RESUMO
Two closely related and commonly found human herpesviruses HHV-6 A and HHV-6 B are classified into the sixth human herpes virus complex (HHV-6). Primary infection with HHV-6 often takes place in early childhood and it can be either asymptomatic or manifests itself as sixth disease (caused by HHV-6 B). HHV-6 remains present in a latent form in the body with the potential for virus reactivation. The article points out the phenomenon of chromosomal integration of HHV-6 (Ci-HHV-6) which is found in about 1% of the population and, unlike the commonly spread HHV-6 infection, has become hereditary, with its pathological potential in Ci-HHV-6 DNA carriers remaining unknown. Therefore, the focus on clinical consequences of Ci-HHV-6 is of high relevance to the therapeutic strategy for patients with high HHV-6 positivity in molecular biological tests.
Assuntos
Exantema Súbito/virologia , Herpesvirus Humano 6/genética , Integração Viral/genética , Portador Sadio/virologia , Exantema Súbito/diagnóstico , Exantema Súbito/genética , Exantema Súbito/terapia , HumanosRESUMO
Chromosomal integration of human herpesvirus 6 (HHV-6) is a novel situation found in a small percentage of individuals. While active HHV-6 infection is treatable using antivirals, the abnormally high level of HHV-6 DNA found in chromosomal integration of HHV-6 (CI-HHV-6) is not affected by such drugs. Stored DNA samples taken originally for detection of fusion genes and minimal residual disease from 339 pediatric patients treated for leukemia in the Czech Republic between the years 1995-2007 were tested retrospectively. Using real-time quantitative PCR technology, the quantity of HHV-6 DNA detected was normalized to 100,000 human genome equivalents as assessed by quantitation of the albumin gene. HHV-6 DNA was detected in 107 samples from 91 patients (26.8%). In the majority of samples (99) only a minute level of normalized viral copies (NVCs) (median 1.84 NVCs) was detected. A high viral load of approximately 100,000 NVCs was detected in 5 patients (1.5%; median 140,150 NVCs), in all of whom were confirmed subsequently CI-HHV-6 by a detection of HHV-6 DNA in hair follicles or in the nails. In all but one patient with HHV-6 variant B, variant A of the virus was detected. None of the patients with CI-HHV-6 had complications attributable to HHV-6 infection. The prevalence of CI-HHV-6 in childhood leukemia does not differ from that published for other patients or healthy populations. Where high levels of HHV-6 DNA are present, CI-HHV-6 should be confirmed as soon as possible so that potentially toxic but ineffective antiviral treatment can be stopped.