The 21st Annual International Meeting on the Molecular Biology of the Hepatitis B Virus, held Sept. 17-20, 2006 in Vancouver, Canada, continues to be the definitive international scientific meeting on hepatitis B and D.
More than 150 oral and poster
presentations were given, and 200
scientists from around the world
attended the meeting, which was
co-chaired by Drs. Ben Yen (U.S.)
and Ulrike Protzer (Germany) with
assistance from Ms. Fonta Reilly, HBF grants and education coordinator.
The Hepatitis B Foundation has
coordinated this meeting for the past
two years, and is pleased to accept the
steering committee’s invitation to become the official host of the meeting.
In a special ceremony, Dr. Jesse Summers was honored for his role in
co-founding the meeting and for his
outstanding science.
Some of the most exciting and hopeful reports at the HBV Meeting 2006 were about possible mechanisms of how HBV chronic infections are established.
Dr. Frank Chisari (Scripps Research Institute) – although hepatitis C virus induces more than 25 innate host defense type genes – a form of the immune system thought to be
important in chronic infections –
following infection, HBV induces
none that he could detect.
Dr. Rafi Ahmed (Emory U.) – a
molecule called PD1 on the surface
of an HBV-infected liver cell interacts with T-cells and results in a compromised immune response, which could explain why a chronic infection occurs.
Dr. Jorg Reimann (U. Ulm, Germany) – liver cells are deficient in proteins needed for “co-stimulation” of T-cells, which may explain why they are such good “homes” for chronic infection.
Drs. Jiaming Hu (Hershey Medical College) and Ju Tao Guo (Drexel U. and HBF) – independently reported that a protein-free, relaxed form of cccDNA accumulates in the liver
cell before becoming established,
suggesting a precursor state that
could explain how cccDNA is made.
Dr. Lorne Tyrell and colleagues
(U. Alberta, Canada) – provocative data that a new drug could destroy cccDNA!
Dr. Yosef Shaul (Weizman Institute, Israel)– reported a curious relationship between nutrition and HBV replication: in a starving mouse model, a cell
protein involved in “gluconeogenesis” was shown to activate HBV replication in a way that could be reversed by feeding the mouse.
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