Virion Structure and Genome Features
The virus is spherical with a complex organization. The virion diameter is 55–65 nm (with a core size of 70–80 nm).
- Capsid: Has an icosahedral symmetry. It contains the core structural protein forming the HCc antigen, as well as several non-structural enzymatic proteins (NS2, NS3, NS4, NS5) required for replication. Inside the capsid is the nucleoprotein.
- Envelope: Represents a lipoprotein membrane with glycoprotein spikes (gpE1, gpE2/NS1).
The genetic material is represented by a single-stranded linear positive-sense RNA. There are about 14 viral genotypes, among which genotype 1b is considered the most virulent. A key feature of the virus is high genome variability. The region encoding the E1 and E2 glycoproteins (targets for antibodies) is extremely variable, causing hypermutability of the pathogen.
Epidemiology and Stability
The infection is widespread globally. A relatively large infectious dose is required for transmission (higher than for Hepatitis B).
Main routes of transmission:
- Parenteral / blood transfusion — the leading route, accounting for 2/3 of all cases.
- Vertical (transplacental) — from mother to fetus (about 10%).
- Sexual — accounts for approximately 7%.
In the environment, the virus has low stability: it is sensitive to heating up to 50 °C, UV irradiation, ether, and detergents. The pathogen lacks hemolytic and hemagglutinating activity. It is extremely difficult to cultivate in standard cell cultures.
Clinical Course and Pathogenesis
The incubation period is prolonged, ranging from 6 to 120 weeks.
The acute phase of the infection is often milder than in Hepatitis B and frequently presents with anicteric forms. The primary blood marker of this period is an elevation in alanine aminotransferase (ALT).
Despite a mild onset, the disease has a pronounced tendency toward chronicity, occurring in up to 50% of cases. Chronic Hepatitis C frequently leads to cirrhosis and hepatocellular carcinoma.
The high rate of chronicity is explained by two main factors:
- Immune evasion: due to continuous genome mutations, neutralizing antibodies fail to effectively block the virus.
- Lack of a robust cellular response: CD4+ lymphocytes target the epitope of the non-structural protein NS3. When this immune arm is weakened, viral reactivation occurs.
The virus is also capable of long-term persistence in lymphoid tissues.
Diagnostics, Treatment, and Prevention
Blood is the primary specimen for microbiological analysis.
- PCR (Polymerase Chain Reaction): Serves as the gold standard for early diagnosis as it detects viral RNA directly. The test becomes positive within days of infection, confirming an active process.
- ELISA (Enzyme-Linked Immunosorbent Assay): Used to detect antibodies. The method has an important limitation — the seronegative window, a period of several weeks when the virus actively circulates and blood is infectious, but antibodies have not yet been produced. Therefore, PCR remains the clinical method of choice.
Specific prophylaxis (vaccine) is not available. Non-specific prevention focuses on intercepting parenteral and sexual transmission routes. Treatment of chronic hepatitis C involves combination direct-acting antiviral therapy.