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Updated: Jun 14, 2026

Ex Vivo Infection of Murine Epidermis with Herpes Simplex Virus Type 1
Published on: August 24, 2015
[Human herpesvirus 6]
József Ongrádi1, Valéria Kövesdi, G Péter Medveczky
1Semmelweis Egyetem, Altalános Orvostudományi Kar, Közegészségtani Intézet, Budapest, Nagyvárad tér 4. 1089. ongjos@hotmail.com
Abstract:
Human herpesvirus 6 discovered in 1986 is the most ancient human herpesvirus shown by molecular characteristics. Variant B infects children under the age of 2 years by droplets from asymptomatic virus shedding adults occasionally causing exanthema subitum. The virus infects CD4+ macrophages and lymphocytes; subsequently establishes lifelong latency and persistence with occasional shedding through the saliva. This variant frequently reactivates in bone marrow and organ transplant recipients with concomitant immunosuppression causing even fatal complications. It is a cofactor in the pathogenesis of multiple sclerosis, chronic fatigue syndrome, Hodgkin and non-Hodgkin lymphomas. The direct consequences of variant A infection and latency in CD4+ cells are not known. It transactivates HIV infection in vitro and in humans, and facilitates tumor progression induced by human papilloma viruses. Pathogenic effects of both variants are mediated by altered cytokine and chemokine profiles. Serological differentiation of the two variants is unreliable; however, it is possible by using PCR. Ganciclovir, foscarnet and cidofovir can be used for treatment and chemoprophylaxis of severe complications.
Insights
Human herpesvirus 6 (HHV-6) infects young children and establishes lifelong latency. Reactivation in transplant recipients can be fatal, and HHV-6 is linked to chronic diseases and cancers.
Area of Science:
- Virology
- Immunology
Context:
- Human herpesvirus 6 (HHV-6), discovered in 1986, is the most ancient human herpesvirus.
- Variant B commonly infects young children, causing exanthema subitum and establishing lifelong latency.
- Reactivation of HHV-6, particularly in immunosuppressed individuals like transplant recipients, can lead to severe or fatal complications.
Purpose:
- To review the molecular characteristics, pathogenesis, and clinical implications of Human Herpesvirus 6 variants.
- To highlight the role of HHV-6 as a cofactor in various diseases and its interaction with other infections.
- To discuss diagnostic challenges and therapeutic options for HHV-6 infections.
Summary:
- HHV-6 infects CD4+ cells, establishes lifelong latency with salivary shedding, and reactivates under immunosuppression.
- HHV-6 is implicated as a cofactor in multiple sclerosis, chronic fatigue syndrome, lymphomas, and facilitates HIV and HPV progression.
- While serological differentiation is unreliable, PCR can distinguish variants. Antiviral drugs like ganciclovir are used for treatment and prophylaxis.
Impact:
- Understanding HHV-6 pathogenesis is crucial for managing post-transplant complications and associated chronic diseases.
- Accurate diagnosis through PCR is essential for effective treatment and chemoprophylaxis of severe HHV-6 manifestations.
- Further research into HHV-6 variant A's specific role in CD4+ cells and disease progression is warranted.
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