Hepatitis C

Clinical Description


Onset is usually insidious, with anorexia, vague abdominal discomfort, nausea and vomiting; progression to jaundice less frequent than with hepatitis B. Although initial infection may be asymptomatic (more than 90% of cases) or mild, a high percentage of cases (50%–80%) develop a chronic infection. Of chronically infected persons, about half will eventually develop cirrhosis or cancer of the liver.

Infectious Agent

The hepatitis C virus is an enveloped RNA virus classified as a separate genus (Hepacivirus) in the Flaviviridae family. At least 6 different genotypes and approximately 100 subtypes of HCV exist. Evidence is limited regarding differences in clinical features, disease outcome or progression to cirrhosis or hepatocellular carcinoma (HCC) among persons with different genotypes. However, differences do exist in responses to antiviral therapy according to HCV genotypes.


Diagnosis depends on detecting antibody to the hepatitis C virus (anti-HCV). Various tests are available for the diagnosis and monitoring of HCV infection. Tests that detect antibodies against the virus include the enzyme immunoassay (EIA) and the recombinant immunoblot assay. The same HCV antigens are used in both EIAs and the immunoblot assays. These tests do not distinguish between acute, chronic, or resolved infection. Reproducible and inexpensive EIA tests for the diagnosis of HCV are suitable for screening at-risk populations and recommended as the initial test for patients with clinical liver disease. A negative EIA test suffices to exclude a diagnosis of chronic HCV infection in immunocompetent patients. The high sensitivity and specificity of third-generation EIAs obviate the need for a confirmatory immunoblot assay in the diagnosis of individuals with clinical liver disease, particularly those with risk factors for HCV. Immunoblot assays are useful as a supplemental assay for persons screened in non-clinical settings and in persons with a positive EIA who test negative for HCV RNA.

Acute or chronic HCV infection in a patient with a positive EIA test should be confirmed by detection of the presence of HCV RNA in the serum using a sensitive assay. Target amplification techniques using polymerase chain reaction (PCR), transcription-mediated amplification (TMA) and signal amplification techniques (branched DNA) may be used to measure HCV RNA levels. A single positive qualitative assay for HCV RNA confirms active HCV replication, but a single negative assay does not exclude viremia and may reflect a transient decline in viral level below the level of detection of the assay. Therefore, a follow-up HCV RNA detection should be performed to confirm the absence of active HCV replication. Quantitative determination of HCV RNA levels and of HCV genotype provides information on the likelihood of response to treatment in patients undergoing antiviral therapy. Liver biopsy can provide direct histological assessment of liver injury due to HCV, but cannot be used to diagnose HCV infection.


Mode of Transmission

HCV is primarily transmitted parenterally. The primary sources of HCV infection include transfusion of blood or blood products from unscreened donors; transfusion of blood products that have not undergone viral inactivation; parenteral exposure to blood through the use of contaminated or inadequately sterilized instruments and needles used in medical and dental procedures; the use of unsterilized objects for rituals (e.g. circumcision, scarification), traditional medicine (e.g. blood-letting) or other activities that break the skin (e.g. tattooing, ear or body piercing); and intravenous drug abuse. Household or sexual contacts of HCV-infected persons are marginally at risk. Sexual and mother-to-child transmissions have both been documented, but appear rare.

Incubation Period

Ranges from 2 weeks to 6 months; commonly 6–9 weeks. Chronic infection may persist for up to 20 years before the onset of cirrhosis or hepatoma.

Period of Communicability

From one or more weeks before onset of the first symptoms; may persist in most persons indefinitely. Peaks in virus concentration appear to correlate with peaks in ALT activity.


Humans; virus has been transmitted experimentally to chimpanzees.


Susceptibility is general. The degree of immunity following infection is not known; repeated infections with HCV have been demonstrated.


Worldwide distribution. HCV prevalence is directly related to the prevalence of persons who routinely share injection equipment, and to the prevalence of unsafe parenteral practices in health care settings. WHO estimates that some 130–170 million people (approximately 2%–3% of world population) are chronically infected with HCV, like HBV one of the most common global causes of chronic hepatitis, cirrhosis, and liver cancer. Most populations in Africa, the Americas, Europe and southeast Asia have anti-HCV prevalence rates under 2.5%. Prevalence rates for the Western Pacific regions average 2.5–4.9%. In the Middle East, the prevalence of anti-HCV ranges from 1% to more than 12%. The number of people with serological manifestation of HCV infection in Europe is estimated at 8.9 million, and at 12.6 million in the Americas; the majority of infected individuals live in Asia (60 million in eastern Asia, 32 million in southeastern Asia) and Africa (28 million).

Prevention and Control

1)    Preventive measures:

General control measures against HBV infection apply. Prophylactic IG is not effective. In blood bank operations, all donors should be routinely screened for anti-HCV and all donor units with elevated liver enzyme levels should be discarded. Routine virus inactivation of plasma-derived products, risk reduction counseling for persons uninfected but at high risk (e.g. health care workers) and nosocomial control activities must be maintained.

2)    Control of patient, contacts and the immediate environment:

General control measures against HBV apply. Post-exposure prophylaxis with IG is not effective in preventing infection. For the treatment of chronic hepatitis C, highest response rates (40–80%) have been achieved with a combination therapy of ribavirin and slow-release interferons (“pegylated interferons”), making this the treatment of choice. Genotype determinations influence treatment decisions and treatment duration. These medications have significant side-effects that require careful monitoring. Ribavirin is a teratogen; thus pregnancy should be avoided during treatment. Corticosteroids and acyclovir have not been effective.

3)    Epidemic measures:

Same as for hepatitis B.

4)    Disaster implications:

Same as for hepatitis B.

5)    International measures:

Ensure adequate virus inactivation for all internationally traded biological products.

Source: Heymann (Ed.). (2008). Control of Communicable Diseases Manual, 19th edition. Washington, DC: American Public Health Association.

Common Disease Taxonomy: