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Three cases with TT virus infection and idiopathic neonatal hepatitis
1Department of Pediatrics, Osaka University Graduate School of Medicine, Osaka, Japan. tajiri@ped.med.osaka-u.ac.jp
Insights
This study suggests Torque teno virus (TTV) infection may contribute to neonatal cholestasis in some infants. Gammaglobulin therapy showed promise in treating these TTV-infected cases.
Area of Science:
- Hepatology
- Virology
- Neonatology
Background:
- Idiopathic neonatal hepatitis is a significant cause of prolonged cholestasis in infants.
- Intrahepatic fatty degeneration can be a feature of neonatal hepatitis.
- Torque teno virus (TTV) is a common, yet often asymptomatic, human virus.
Observation:
- Three infants with idiopathic neonatal hepatitis and fatty liver changes presented with prolonged cholestasis.
- All patients showed immediate improvement in cholestasis following high-dose intravenous gammaglobulin therapy.
- TTV DNA was detected in serum, duodenal fluid, and liver tissue of the affected infants.
Findings:
- Sequence analysis confirmed identical TTV strains in serum, duodenal fluid, and liver tissue within individual patients.
- Maternal TTV strains were nearly identical to those found in two of the infants, suggesting vertical transmission.
- These findings indicate TTV infection as a potential contributing factor to neonatal cholestasis.
Implications:
- This research identifies a potential subset of idiopathic neonatal hepatitis cases linked to TTV infection.
- Gammaglobulin therapy may be a beneficial treatment for TTV-associated neonatal cholestasis.
- Further investigation into TTV's role in neonatal liver disease is warranted.
Abstract:
We present three cases of infants with idiopathic neonatal hepatitis showing diffuse intrahepatic fatty degeneration. Prolonged cholestasis has improved immediately upon intravenous administration of a high-dose gammaglobulin treatment in all three patients. The TT virus (TTV) genome was detectable in the serum of two patients, in the duodenal fluid of one and in the liver of all three. By analyzing sequence homology, we observed that the respective TTV isolated from serum, duodenal fluid and liver tissue were completely identical in cases 2 and 3. These findings suggest that TTV infection was one of the contributing factors for neonatal cholestasis in these patients. TTV was isolated from the serum of two out of the three mothers. The viruses were either completely or almost identical in sequence to those isolated from their respective infants, suggesting that they had been transmitted from mother to infant in these 2 cases. The patients presented here, whose livers were infected with the TTV and showed a favorable response to gammaglobulin therapy, may represent a subset of idiopathic neonatal hepatitis patients.