Abstract
Human herpesvirus-6 (HHV-6) exists in latent form either as a nuclear episome or integrated into human chromosomes in more than 90% of healthy individuals without causing clinical symptoms. Immunosuppression and stress conditions can reactivate HHV-6 replication, associated with clinical complications and even death. We have previously shown that co-infection of Chlamydia trachomatis and HHV-6 promotes chlamydial persistence and increases viral uptake in an in vitro cell culture model. Here we investigated C. trachomatis-induced HHV-6 activation in cell lines and fresh blood samples from patients having Chromosomally integrated HHV-6 (CiHHV-6). We observed activation of latent HHV-6 DNA replication in CiHHV-6 cell lines and fresh blood cells without formation of viral particles. Interestingly, we detected HHV-6 DNA in blood as well as cervical swabs from C. trachomatis-infected women. Low virus titers correlated with high C. trachomatis load and vice versa, demonstrating a potentially significant interaction of these pathogens in blood cells and in the cervix of infected patients. Our data suggest a thus far underestimated interference of HHV-6 and C. trachomatis with a likely impact on the disease outcome as consequence of co-infection.
Highlights
IntroductionHuman herpes virus 6 (HHV-6) is a ubiquitous pathogen with more than 90% seroprevalence in healthy adults
Total DNA extracted at 2 days post infection and 9 dpi was used for quantitative PCR [23] against Human herpes virus 6 (HHV-6) U94 ORF (Table S1)
We showed that active HHV-6 infection induces chlamydial persistence in HeLa cells
Summary
Human herpes virus 6 (HHV-6) is a ubiquitous pathogen with more than 90% seroprevalence in healthy adults. Chronic viral replication mostly occurs in salivary glands whereas HHV-6 persists in a latent stage in various tissue types including monocytes and bone marrow progenitor cells. Latent HHV-6 resides in the host cell as nuclear episome [1,2] or integrated into telomeric ends of host cell chromosomes. The later form of latent HHV-6 can be vertically transmitted in the germ line [3,4,5]. HHV-6 persists in a dormant state with minimal viral transcription or translation in human host cells without any clinical complications. Under various physiological conditions, latent HHV-6 is reactivated to form infectious viral particles (for further details see reviews [6,7,8]). Reactivation of latent HHV-6 can be achieved by treatment with chemical stimulators like
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