and is less prone to contamination and is more accurate when measuring higher levels of the virus as compared to RT-PCR. However, the bDNA assay is not as sensitive as the RT-PCR and is unable to measure levels of virus below 200,000 copies/ml.

Transcription mediated amplification (TMA) is a qualitative technique that is distinct from PCR. This test can measure as few as 2 to 5 copies of virus/ml.

Anti-HCV (EIA)	Anti-HCV (RIBA)	HCV RNA (Qualitative RT- PCR or TMA)	Interpretation
Non-reactive	Non-reactive	Undetectable	No present or past infection
Reactive	Non-reactive	Undetectable	False positive EIA; no present or past infection
Reactive	Undeterminate	Undetectable	In the absence of risk factors, probable false positive EIA
Reactive	Positive	Undetectable	Probable past exposure with clearance of infection. Qualitative RNA testing should be repeated to exclude fluctuating low levels of viremia
Reactive	Positive	Detectable	Ongoing infection
Non-reactive	Non-reactive	Detectable	Acute HCV infection or chronic HCV infection in an immunocompromised person unable to make adequate antibodies

End stage (advanced, with complications) liver disease that is associated with chronic hepatitis C infection is the leading reason for liver transplantation in the U.S. today. The recurrence of the hepatitis C virus in the blood, however, is almost universal after liver transplantation for hepatitis C virus liver disease. In fact, about 25 % of patients will develop significant recurrence of hepatitis (seen on liver biopsy) in the new grafted liver. Moreover, these patients with recurrent hepatitis will develop cirrhosis within five years of their transplant.

Despite these findings of recurrence, the five-year survival rate for hepatitis C patients is comparable to that of patients who are transplanted for other types of liver disease. Still, the failure of the transplanted liver that is caused by recurrent hepatitis C virus infection is the number one reason to consider re-transplantation.

Treatment is recommended for patients with detectable hepatitis C virus RNA who have persistently elevated liver tests and evidence of scarring and at least moderate inflammation on their liver biopsy, but without outward signs of liver failure.

Treatment results in improvement in the inflammation and scarring of the liver in most sustained responders and also occasionally (and to a much lesser extent) in relapsers and non-responders.

Trials are underway that are examining other combinations of medications. These combinations include pegylated interferon+ribavirin+amantadine (Symmetrel, an antiviral agent approved for influenza), pegylated interferon+ribavirin+mycophenylate mofetil (CellCept, an anti-rejection medication), and pegylated interferon+thysmosin (thymus gland proteins that enhance the immune system).