Acute and Chronic Hepatitis C
المؤلف:
Mary Louise Turgeon
المصدر:
Immunology & Serology in Laboratory Medicine
الجزء والصفحة:
5th E, P305-306
2025-09-07
429
Acute Hepatitis C
The coordinated activities of CD4+ T cells and cytotoxic CD8+ T cells, primed in the context of human leukocyte antigen (HLA) class II and I alleles, respectively, on antigen-present cells are critically important for the control of acute HCV infections. The signs and symptoms of acute hepatitis C infection usually include jaundice, fatigue, and nausea. Laboratory manifestations include a significant increase in serum liver enzyme levels (usually >10-fold) and the presence or de novo development of anti-HCV.
Demonstration of HCV antibodies can be problematic because anti-HCV is not always present in the patient with symptoms. In 30% to 40% of patients, anti-HCV is not detected until 2 to 8 weeks after the onset of symptoms. Acute hepatitis C can also be diagnosed by testing for HCV RNA, apparently the earliest detectable marker of acute HCV infection, preceding the appearance of anti-HCV by several weeks. The current ELISA for antibodies to recombinant HCV antigens becomes positive earlier and is more sensitive than preceding ELISAs. Another approach is to repeat the anti-HCV testing 1 month after the onset of illness.
Hepatitis C viremia may persist despite the normalization of serum ALT levels. Intracytoplasmic HCV antigen has been found in the hepatocytes of acutely infected chimpanzees and, by analogy, is presumed to be present in acute hepatitis C in human beings. HCV antigens were not detected in hepatocyte nuclei, Kupffer or sinusoidal lining cells, bile duct epithelium, or blood vessels.
Chronic Hepatitis C
Chronic hepatitis C varies greatly in its course and outcome. At one end of the spectrum are asymptomatic patients who generally have a favorable prognosis; at the other end are patients with severe hepatitis C who have symptoms, HCV RNA in their serum, and elevated serum liver enzyme levels. These patients typically develop cirrhosis and end-stage liver disease.
Episodic fluctuations in serum liver enzyme levels appear to be a feature of chronic hepatitis C. This pattern, presumably reflecting waves of hepatocellular inflammation and necrosis, may last for months to years. Such episodes of disease activity may be related to the emergence of so-called HCV neutralization escape mutants, but other poorly defined mechanisms also may play a role. HCV RNA is detected in the serum by PCR in almost all patients with chronic hepatitis C. HCV replication may be increased in advanced liver disease and may con tribute to the progression of disease.
At least 20% of patients with chronic hepatitis C develop cirrhosis, a process that takes 10 to 20 years. After 20 to 40 years, a smaller percentage of patients with chronic disease develop liver cancer. Liver failure from chronic hepatitis C is one of the most common reasons for liver transplantation in the United States.
Chronic hepatitis C is diagnosed when anti-HCV is present and serum liver enzyme levels remain elevated for more than 6 months. Testing for HCV RNA by PCR assay confirms the diagnosis and documents that viremia is present. Most patients with chronic infection will have the viral genome detectable in serum by PCR.
Approximately one third of those infected with HCV mani fest anti-HCV antibodies within several weeks; others may take months or, less often, as long as 1 year to express antibodies. The current test antigen represents only 12% of the encoding capacity of the virus.
A reactive test implies infection with HCV, but not infectivity or immunity.
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