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Pathological Anatomy · Diseases of the Liver, Biliary System, and Exocrine Pancreas

Understudied viral hepatitides

Hepatitis viralis

Little-studied viral hepatitis is a specific group of infectious liver lesions caused by relatively recently discovered hepatotropic viruses (HGV, TTV, SEN, GB agents). In clinical practice, they often act as a coinfection that joins classical hepatitis, significantly worsening the disease course and repeatedly accelerating the formation of irreversible changes in liver tissue.

HGV and HCVBelong to the same family of RNA-containing viruses — Flaviviridae.
DNA virusesUnlike many hepatotropic agents, TTV and SEN viruses contain DNA.
TTV incubationPost-transfusion hepatitis manifests 8–11 weeks after transfusion.
Risk of chronic progressionAcute HGV superinfection progresses to a chronic form in 75% of cases.
4 min readFor medical studentsUpdated Sep 25, 2026
Material prepared by WhiteCoat Pro editorial team based on platform study guidesReviewed by medical editor: Aulov A. A., general practitioner · 09/24/2026

Hepatitis G virus (HGV)

The HGV causative agent is an RNA-containing virus belonging to the Flaviviridae family (the hepatitis C virus belongs to the same family). It is important to emphasize that it is not a simian virus.

The clinical significance of HGV lies in its ability to cause severe and rapidly progressive forms of infection.

  • Superinfection: If HGV infection occurs against the background of a pre-existing liver lesion, the acute phase progresses to chronic hepatitis in 75% of cases.
  • Severity of the process: In patients with severe chronic hepatitis, markers of active HGV replication are detected in the vast majority of cases — from 79% to 86%.
  • Pathogenesis: According to the working hypothesis, the classical hepatitis B virus (HBV) itself often causes an infection with low or moderate activity. However, the addition of HGV acts as a trigger that sharply increases the activity of the inflammatory process.
  • Prognosis: HGV-associated infection is highly likely to lead to the rapid development of liver cirrhosis.

GB agents (GBV-A and GBV-B)

A group of viruses designated as GBV was identified in the mid-1990s by a research team led by J.N. Simons. The discovery was made possible by the application of the representational difference analysis method using PCR.

The history of the discovery of these viruses is quite specific. Initially, the infectious agent was obtained from the blood serum of a surgeon (whose initials were G.B.) suffering from unverified hepatitis. This serum had been stored frozen since the early 1960s. Subsequently, new viruses, named GBV-A and GBV-B, were successfully isolated from the blood of a tamarin (a primate species) experimentally infected with the preserved GB agent.

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DNA-containing hepatotropic viruses: TTV and SEN

In the late 1990s, new viruses were discovered whose genome, unlike HGV and HCV, is represented by a DNA molecule.

CharacteristicTTV virus (Transfusion Transmitted Virus)SEN virus
Year and place of discovery1997, Japanese researchers1999, Italian researchers
Type of nucleic acidDNADNA
Primary source of isolationPatients with post-transfusion hepatitisHIV-infected patient with liver damage
Genetic diversity3 genotypes and 9 subtypes identifiedNo precise data within the current review

Features of the TTV virus: The virus is associated with cases of post-transfusion hepatitis. The clinical picture of the disease usually develops 8–11 weeks after a blood transfusion procedure. The main diagnostic marker is the isolation of TTV-DNA. In the Russian Federation, the virus has been isolated in the European part and Western Siberia, and it is detected both in patients with hepatitis of unknown etiology and in absolutely healthy people.

Features of the SEN virus: According to Italian authors, the SEN virus has a specific prevalence in risk groups. It is detected in 3% of hemophilia patients, 40–60% of injection drug users, and 60% of patients with hepatitis of unknown etiology.

Briefly: answers to topical questions

What are the transmission routes of hepatitis G virus (HGV)?

Hepatitis G virus transmission routes include parenteral and vertical mechanisms.

  • Parenteral route — is the leading one. The high-risk group includes recipients of donor blood and its components, organ transplant patients, and injection drug users.
  • Vertical route — the possibility of virus transmission from an infected pregnant woman to the fetus has been proven.

To which families do the DNA-containing hepatotropic viruses TTV and SEN belong?

DNA-containing hepatotropic viruses TTV and SEN are classified differently depending on the source.

  • Family (Circoviridae) — both viruses (TTV and SEN) are assigned to this group.
  • Family (Anelloviridae) — the type representative, TTV virus (Torque Teno virus), belonging to the genus Alphatorquevirus, is assigned to this family.

What clinical symptoms are characteristic of the acute phase of hepatitis caused by the SEN virus?

SEN virus-associated infection is characterized by a predominantly latent (asymptomatic) course. The independent role of the SEN virus as a causative agent of hepatitis has not been conclusively confirmed; a clear link between SEN infection and the development of acute or chronic hepatitis has not been established.

How to memorize

To avoid confusing the type of nucleic acid, remember: HGV is a "relative" of hepatitis C (Flaviviridae family), and therefore it contains RNA. And viruses with three-letter abbreviations (TTV, SEN) are DNA viruses.

Class and exam questions

How does the HGV virus affect the course of hepatitis B?

According to the existing hypothesis, hepatitis B virus (HBV) frequently causes a process with low or moderate activity. Superinfection with HGV sharply increases the inflammatory activity and accelerates the development of liver cirrhosis.

Where did the name of the GBV group of viruses come from?

The name comes from the initials of a surgeon (G.B.) from whose blood serum, frozen back in the early 1960s, the infectious agent was initially obtained.

How long does it take for TTV-induced hepatitis to manifest?

The clinical picture of TTV-associated post-transfusion hepatitis develops on average 8–11 weeks after transfusion of infected blood.

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What else to study on this topic

  • Mechanisms of fibrosis progression in HBV and HGV coinfection.
  • The role of the SEN virus in the development of hepatitis of unknown etiology.
  • Methods of PCR diagnostics and TTV genotype typing.
  • Differential diagnosis of post-transfusion viral hepatitis.
  • Epidemiological significance of detecting TTV-DNA in healthy individuals.

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