This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. As the 20th anniversary for recognition of HIV-1 as the causative agent for AIDS and wasting syndrome is marked, HIV-1 and associated opportunistic infections are increasing world-wide. During these two decades, many emerging opportunistic pathogens have been recognized to infect humans, including Microsporida. These eukaryotic, intracellular parasites could conservatively account for chronic diarrhea in approximately 2.9 million people in the Sub-Saharan region alone posing life-threatening loss of nutrients and liquids. While microsporidians have been classified as both emerging/re-emerging pathogens and category B class of food and waterborne agents with bioterrorism potential, little is understood about the host response to these opportunistic pathogens. The proposed studies will define one of the mechanisms by which Encephalitozoons: E. intestinalis, E. cuniculi, and E. hellem 1) induce activation of macrophages 2) leading to augmentation of HIV-1 replication and 3) the secretion of a chemoattractant gradient, resulting in recruitment of monocytes which then can harbor and disseminate both the viral and parasitic infection to distant tissues. Development of specific therapies could be better designed if the basic mechanisms for how these microsporidians alter the immune system are defined. Introducing an in vitro assessment that mimics these mechanisms will not only help to elucidate possible areas for intervention such as interfering with the initiation of a chemokine cascade, but also provide and economical approach to look at drug therapies before going into animal models.
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