Вирустық гепатит: қабыну және емдеу жолдары

Liver inflammation from a viral infection

Viral hepatitis is liver inflammation due to a viral infection. It may present in acute form as a recent infection with relatively rapid onset, or in chronic form, typically progressing from a long lasting asymptomatic condition up to a decompensated hepatic disease and hepatocellular carcinoma (HCC).

Viral hepatitis is either transmitted through contaminated food or water (A, E) or via blood and body fluids (B, C). The viruses transmitted through water and food are mostly self limited, resulting in acute illness with full resolution. The blood borne viruses (B, C) can cause both acute and chronic liver disease and can be transmitted from mother to child during birth, through contact with body fluids during sex, unsafe injections and through unscreened blood transfusions. The most common types of hepatitis can be prevented or treated.

Hepatitis B is caused by the hepatitis B virus, a hepadnavirus that can cause both acute and chronic hepatitis. Chronic hepatitis develops in the 15% of adults who are unable to eliminate the virus after an initial infection. Identified methods of transmission include contact with blood, blood transfusion (now rare), unsanitary tattoos, sex (through sexual intercourse or contact with bodily fluids), or mother to child by breast feeding; there is minimal evidence of transplacental crossing. However, in about half of cases the source of infection cannot be determined. Blood contact can occur by sharing syringes in intravenous drug use, shaving accessories such as razor blades, or touching wounds on infected persons. Needle exchange programmes have been created in many countries as a form of prevention. Patients with chronic hepatitis B have antibodies against the virus, but not enough to clear the infected liver cells. The continued production of virus and countervailing antibodies is a likely cause of the immune complex disease seen in these patients. A vaccine is available to prevent infection for life. Hepatitis B infections result in 500,000 to 1,200,000 deaths per year worldwide due to the complications of chronic hepatitis, cirrhosis, and hepatocellular carcinoma (HCC). Hepatitis B is endemic in a number of (mainly South East Asian) countries, making cirrhosis and hepatocellular carcinoma big killers. There are eight treatment options approved by the U. S. Food and Drug Administration (FDA) available for persons with a chronic hepatitis B infection: alpha interferon, pegylated interferon, adefovir, entecavir, telbivudine, lamivudine, tenofovir disoproxil and tenofovir alafenamide with a 65% rate of sustained response.

Hepatitis C (originally "non A non B hepatitis") is caused by hepatitis C virus (HCV), an RNA virus of the family Flaviviridae. HCV can be transmitted through contact with blood (including through sexual contact if the two parties' blood is mixed) and can also cross the placenta. Hepatitis C usually leads to chronic hepatitis, culminating in cirrhosis in some people. It usually remains asymptomatic for decades. Patients with hepatitis C are susceptible to severe hepatitis if they contract either hepatitis A or B, so all persons with hepatitis C should be immunized against hepatitis A and hepatitis B if they are not already immune, and avoid alcohol. HCV can lead to the development of hepatocellular carcinoma, however, only a minority of HCV infected individuals develop cancer (1–4% annually), suggesting a complex interplay between viral gene expression and host and environmental factors to promote carcinogenesis. The risk is increased two fold with active HBV coinfection and a 21% increase in mortality compared to those with latent HBV and HCV. HCV viral levels can be reduced to undetectable levels by a combination of interferon and the antiviral drug ribavirin. The genotype of the virus is the primary determinant of the rate of response to this treatment regimen, with genotype 1 being the most resistant. Hepatitis C is the most common chronic bloodborne infection in the United States, and the leading cause of liver tranplants. +Hepatitis C Marker Detection Time Description Significance Note HCV RNA 1–3 weeks or 21 days PCR Demonstrates presence or absence of virus Results may be intermittent during course of infection. Negative result is not indicative of absence. anti HCV 5–6 weeks Enzyme Immunoassay for antibodies Demonstrates past or present infection High false positive in those with autoimmune disorders and populations with low virus prevalence. ALT 5–6 weeks – Peak in ALT coincides with peak in anti HCV Fluctuating ALT levels is an indication of active liver disease.

Hepatitis D is caused by the hepatitis D virus (HDV), or hepatitis delta virus; it belongs to the genus Deltavirus. HDV is similar to a satellite virus as it can only propagate in the presence of the hepatitis B virus, depending on the helper function of HBV for its replication and expression. It has no independent life cycle, but can survive and replicate as long as HBV infection persists in the host body. It can only cause infection when encapsulated by hepatitis B virus surface antigens. The vaccine for hepatitis B protects against hepatitis D virus because of the latter's dependence on the presence of hepatitis B virus for it to replicate.

Hepatitis E is caused by the Hepatitis E virus (HEV), from the family Hepeviridae. It produces symptoms similar to hepatitis A, although it can take a fulminant course in some patients, particularly pregnant women (mortality rate about 20%); chronic infections may occur in immune compromised patients. It is more prevalent in the Indian subcontinent. The virus is feco orally transmitted and is usually self limited.

Hepatitis F virus (HFV) is a hypothetical virus linked to certain cases of hepatitis. Several hepatitis F virus candidates emerged in the 1990s, but none of these reports have been substantiated.

The GB virus C is a virus that is probably spread by blood and sexual contact. It was initially identified as Hepatitis G virus. There is very little evidence that this virus causes hepatitis, as it does not appear to replicate primarily in the liver. It is now classified as GB virus C.

In 2022, several hundred cases of acute hepatitis of probable infectious origin were reported worldwide. As of May 2023, the virus causing these cases has not been identified, but an adenovirus is suspected.