Analysis of cytomegalovirus binding/entry-mediated events.

The broad cellular tropism of human cytomegalovirus (HCMV) is a direct consequence of the multifaceted viral entry process involving a combination of viral glycoprotein and cellular receptor interactions that carefully orchestrate viral binding and penetration events. Although recent strides have been made in elucidating the molecular mechanisms of HCMV entry, it has become increasingly clear that the first step of the viral life cycle is exquisitely complex and dependent on several factors including virus strain and cell type. The lack of a full understanding about HCMV entry emphasizes the need for molecular techniques that can help to identify the specific roles of viral glycoproteins and cellular receptors during the viral entry process.

The HCMV gH/gL/UL128-131 complex triggers the specific cellular activation required for efficient viral internalization into target monocytes.

We have established that HCMV acts as a specific ligand engaging and activating cellular integrins on monocytes. As a result, integrin signaling via Src activation leads to the functional activation of paxillin required for efficient viral entry and for the biological changes in monocytes needed for viral dissemination. These biological/molecular changes allow HCMV to use monocytes as "vehicles" for systemic spread and the establishment of lifelong persistence.

A quantitative evaluation of cell migration by the phagokinetic track motility assay.

Cellular motility is an important biological process for both unicellular and multicellular organisms. It is essential for movement of unicellular organisms towards a source of nutrients or away from unsuitable conditions, as well as in multicellular organisms for tissue development, immune surveillance and wound healing, just to mention a few roles(1,2,3). Deregulation of this process can lead to serious neurological, cardiovascular and immunological diseases, as well as exacerbated tumor formation and spread(4,5).