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"That stretch fascinates me," Whittaker says. "No other influenza ever in any species has this sequence apart from equine H7 virus."
It's the exposure of this sequence that Whittaker believes controls the virus's ability to invade the tissues of many regions of the body rather than just the lungs, as do the currently circulating equine influenza (H3) and human influenza (H1 and H3).
Structural biologist and co-investigator Brian Crane, an associate professor of chemistry and chemical biology, is focusing on the static structure of HA. It is known that when viruses enter cells they undergo a change in their structure. Collaborator Lois Pollack, an associate professor of applied and engineering physics, is interested in the dynamics of this change -- how the protein undergoes a change in shape and structure when entering the cell. Susan Daniel, an assistant professor of chemical and biomolecular engineering and an expert in using solid-supported lipid bilayers as mimics of cell membranes, is looking at what happens next, when the virus enters the host's cell and contacts the plasma membrane of the cell (which is a lipid).
"With this highly talented group of people, we can go deeper and deeper into the mechanism of how the virus recognizes the cell and undergoes its conformational change, right through to when it fuses with the lipids," Whittaker explains.
There is another equally compelling reason to study the activity of surface proteins of the equine influenza virus.
"Mutations occurring at the entry site are very often what allow host switching; that is, the virus's ability to jump from one species to another -- say from birds to horses or from birds to people," Whittaker points out.
The H7 serotype -- the first documented equine influenza virus -- was isolated from an equine outbreak in Czechoslovakia in 1956 that spread around the world. Subsequently it was shown that the virus was a very highly pathogenic H7 virus in chickens and other birds that had moved into horses. Now H7 is prevalent in birds, a fact that gives public health officials great concern.
Whittaker thinks there's a significant probability that the characteristics of H7 (which has never been studied in any kind of molecular detail before) as it infected horses in the 1950s would be similar to the characteristics of virus behavior when the next virus pandemic occurs in horses and in humans.
"The horse," Whittaker says, "can give incredibly valuable information for our global understanding of influenza."
The investigators also plan to study the serotype of the virus that caused the 1918 flu pandemic and today's avian influenza serotypes to try to figure out what distinguishes those from flu viruses now circulating in the human population.
SYMPTOMS OF THE CYTOKINE STORM:
The end stage, or final result, of cytokine storm (SIRS) or sepsis is multiple organ dysfunction syndrome (MODS). The end-stage symptoms of the bird flu, or other infection precipitating the cytokine storm may include:
fever (temperature of >38°C or >100.4°F)
Ischemia, or insufficient tissue perfusion (especially involving the major organs)
and multisystem organ failure (caused primarily by hypoxia, tissue acidosis, and severe metabolism dysregulation