ПЦР. Гепатит C, HCV генотипирование, кровь

Hepatitis C Virus (HCV) Genotyping by real-time RT-PCR identifies the viral genotype or subtype (1a, 1b, 2, 3a, 4) to guide antiviral management. Results help determine whether to treat, anticipate the clinical course, set treatment duration and dosing, estimate probability of therapeutic response, and decide whether a liver biopsy is warranted. The assay is also known as HCV genotype analysis or HCV subtype testing.

Hepatitis C virus infects hepatocytes and can also involve select blood cells, including neutrophils, monocytes, and B lymphocytes. Transmission occurs primarily via blood exposure—such as transfusion of blood components or plasma, transplantation of donor organs, or use of nonsterile syringes, needles, and instruments—and less often through sexual contact. Acute infection is frequently asymptomatic and therefore often unrecognized. Chronic infection develops in 60–85 %, increasing the risk of cirrhosis, hepatic failure, and hepatocellular carcinoma; because of this indolent but progressive injury, HCV is often described as a silent infection. HCV exhibits marked genetic diversity due to a high mutation rate, which facilitates immune evasion. Viral genomes vary across regions and differ in their responsiveness to interferon-based regimens. There are 6 major genotypes and approximately 500 subtypes. Globally, genotype 1 is most prevalent (40–80 %); subtype 1a is common in the United States and 1b in Western Europe and South Asia. Genotype 2 occurs with a frequency of 10–40 %. Genotype 3 is frequent in Scotland, Australia, India, and Pakistan. Genotype 4 predominates in Central Asia and North Africa, genotype 5 in South Africa, and genotype 6 in parts of Asia. In Russia, genotype 1b predominates, followed by genotypes 3, 1a, and 2; in the United States, 1a/1b, 2b, and 3a are common. Genotyping assists in estimating the likelihood of response to therapy. Genotype 1 responds less favorably than genotypes 2 and 3, and liver biopsy is more consequential for patients with genotype 1. Higher interferon doses are recommended for genotypes 1 and 4, and treatment is extended to 48 weeks even when viremia is absent for more than 24 weeks. A rapid on-treatment decline in viral load (< 50 IU/mL at 4 weeks) supports the possibility of a shorter course, whereas failure to achieve a 2-log reduction by 12 weeks suggests treatment is ineffective and should be reconsidered. Genotypes 2 and 3 respond well in 80 % of cases, typically over 24 weeks. Therapeutic planning incorporates sex, age, symptom burden, prior therapy, hepatic structure and function, and laboratory parameters.