ENVELOPMENT
We are interested in understanding how viruses, particularly HCMV, obtain their final lipid envelope. While many viruses utilize the host ESCRT machinery in this process, we and others have found that HCMV envelopment is independent of ESCRT function. Our lab is interested in understanding this ESCRT-independent process. This includes identifying the viral factors involved and which, if any, cellular factors are utilized. We aim to elucidate both the players involved and the mechanism by which they cooperate to constrict and scission membrane as part of the envelopment process.
MEMBRANE TRAFFICKING
Viruses often rearrange host membranes and organelles to generate novel compartments to both protect viral products during replication and increase efficiency of the replication process. In the case of HCMV, viral organelles are organized in a juxtanuclear position referred to as the cytoplasmic viral assembly compartment. Rearrangement of these membranes, although not absolutely required for, greatly increases the efficiency of production of infectious virions. We are interested in understanding how this rearrangement of cellular organelles occurs. This includes understanding both the viral and cellular factors involved in both the initial rearrangement as well as the maintenance of this compartment.
PROTEIN TRAFFICKING
It is clear that HCMV induces a drastic change in the host proteome of the cell. Of particular interest are proteins that normally localize to the plasma membrane, many of which have been shown to be removed form their normal localization during infection. While the regulation of some these plasma membrane proteins, mainly those with immune implications, have been well characterized, how and why the virus down regulates the plasma membrane expression of many other proteins is not yet known. We are interested in understanding the regulation of these proteins. Is it merely a byproduct of infection or are they specifically targeted by the virus? Understanding which of these proteins are specifically downregulated by the virus and the functional consequences of blocking this regulation may identify new antiviral targets.