Human herpes virus type 6 (HHV 6), IgG antibodies
Why this test?
To establish HCV-6 infection and the nature of the infection:
- primary infection (acute course, latent course, carriage);
- secondary infection (chronic course, exacerbation / relapse, reinfection).
In what cases is it prescribed?
In the differential diagnosis of children's infections with high temperature and rash. In the diagnosis of infectious mononucleosis, negative for the Epstein-Barr virus.
In the complex of examinations of patients with lymphoproliferative diseases and hemoblastoses.
In the complex of examinations of recipients of organs and tissues before and after transplantation.
In the diagnosis of virus-associated diseases in HIV-infected patients and in other immunodeficiency conditions (chronic fatigue syndrome).
Human herpes virus type 6 (HCV-6) was first isolated relatively recently, in 1986 (in the blood cells of patients infected with HIV).
To date, it has been established that HCV-6 infection is widespread and has 2 subtypes - A and B - which differ genetically and epidemiologically: subtype B is more common, and subtype A is usually found in patients with immunodeficiencies.
Subtype B is the main cause of sudden exanthema - a childhood disease that is accompanied by a high temperature and a rash. In addition, the herpes virus can be asymptomatic and in the form of a non-specific febrile illness. In some cases, complications from the central nervous system are observed (convulsions against the background of high fever, rarely other neurological complications, including encephalitis, meningoencephalitis, serous meningitis).
IgG antibodies to this virus are found in 70-90% of adults. Primary HCV-6 infection in adults is rare, it can be associated with fulminant hepatitis, infectious mononucleosis, negative for the Epstein-Barr virus. The most likely way of transmission of infection is airborne, with saliva, vertical transmission is not excluded - from mother to child during pregnancy.
The virus tends to infect lymphocytes. Replication of the virus occurs mainly in T-lymphocytes, but it can also be detected in other cells - monocytes, B-lymphocytes - as well as in brain tissue, liver, salivary glands, and endothelium. Like other herpes viruses, HCV-6 is able to persist in the body after primary infection, activating when the immune system is suppressed.
Transplantation of stem cells and transplantation of internal organs increases the risk of infections caused by HCV-6 (in most cases, this is probably due to reactivation of latent infection as a result of suppression of immunity against the background of immunosuppressive therapy).
Testing for HCV-6, along with testing for cytomegalovirus and Epstein-Barr virus, is recommended for the earliest possible detection of virus-associated diseases and transplant success. Currently, the possible role of HCV-6 in the development of multiple sclerosis, chronic fatigue syndrome, lymphoproliferative diseases, and its influence on the course of HIV infection is being actively investigated.
Detection of virus-specific antibodies of the IgG class, which are divided into subclasses, is widely used for the diagnosis of HCV-6: 1) IgG antibodies to pre-early (non-structural) proteins of HCV-6 These antibodies appear in response to the activation of the virus in the cell infected with it. They are very specific, so there are no false positive results when they are detected. The presence of IgG to the early proteins of HCV-6 is a clear sign of virus activity. They are produced both during primary acute infection and during relapse of chronic infection and re-infection of HCV-6. 2) low-affinity IgG antibodies to HCV-6 10-14 days after the primary infection with HCV-6, IgG antibodies with low avidity (weak binding force of HCV-6 antigens) appear in a person without immunodeficiency, while the avidity of IgG antibodies constantly increases, and the proportion of low-avidity IgG antibodies decreases. so that they completely disappear after 1-3 months.
Detection among IgG of more than 50% of low-avid IgG to HCV-6 is an unequivocal sign of primary infection with this virus. 3) high-avidity IgG antibodies to HCV-6 They begin to be produced almost simultaneously with low-avidity IgG antibodies and circulate in the blood of the HCV-6 carrier throughout his life. The analysis of IgG to HCV-6 with their classification according to the subclasses described above is certainly very informative, but it is rarely used because it requires expensive immunodiagnostic kits. In connection with this, the standard test for IgG antibodies to HCV-6 is enzyme-linked immunosorbent assay (ELISA) of blood serum with the determination of the diagnostic titer of all virus-specific IgG in general and accounting for its changes.
Primary infection with HCV-6, as a rule, occurs in childhood (up to 3 years) and in most cases (70-80%) does not lead to an acute infectious process, but passes into a latent, asymptomatic period (carriage of the virus).
However, the human immune system responds to the invasion of the virus by producing antibodies. IgG appear in the 2nd week after infection in a small concentration, which continuously increases and reaches a maximum after a month. In the absence of active reproduction of the virus, the level of specific IgG-antibodies reached remains with minor fluctuations throughout life. It follows from this that if no virus-specific IgG is detected during the analysis or if they are detected in a low titer, then a repeat test is necessary 2 weeks after the first one. If after the initial infection, the virus begins to multiply actively, an acute primary HCV-6 infection develops, which in the vast majority of cases is manifested by large rashes on the skin and an increase in temperature. At the same time, virus-specific IgG antibodies also reach a peak after a month, but their titer is 2-4 times higher than during the latent course.
After the neutralization of active viruses, the titer of virus-specific IgG begins to gradually decrease and after 1-1.5 months the blood is approaching the level of antibodies during the latent course.
Secondary infection The chronic (latent) course of HCV-6 may be accompanied by exacerbations of the primary latent process or relapses of the primary infection. In addition, rarely, when as a result of antiviral therapy, effective immune protection, the primary infection with HCV-6 ended with the elimination of the virus, re-infection with HCV-6 or reinfection is possible. All cases of secondary infection are characterized by the presence of already existing IgG antibodies to HCV-6 in the body. However, exacerbation, relapse and reinfection stimulate additional production of virus-specific IgG, and their titer begins to increase on the 1st-3rd day of the infectious process.
However, since the secondary infection develops, as a rule, due to a decrease in the existing antiviral immunity, the titer of IgG antibodies can be significantly lower, and the time to reach the peak of their production is significantly longer than that observed with a normally functioning immune system. As with primary acute infection, after neutralization of active HC-6 viruses, the IgG level begins to decrease and reaches the initial value 1-1.5 months after the onset of clinical remission.
Thus, when IgG antibodies to HCV-6 are detected in the blood, the study should be repeated 2 weeks after the previous one and 1-1.5 months after remission.