This article is more than 5 years old. Information may no longer be current.
Molecular switch deactivates HCMV; may benefit organ transplantation
Click Here to Manage Email Alerts
Swiss researchers have discovered a molecular switch that operates human cytomegalovirus and may lead to new approaches for treatment and removal of the virus from organ transplants, according to study results.
The highly prevalent human cytomegalovirus (HCMV) causes lifelong infection, persisting in hematopoietic stem cells, researchers at the École Polytechnique Fédérale de Lausanne in Switzerland wrote in their study published in eLife.
The virus can remain dormant for years until it is reactivated and begins to multiply. In healthy people, the reactivated virus is quickly subdued by the immune system; however, these bouts can be fatal in people who are immunocompromised.
The researchers determined that a protein called KAP1, along with the protein HP1 and the SETDB1 histone methyltransferase, act as an off switch for the virus. In addition, the researchers found that HCMV could be forced out of latency with drugs that block KAP1 activity. In this study, they found that the malaria treatment chloroquine reactivated HCMV.
“Our discovery that HCMV can be forced out of latency by pharmacological manipulation suggests new avenues to eradicate infection by combing ATM and NF-kappa B activation with immune- or drug-based approaches aimed at killing HCMV-infected cells,” the researchers wrote.
As an example, the researchers said it may lead to treatments that purge dormant HCMV from bone marrow before it is transplanted into immunocompromised patients. – by Colleen Owens
Disclosure: The researchers report no relevant financial disclosures.
Click Here to Manage Email Alerts