Chlamydia – HHV6 co-infections as promoter for ovarian cancer development
More than 95% of the human population is infected with Human herpesvirus-6 (HHV-6) during early childhood and maintain latent HHV-6 genomes for lifelong. Latent HHV-6 remains in a non-infectious state with limited activity in their host and not accessible to the host’s immune system. One possible way by which HHV-6 achieves this stage is by integrating into telomeric ends of human chromosomes, highly repetitive sequences that protect ends of chromosomes from damage. About 1% of humans are born with an inheritable form of HHV-6 (ciHHV-6). Various stress conditions can reactivate latent HHV-6 thus causing severity in multiple human disorders. Recently, we have identified Chlamydia infection as a natural cause of latent HHV-6 reactivation. Such viral reactivation and subsequent removal of viral genome from telomere can end up in telomere fusion leading to subsequent genomic instability. We investigate the hypothesis that Chlamydia-induced HHV-6 reactivation in ovarian epithelial cells can contribute to development of ovarian cancer.