In industrialized countries cytomegalovirus (CMV) infects approximately half of the human population. However, due to the mild symptoms, most of the infected individuals are unaware of the infection. As a true member of the herpesvirus family, after initial infection, HCMV stays dormant in specific cell types. Occasionally, the virus wakes up (“reactivates”) and is shed in body fluids such as saliva to get transmitted to other individuals. In immunocompromised patients (e.g., transplant recipients) or following congenital infection of unborn children, CMV can lead to severe life threatening complications. Understanding how the virus persists, i.e. enters the dormant state (“latency”) and reactivates from it, is a prerequisite to develop new intervention strategies.
CMV infects a range of different cell types and is closely associated with these cells. Regardless of whether infection is initiated by newly entering virions or by reactivation from latency, the virus must reprogram the infected cells to ensure efficient transmission of viral progeny to neighboring cells. In tissues, CMV is mainly transmitted through direct cell-cell contacts. The way in which CMV mediates cell-to-cell transfer is not well understood, but it is believed that the virus utilizes the cytoskeleton of infected cells for this process.
By combining virological, biochemical and cell biological techniques we aim to understand how the cytomegalovirus UL25 proteins – a class of viral tegument proteins – alter the cytoskeleton and interfere with cellular pathways in order to facilitate viral cell-cell transfer and to ensure persistent infection.