The ongoing studies in our laboratory are concerned with making life as difficult for viruses as they do for us. To this end, we focus on several aspects of the interaction between viruses and their hosts. This approach has great promise but, surprisingly, the precise mechanism that underlies this technology remains unclear.
T cells play a key role in combating most viral infections.
Cytotoxic T lymphocytes lyse infected target cells and can also counter viral infection by secreting antiviral cytokines. However cytokine production is turned on within minutes after the cells encounter the appropriate antigenic stimulus. Remarkably, if the contact between T cells and antigen-presenting cells is disrupted, cytokine production ceases instantly, but production restarts immediately upon restoration of the antigenic stimulus. Such cells can limit viral replication and dissemination without destroying the infected cell. It is strongly implicated as an underlying cause of idiopathic dilated cardiomyopathy, the most common indicator for heart transplantation in young males.