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Hepatitis caused by human herpes viruses types 6 and 7

 
, medical expert
Last reviewed: 04.07.2025
 
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Human herpes virus type 6 (HHV 6) was first discovered by H. Salahuddin et al in 1986 in adult patients with lymphoreticular diseases infected with HIV. HHV 6 is a member of the Roseolovirus genus, beta-Herpesvirus subfamily. HHV 6 has an electron-dense core and an icosahedral capsid surrounded by an envelope and an outer membrane, which is the location of glycoproteins and proteins. The virion diameter is 160-200 nm, containing 162 capsomeres. The genome is represented by double-stranded DNA. Restriction analysis of HHV 6 DNA has established variability in the genome of different isolates of the virus. HHV6 is represented by two variants: HHV 6A and HHV6B.

Human herpes virus type 7 (HHV 7) was first identified in cells from a healthy adult in 1990 by M. Frenkel et al. HHV 7 is a member of the Roseolovirus genus, beta-Herpesvirus subfamily, and has morphological, antigenic, and genomic similarities to HHV 6. It has a nucleocapsid containing DNA surrounded by a dense membrane and lipid coating. The diameter of HHV 7 virions is up to 170 nm.

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Symptoms of hepatitis caused by human herpes viruses types 6 and 7

HHV 6 and HHV 7 infection in patients who have undergone solid organ or bone marrow transplantation manifests itself as fever, maculopapular rash, pneumonia, encephalitis, bone marrow damage, and hepatitis. The etiology of the disease is confirmed using all existing methods. HHV 6 itself can also exert an immunosuppressive effect and aggravate the course of hepatitis caused by cytomegalovirus and other pathogens in transplant recipients. At the same time, HHV 6 infection (including hepatitis) can be asymptomatic, which increases the role of laboratory diagnostic methods.

Acute cholestatic afebrile HHV 6 hepatitis may develop in patients who have undergone solid organ transplantation. HHV 6 infection may cause graft rejection in patients who have undergone liver transplantation.

HHV 6 is capable of causing fulminant hepatitis in immunocompetent individuals. In these cases, the diagnosis is confirmed by the detection of high concentrations of HHV 6 DNA and antigens in hepatocytes and mononuclear cells of the peripheral blood and characteristic morphological changes in the liver tissue. In this case, anti-HHV 6 is detected in the blood serum of patients.

There is evidence of the etiologic role of HHV 6 in the development of giant cell hepatitis in newborns. The diagnosis is established based on the presence of multinucleated giant cells, which are derivatives of hepatocytes. The disease can also take a fulminant form, rapidly progressing liver cirrhosis can develop, in addition, the disease can occur with an autoimmune component. During the remission period, symptoms of intoxication in patients with congenital HHV 6 hepatitis were virtually absent. Extrahepatic manifestations disappeared in most children. The size of the liver and spleen decreased, but their complete normalization was not observed. Usually, the edge of the liver protruded from under the costal arch by no more than 1-2 cm. The spleen was palpated less than 1 cm below the edge of the costal arch in most patients with splenomegaly. In the blood serum, enzyme activity did not exceed normal values.

Treatment of hepatitis caused by human herpes viruses types 6 and 7

For the purpose of etiotropic treatment of HHV6 hepatitis, ganciclovir and foscarnet sodium, which have activity against HHV 6 in vitro and in vivo, can be used. Information is accumulating on the successful use of Viferon for the treatment of chronic HHV 6 hepatitis in children.

Prevention of hepatitis caused by human herpes viruses types 6 and 7

Specific prophylaxis for HHV6 and HHV7 infections has not yet been developed.

Thus, it can be concluded that in children, human herpes virus type 6 can have a hetatotropic effect, which is confirmed by the results of clinical and laboratory research, including the detection of HHV 6 DNA by PCR (in all 3 children examined by us) in hepatocytes. Clinical manifestations of chronic HHV 6 hepatitis correspond to those in chronic viral hepatitis of varying degrees of activity. Recognize liver cirrhosis was not detected in any patient.

Summarizing the above, it can be said that HHV 6 and HHV 7 can cause both acute and chronic hepatitis in various categories of patients. However, given that these pathogens have become the subject of close attention of researchers relatively recently, many issues remain unresolved and further study of the problem is required.

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