Date: Monday, June 17th 2013
Gyan Bhanot, Rutgers University, USA
Room: 5161.0267 (Bernoulliborg)
FLU Pandemics, past, present and future.
Viruses are obligate parasites, needing hosts to survive, replicate and proliferate. Because of a high mutation rate and lack of error correction machinery, viral genomes evolve rapidly and become exquisitely adapted to specific hosts. However, spillovers between species are common. When such events occur, they can cause pandemics. As an example of this general theme, I will describe how the H1N1 Influenza A virus, which entered the human reservoir from birds, has adapted and evolved in humans since 1918. A study of viral sequences in humans shows that H1N1, while remaining highly infective, is evolving to become less visible to the immune system, thereby gradually coming to equilibrium (reducing its pathogenicity) in human hosts. It does so by changing the frequencies of certain sequence combinations in its RNA in a context dependent manner. Using oligonucleotides to infect dendritic cells, we showed that this effect can be traced to Toll-like receptors. As a second example, we will study the H5N1 virus, which caused a mini-pandemic a few years ago. This virus is also lethal in humans, but seems not to be transmissible between humans. A comparative study of H5N1 viral amino sequences in humans and birds shows that specific residues at loci on the HA protein are necessary for the virus to infect humans. Further, birds that become infected in spite of inoculation, have viral strains that do not have these mutations in the viral strains infecting humans. This suggests that inoculation of poultry may be a mechanism to keep the virus away from infecting humans. Our studies raise some novel hypotheses about how to approach emerging pandemics.
Colloquium coordinators are Prof.dr. M. Aiello (e-mail :
Prof.dr. M. Biehl (e-mail:
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