Anice Lowen, PhD
Emory University School of Medicine
Dr. Lowen is an Associate Professor in the Department of Microbiology and Immunology, Emory University School of Medicine. She obtained her PhD from the University of Glasgow, UK, and carried out postdoctoral training at Mount Sinai School of Medicine in New York, NY.
Despite its clear importance to the epidemiology of influenza, the process by which human influenza viruses travel from one individual to another is not well understood. Prior to the zoonotic outbreak of H5N1 influenza viruses in Southeast Asia, it was generally assumed that if an influenza virus could productively infect a given host species, that virus would also transmit among individuals of that species. The lack of transmission of H5N1 influenza viruses among humans and other mammals has shown that, on the contrary, viral growth is not the only prerequisite for transmission. Research over the past six years has revealed that viral, host and environmental factors each play a role in determining the efficiency with which an influenza virus transmits. We previously showed, for example, that ambient conditions of humidity and temperature have a strong impact on the efficiency of transmission, that host-specific adaptive changes in the viral polymerase can alter transmission efficiency, and that host immunity resulting from either vaccination or natural infection limits transmission to varying degrees. Despite such progress, an in-depth understanding of transmission remains a high priority in the influenza field. Going forward, my research will focus on the viral traits which allow transmission to proceed in guinea pigs, a mammalian model system which we have demonstrated to reflect humans well in terms of influenza virus transmissibility.
Reassortment is the process by which influenza viruses, which carry RNA genomes comprising eight segments, exchange genetic material. Reassortment of the genome segments of two differing influenza strains has the potential to vastly increase the diversity of circulating influenza viruses. The contribution of reassortment to the process of antigenic shift has long been recognized: the viral strains which initiated the 1957, 1968 and 2009 pandemics all arose through reassortment. That reassortment also makes a major contribution to the more gradual process of antigenic drift has more recently become apparent with the increased availability of whole genome sequences. Despite its importance to influenza virus evolution, the frequency with which reassortment occurs in an animal infected with two or more variant viruses is unclear. I therefore propose to assess the incidence of reassortment in experimentally infected guinea pigs. By studying the process under well-controlled conditions, I aim to identify factors which dictate how readily reassortment can occur. For example, the roles of pre-existing immunity to one subtype, sequential rather than coincident infection, genetic compatibility between differing viruses, and the likelihood of two distinct strains to infect the same cell type will be studied.
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