What Is Hepatitis G?

Hepatitis G Virus ( HGV )

Hepatitis G virus

Hepatitis G virus discovery and nomenclature

Hepatitis G Virus ( HGV )

In 1967, DEINHARDT et al. Found that tamarins from serum samples taken from a jaundice patient could cause tamarins to develop hepatitis and to pass on infections in tamarins. The pathogenic factor is named GB factor.

In 1995, American scientists obtained two flavivirus-related gene sequences from marmosets inoculated with GB factor, named GBV-A and GBV-B. Subsequently, a human GBV nucleic acid sequence was amplified from a non-A to E patient and named GBV-C. At about the same time, another laboratory scientist in the United States also found a similar gene sequence from a patient with non-A to E hepatitis after blood transfusion, called HGV. Further research shows that the gene sequence of HGV has high homology with GBV-C. The nucleotide homology of the NS3 region of the two is 85% and the amino acid homology is 100%. Therefore, it is determined that the two are identical. Different isolates of this virus are collectively referred to as Hepatitis G Virus ( HGV ).

Biological characteristics of hepatitis G virus

HGV is now considered to be a member of the Flaviviridae family, and its genome structure is similar to HCV (Hepatitis C virus, the same below). It is about 9.5 kb in length and is a single positive-strand RNA virus. The genome has only one ORF,

It encodes a precursor protein with a length of about 2900 amino acids. It is hydrolyzed by viruses and host cells to form different structural and non-structural proteins.

Hepatitis G virus pathogenicity

The transmission route of HGV is similar to HBV (Hepatitis B virus, the same below) and HCV. It is mainly transmitted through parenteral routes such as blood transfusion. There can also be mother-to-child transmission and iatrogenic transmission. The clinical symptoms of HGV infection are not obvious and generally do not damage the liver. HGV is longer than HBV or HCV and joint infection occurs, so some scholars believe that HGV may be a helper virus. In some cases of HCV combined with HGV infection, HCV infection disappears, ALT returns to normal, and HGV infection persists, suggesting that HGV can interfere with HCV replication or cooperate with the body to clear HCV. Vaccination of chimpanzees with sera from HGV RNA-positive patients can be seen HGV RNA remained positive in orangutan serum, but there were no significant abnormalities in serum ALT and liver histopathology. However, some scholars have infected rhesus monkeys with the same method, and changes in serum HGV RNA positive conversion, ALT elevation, and anti-HGV positive changes occurred one week later, and the infected primary rhesus monkey serum can be passaged in rhesus monkeys. Therefore, HGV is pathogenic. Sex needs further research.

Hepatitis G virus detection method

PT-PCT method is the most commonly used method for the diagnosis of HGV infection. HGV envelope protein E2 has been expressed in eukaryotic systems, and an ELISA method for detecting E2 antibodies has been established.

Since the appearance of E2 antibody is related to the disappearance of HGV RNA, detection of E2 antibody is considered to be a sign of recovery from HGV infection.

Hepatitis G virus characteristics

(1) Recessive viremia is a recessive infection:

(2) Acute hepatitis has increased ALT, and jaundice is lighter than acute hepatitis C. Most of them can recover quickly and can be infected with hepatitis B and C viruses.

(3) The virus persists. The virus is always in a low titer state, with a few high titers, but often without clinical symptoms.

(4) Duration of illness With the fluctuation of virus titer, ALT increases intermittently, and a few recurrent episodes turn into chronic hepatitis.

(5) Subacute severe hepatitis may cause fulminant hepatitis.

(6) It takes a long time for liver cirrhosis to develop into cirrhosis after infection with the virus. Once cirrhosis occurs, the condition rapidly changes and develops rapidly.

(7) A small number of liver cancer patients can also develop liver cancer, which has a synergistic effect with hepatitis B and C viruses.