Emory Vaccine Center
Department of Medicine, Division of Infectious Diseases, Emory University School of Medicine
Yerkes National Primate Research Center
The research of Dr. Alberto Moreno focuses on malaria vaccine development and malaria pathogenesis. Dr. Moreno is an Assistant Professor in the Division of Infectious Diseases of the Department of Medicine at the Emory University School of Medicine and Affiliate Scientist at the Yerkes National Primate Research Center. He earned his M.D. from the Pontificia Universidad Javeriana in Bogotá, Colombia. Dr. Moreno was also a Fogarty International Fellow in the Department of Medical and Molecular Parasitology at the New York University Medical Center from 1990-1993. Before joining Emory in 2000, he headed the Immuno-parasitology Division at the Fundación Instituto de Inmunología, National University in Bogotá, Colombia.
Malaria is one of the most widespread infectious diseases, prevalent in over 100 countries worldwide. Although surveillance reports indicate a decline in malaria burden in the past decade that correlates with the local improvement on vector control policies, the development of an effective vaccine is critical for a sustainable malaria control strategy. Understanding of the complexities of the malaria parasite life cycle and the stage-specific immunity acquired by the host are serious obstacles for developing effective vaccines. Our vaccine approach is to induce multi-stage protective immunity by using chimeric constructs that include functional domains and several autologous promiscuous CD4+ T cell epitopes. We have designed and expressed several subunit vaccine candidates that have shown potential for future clinical pathway development using heterologous prime-boost immunization regimens.
A second area of interest is to understand the mechanisms of severe malaria in humans using the NHP models. Severe malaria is a major clinical complication of the two most prevalent human malaria parasites, P. falciparum and P. vivax. The molecular mechanisms involved in severe malaria pathogenesis involve both host and parasite factors. Plasmodium spp, an obligate intracellular parasite, has evolved strategies to modify the morphology and physiology of the parasitized cell and to modulate the immune response of the host. The most characterized pathophysiological event in P. falciparum malaria is the sequestration of infected erythrocytes. Interestingly, severe malaria can also be induced by P. vivax, a parasite that does not sequester, suggesting that a variety of molecular events are involved. We have extensively used the simian malaria parasites in macaques as optimal experimental animal models that reproduce the clinical outcome of humans infected with P. falciparum or P. vivax. The use of animal models in conjunction with omics tools and computational and mathematical analysis will provide robust information to understand in depth the complexity of the parasite-host interaction and to develop novel intervention measures.