Previous work has shown using fixed-cell microscopy and biochemical assays that cAMP is transiently localized to the forming phagosome when the cells are ingesting opsonized zymosan particles. Additionally, increased levels of cAMP have been linked to reduced actin assembly, inhibition of phagosome-lysosome fusion and Sibutramine HCl acidification, and increased intraphagosomal Gelsenicine growth of pathogens. For these reasons, our results showing transient elevation of cAMP during the initial formation of the phagosome appear surprising. It is possible that a transient and localized burst of cAMP plays a role in mediating phagosome formation, although further studies will be necessary to clarify the functional importance of this finding. Additional work is also needed to further elucidate the spatial and kinetic effects of cAMP on phagosome trafficking and eventual pathogen destruction. The regulation of intracellular cAMP is essential to a variety of signal transduction events within cells. Previous work has shown a correlation between the amount of cAMP produced at the phagosome and the ability of the cell to internalize and kill an invading pathogen. The importance of cAMP as a negative regulator of phagocyte function is further indicated by the fact that several pathogenic microorganisms elevate cAMP in target host cells. Pathogens use cAMP to disable phagocytosis, intracellular killing and inflammatory mediator generation, thus allowing the pathogen to gain an advantage against the host. Perhaps premature elevation of cAMP by toxins or immunomodulatory compounds inhibits phagocytosis by prematurely inactivating essential early activities. These studies extend our understanding of cAMP signaling in phagocytosing macrophages by putting its dynamics into the context of signaling for phagocytosis. This is essential for understanding host pathogen interactions and the immunomodulatory effects of therapeutic agents that modulate cAMP levels. In single-stranded RNA viruses, genome sequence diversity affects infectiousness and pathogenicity in two ways.