Epidemiological characteristics and routes of transmission
Hepatitis C virus is sensitive to heat: boiling completely inactivates it within 2 minutes. The disease holds immense clinical and social significance as a leading cause of cirrhosis and hepatocellular carcinoma. The source of infection is patients with acute and chronic forms, with individuals who have a latent course and detectable viral RNA in the blood posing the greatest threat.
The primary mechanism of transmission is parenteral. Blood contagiousness is 1–2 orders of magnitude lower than that of hepatitis B.
Routes of transmission are divided into:
- Artificial (high risk): instrumental medical and non-medical procedures (hemodialysis, tattoos, reusable needles). Intravenous drug use remains the leading factor in spread. The transfusion route has been minimized by screening, but a risk remains due to the "seronegative window".
- Natural (low risk): sexual and household contact routes are of secondary importance. Vertical transmission from mother to child does not exceed 2%, but the risk increases up to 30% if the parturient woman has a high viral load (over $10^6$ copies/µL).
Features of pathogenesis and immune response
Specific protective immunity after a past infection is not formed due to the high mutation rate of the pathogen, which makes reinfection and superinfection possible. The virus possesses "immune escape" mechanisms, hiding in extrahepatic reservoirs (lymph nodes, bone marrow, spleen) and infecting immunocompetent cells.
T-cell anergy develops, and the produced antibodies lack virus-neutralizing potential. Classical immune-mediated hepatocyte cytolysis plays a secondary role. The foreground is taken by pathological polyclonal activation of B-lymphocytes, leading to the synthesis of cryoglobulins and increasing the risk of B-cell lymphomas. Liver damage is largely autoimmune in nature.
Due to immune failure, spontaneous viral clearance is observed in only 20–25% of patients (more often in young women with a specific HLA phenotype), while in the remaining cases, the disease transitions into a chronic form with prolonged HCV RNA persistence.
Clinical presentation of acute hepatitis C
Acute viral hepatitis C (coded as B17.1 in ICD-10) is characterized by a predominantly latent or paucisymptomatic course. The incubation period lasts from 2 to 26 weeks.
Pre-jaundice period (1–2 weeks) may present with dyspeptic, asthenovegetative, arthralgic, or latent variants. Extrahepatic manifestations (arthralgia, rashes) due to immune complex reactions are possible during this period.
Jaundice period (2–4 weeks) develops in only 5% of patients, usually upon receiving a massive infecting dose. Jaundice is mild, and intoxication is minimal. Characteristically, dyspepsia does not resolve with the onset of jaundice. Objectively, hepatomegaly and, less frequently, splenomegaly are noted.
A specific laboratory sign is fluctuating hyperfermentemia (a 10–100-fold increase in transaminases) not accompanied by a subjective deterioration in well-being. Severe fulminant forms with hepatic encephalopathy are not characteristic of this infection.
Diagnostics and treatment principles
The diagnosis of the acute phase is most often established incidentally. A biochemical blood test demonstrates a sharp increase in ALT and AST (with a de Ritis ratio < 1).
The basis for confirmation is the detection of viral RNA by PCR (an early marker, appearing in 1–3 weeks). Serological diagnostics (detection of anti-HCV) is retrospective in nature. The presence of IgM is not a reliable criterion for the acute phase, as they also circulate during a chronic course. Key evidence of an acute process is a documented seroconversion of antibodies in a previously seronegative patient.
Treatment of mild forms is possible on an outpatient basis, while moderately severe forms require hospitalization. Basic therapy includes diet and detoxification. In modern practice, early initiation of specific antiviral therapy is considered to prevent chronification. There is no vaccine against the disease.
Briefly: answers to topical questions
What are the main pathogenetic mechanisms (theories) explaining the development of acute hepatic encephalopathy?
The development of acute hepatic encephalopathy is explained by several theories based on the action of neurotoxins on the central nervous system.
- Glial hypothesis — the leading theory, according to which endogenous neurotoxins, against the background of an amino acid imbalance, cause edema and impaired function of astroglia.
- Ammonia theory — when liver function is impaired, ammonia crosses the blood-brain barrier, reduces ATP synthesis in mitochondria, and causes energy deprivation in neurons.
- Amino acid metabolism disorder theory — the accumulation of aromatic amino acids (phenylalanine, tyrosine, tryptophan) in the blood and their penetration into the brain leads to a decrease in intracerebral synthesis of dopamine and norepinephrine.
How does the value of the de Ritis ratio differ in viral hepatitis versus alcoholic liver disease?
The de Ritis ratio (the ratio of AST to ALT enzymes) is used for the differential diagnosis of liver lesions and has different values for viral and alcoholic etiologies.
| Disease | Features of the de Ritis ratio |
|---|---|
| Acute viral hepatitis | Preponderance of ALT over AST |
| Alcoholic liver disease | AST/ALT ratio is usually above 2 |
Which groups of drugs are used for the medical therapy of acute hepatic encephalopathy?
For the medical therapy of acute hepatic encephalopathy, groups of drugs aimed at combating hyperammonemia are used.
- Antibacterial drugs — suppress ammonia-producing intestinal microflora (metronidazole, rifaximin, ciprofloxacin).
- Osmotic laxatives — reduce the absorption of ammonia and other toxins into the systemic circulation (lactulose).
- Ornithine cycle stimulators — intermediate metabolites of the ornithine cycle for binding ammonia in the liver (ornithine aspartate, ornithine α-ketoglutarate, and arginine malate).
To remember the risk of chronification: the "80/20 rule" — 80% of cases progress to a chronic form (latent course), and only 20% end in spontaneous recovery.
Class and exam questions
Can you get infected with hepatitis C through a kiss?
Viral RNA and antibodies can be detected in saliva, but there is no reliable clinical data on the transmission of infection via household contact through kissing.
Are pregnancy and lactation contraindicated for infected women?
No, they are not contraindicated provided there is no immunodeficiency, viral load is low, and liver function is preserved. The baseline risk of fetal infection is minimal (about 2%).
Does the presence of antibodies in a newborn mean they are infected?
Not always. Most often, the presence of anti-HCV in an infant is the result of passive transfer of maternal antibodies across the placenta (false-positive result).
Does severe liver failure develop in the acute form?
Fulminant forms capable of leading to acute hepatic encephalopathy and death are extremely atypical for acute viral hepatitis C.
What else to study on this topic
- Mechanisms of development of mixed cryoglobulinemia and glomerulonephritis in the chronic form
- The link between hepatitis C virus and the development of B-cell lymphomas
- Differential diagnostics of icteric and cytolytic syndromes
- The theory of the origin of "cryptogenic hepatitis" in delayed seroconversion
- Histological markers of progression: piecemeal necrosis and steatosis
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