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Varicella-zoster hepatitis.
Last reviewed: 07.07.2025
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Elementary bodies of the virus were first discovered by H. Argao in 1911. The varicella-zoster virus was first cultured in tissue culture by T. H. Weller in 1953. The virus is a spherical particle with a diameter of 150-200 nm, containing DNA; its properties are similar to those of the herpes simplex virus and are indistinguishable from the causative agent of herpes zoster, which is why it is designated as the varicella-zoster virus or VZV for short. According to modern classification, it is human herpes virus type 3 (HHV 3).
The virus is unstable in the external environment and is not pathogenic for animals. It is well cultivated in transplantable cultures of humans and monkeys. The best culture for VZV replication is human hepatocytes, in second place are lung fibroblasts.
Epidemiology of varicella-zoster hepatitis
Almost the entire population suffers from chickenpox by the age of 10-14. The only source of infection is a sick person. The source of infection can also be people with herpes zoster.
The infection is transmitted by airborne droplets, less often by contact, and infection is possible over a long distance. Transplacental transmission from mother to fetus has been proven.
[ Pathogenesis of varicella-zoster hepatitis
The pathogenesis of VZV hepatitis has not been studied. The idea of the hepatotropism of the herpes virus type 3 first arose during the development of a live vaccine against chickenpox, when it was convincingly shown that it has a pronounced tropism for hepatocytes. This property of the virus was successfully used by Japanese scientists for its cultivation. Hepatocytes turned out to be the best culture for replication, with lung fibroblasts in second place.
Generalized forms of chickenpox and isolated varicella-zoster hepatitis are extremely rare, mainly in children with altered immunological status.
Pathomorphology
The virus infects the cell nuclei, forming eosinophilic intranuclear inclusions. It can cause the formation of giant multinucleated cells.
In the internal organs, primarily in the liver, kidneys, lungs, and central nervous system, small foci of necrosis with hemorrhages at the periphery are detected.
Symptoms of Varicella-Zoster Hepatitis
Currently, varicella-zoster hepatitis is described mainly in immunocompromised patients. It can occur both as part of a generalized infection and in isolation. The spectrum of VZV liver lesions varies from mild and subclinical to severe and fulminant forms of hepatitis. Varicella-zoster hepatitis always has an acute course. Chronic course of the disease is not observed.
Mortality in disseminated VZV infection in adult kidney transplant recipients is 34%. In 82% of cases, primary chickenpox occurs, and in 18%, reactivation of the infection occurs. The main clinical manifestations are hepatitis, pneumonitis, and DIC syndrome. However, no specific cytostatic drug has been identified that would be associated with the risk of dissemination of the infection. VZV hepatitis can also occur in HIV-infected patients.
Isolated varicella-zoster hepatitis may develop in immunocompromised patients (liver transplant recipients, patients with acute lymphoblastic leukemia, etc.). Liver damage is not accompanied by vesicular rashes on the skin and mucous membranes.
Acute varicella-zoster hepatitis develops in immunocompetent children and adolescents extremely rarely. In addition, a typical clinical and biochemical picture of hepatitis can be observed in 3-5% of patients with chickenpox. In this case, the activity of liver cell enzymes in the blood serum exceeds 100 U/l.
Treatment of varicella-zoster hepatitis
The use of high doses of acyclovir in combination with reduction of immunosuppressive therapy leads to a decrease in mortality from disseminated VZV infection in immunocompromised patients.
In disseminated VZV infection involving the liver, acyclovir and ganciclovir therapy may provide only temporary improvement. However, the number of VZV DNA copies in the blood serum often remains high, and the manifestations of hepatitis usually do not disappear. In these cases, the use of foscarnet sodium may lead to a decrease in the level of viremia and normalization of liver function.
The use of acyclovir in immunocompetent children and adolescents with acute VZV hepatitis alleviates the course of chickenpox, but does not have a reliable effect on the course of hepatitis. Hepatitis has an acute course, ending in recovery. In more than 80% of patients, the activity of serum transaminases is normalized by the 25th-30th day of treatment.
Prevention of varicella-zoster hepatitis
For the purpose of specific prevention of VZV infection, including that accompanied by liver damage, a live vaccine is used.
In summary, it can be said that varicella-zoster hepatitis has an acute course and is a relatively rare manifestation of VZV infection, developing mainly in immunocompromised patients. However, given the proven hepatotropism of VZV and the fact that the functional state of the liver is not examined in most patients with chickenpox and herpes zoster, some cases of VZV hepatitis may remain undiagnosed. The issue requires further study.