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Hepatitis caused by human herpes virus types 6 and 7
Last reviewed: 18.10.2021
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Human herpesvirus type 6 (HHV 6) was first detected by H. Salahuddin et al in 1986 in adult patients with HIV-infected lymphoreticular diseases. HHV 6 is a member of the genus Roseolovirus, the subfamily beta-Herpesvirus HHV 6 has an electronically dense nucleus and an icosahedral capsid surrounded by a membrane and an external membrane, the location of glycoproteins and proteins. The diameter of the virion is 160-200 nm, contains 162 capsomers. The genome is represented by double-stranded DNA. Restriction analysis of HHV6 DNA established the variability of the genome of different, virus isolates. HHV6 is represented by two options: HHV 6A and HHV6B.
Human herpesvirus type 7 (HHV 7) was first identified in cells from a healthy adult in 1990. M. Frenkel et al. HHV 7 is a member of the genus Roseolovirus, a subfamily of beta-Herpesvirus, has a morphological, antigenic and genomic similarity to HHV 6. It has a nucleocapsid containing DNA surrounded by a dense membrane and a lipid coating. The diameter of the virions of HHV 7 is up to 170 nm.
[Symptoms of hepatitis caused by human herpes virus types 6 and 7
HHV 6- and HHV 7-infection in patients who undergone transplantation of solid organs or bone marrow, is manifested by fever, patchy-papular rash, pneumonia, encephalitis, bone marrow damage and hepatitis. The etiology of the disease is confirmed with all the existing methods. HHV 6, in addition, is able to exert an immunosuppressive effect and weight the course of hepatitis caused by cytomegalovirus and other pathogens in transplant recipients. At the same time, HHV 6 infection (including hepatitis) can occur in a low symptom, which increases the role of laboratory diagnostic methods.
Possible development of acute cholestatic febrile HHV 6-hepatitis in organ transplant patients. HHV 6-infection can cause transplant rejection in patients who underwent liver transplantation.
HHV 6 is able to cause fulminant hepatitis in immunocompetent individuals. In these cases, the diagnosis is confirmed by the detection of a high concentration of DNA and HHV6 antigens in hepatocytes and peripheral blood mononuclear cells and with characteristic morphological changes in liver tissue. In this case, the serum of patients detected anti-HHV 6.
There is evidence of the etiological role of HHV 6 in the development of giant cell hepatitis of newborns. The diagnosis is established on the basis of the presence of multinucleated giant cells, which are derivatives of hepatocytes. The disease is also capable of taking fulminant form, fast progressive liver cirrhosis can develop, in addition, the disease can occur with an autoimmune component. In the remission period, the symptoms of intoxication in patients with congenital HHV 6-hepatitis were practically absent. The majority of children disappeared extrahepatic manifestations. Dimensions of the liver and spleen were reduced, but complete normalization was not observed. Usually the edge of the liver protruded from under the costal arch not 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 serum, the activity of the enzymes did not exceed normal values.
Treatment of hepatitis caused by human herpes virus types 6 and 7
For the purpose of etiotropic treatment of HHV6-hepatitis, ganciclovir and sodium foscarnet can be used that have activity against HHV 6 in vitro and in vivo. The information on the successful use of viferon for the treatment of chronic HHV 6-hepatitis in children is accumulated.
Prevention of hepatitis caused by human herpes virus types 6 and 7
Specific prophylaxis of HHV6 and HHV7 infections is not currently developed.
Thus, it can be concluded that in children the human herpesvirus type 6 can have a getatropic effect, as evidenced by the results of a clinical laboratory study, including the detection of HHV6 DNA by PCR (in all 3 of the children we examined) in hepatocytes . Clinical manifestations of chronic HHV 6-hepatitis correspond to those with chronic viral hepatitis of varying degrees of activity. Recognize cirrhosis of the liver has not been detected in any patient.
Summarizing the above, we can say 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 questions remain unresolved and further study of the problem is required.