Latent Human Herpes Virus-6: functionally dormant but not extinct - a hidden 'transposon' awaiting the ideal trigger?

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Human herpesvirus-6 (HHV-6) achieves latency by integrating into human genome. Can activation
of integrated HHV-6 shorten telomeres and cause unstable telomeric ends that contribute to
disease? Can activated, partial or full-length viral genome reintegrate into human chromosome
or is it lost completely? Can latent or activated HHV-6 influence the host cell through partial
transcription or translation? Preliminary data shows that chromosomally integrated HHV-6 is not
always silent. Common drugs and environmental exposure can activate it. Whole or parts of viral
genome can shuffle in and out of host chromosomes resulting in genomic instability. Further,
the "semi-latent" virus is functionally active enough to influence cells without forming infectious
viral particles. Over 95% of human population carry latent HHV-6/-7 that can get activated
while exposed to specific, timely, relevant triggers. Hence, it might constitute a prime factor in
effectuating several human diseases, with thus far unidentified and unexplored origins.