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Larry J. Anderson, MD

Professor
Emory Vaccine Center

Professor and Marcus Chair of Infectious Diseases
Department of Pediatrics, Emory University School of Medicine

Phone: 404-712-6604

Fax: 404-727-8249

Email: larry.anderson@emory.edu

Larry J. Anderson, MD joined the Division of Pediatric Infectious Disease, Emory University School of Medicine as Professor and Marcus Chair of Infectious Diseases in 2010 after 33 years at the Centers for Disease Control and Prevention (CDC). His laboratory is focused on studies of the pathogenesis of respiratory syncytial virus (RSV) to guide vaccine development and the asthmatic immune response to RSV and rhinovirus to identify novel approaches to treating asthma exacerbations.

Research Interests

Pathogenesis of Respiratory Syncytial Virus (RSV) Disease: Our laboratory is focusing on pathogenesis of respiratory syncytial virus (RSV) disease to support development of vaccines and anti-viral treatment. RSV is the single most important cause of serious lower respiratory tract disease in the infant and young children and a high priority for vaccine development. Unfortunately, efforts to develop RSV vaccines have failed. Our laboratory is using the BALB/c mouse model and human airway epithelial cell lines plus human peripheral blood mononuclear cell (PBMC) cell culture system to explore virus induced host responses that contribute to disease and ways to prevent these responses. For the last 10 years, we have focused much of this work on the RSV G protein and its CX3C chemokine motif. The G protein and this motif appear to contribute to induction of a Th-2 type T cell response and enhanced pulmonary inflammatory after RSV infection and FI-RSV vaccination. For example, administration of a monoclonal antibody that bind G near the CX3C motif and blocks binding to CX3CR1 before or after challenge decreases the pulmonary inflammatory response in naïve or FI-RSV vaccinated mice. A G peptide vaccine that induces antibodies that block binding to CX3CR1 also blocks the Th2-type pulmonary inflammatory response seen after RSV challenge in FI-RSV vaccinated mice. We are using G peptide vaccines, anti-G monoclonal antibodies, clinical RSV isolates with different disease manifestations in mice, and genetically engineered viruses to 1) understand pathogenesis of RSV disease and especially that associated with the G protein and the CX3C motif on G and 2) develop novel approaches to making a safe and effective RSV vaccine.

Rhinovirus Infection and Asthma: Our laboratory is also looking at rhinovirus and RSV infection as a way to understand asthmatic immune responses and identify novel ways to treat asthma exacerbations. Asthma is a major cause of disease globally and associated with ~1.75 million asthma-related emergency department visits and ~456,000 asthma-related hospitalizations in the United States in 2007. Rhinoviruses and RSV have both been associated development and/or exacerbations of asthma and provide a way to study the “asthmatic immune response”. We are applying our human airway epithelial cell and PBMCs model to rhinovirus and RSV infection as a probe of the asthmatic immune response. These studies should identify 1) viral and host factors associated with asthma and 2) novel approaches to treating the disease.