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Archive - Apr 15, 2012

Blood Type A May Predispose to Some Rotavirus Infections

Whether you become infected by some strains of rotavirus may depend on your blood type. Some strains of rotavirus find their way into the cells of the gastrointestinal tract by recognizing antigens associated with the type A blood group, a finding that represents a new paradigm in understanding how this gut pathogen infects humans, said Baylor College of Medicine (BCM) researchers in an online report published on April 15, 2012 in the journal Nature. Rotavirus is a major intestinal pathogen that is the leading cause of severe dehydration and diarrhea in infants around the world. An estimated 500,000 people worldwide die from the infection annually. The structure of a key part of a strain of the virus known as P[14] provides a clue to how the virus infects human cells, said Dr. B. V. Venkataram Prasad, professor of biochemistry and molecular biology at BCM and the report's corresponding author. In strains of rotavirus that infect animals, the top of a spike on the virus attaches to the cell via a glycan (one of many sugars linked together to form complex branched-chain structures) with a terminal molecule of sialic acid. The same did not appear to be true of virus strains that infect humans, and scientists believed the human rotavirus strains were bound to glycans with an internal sialic acid molecule, but they did not know how this occurs. "We wondered how this genotype of rotavirus recognized a cellular glycan," said Dr. Prasad. "With colleagues at Emory (University School of Medicine), we did a glycan array analysis to see which glycans interacted with the top of the virus spike (called VP8*)." The only type of glycan that interacted with VP8* was type A histo-blood group antigen, he said. "That was surprising," he said.

Pac Bio Sequencing Technology ID’s FLT3 Gene As Therapeutic Target in AML

Through a groundbreaking new gene sequencing technology, researchers have demonstrated that the gene FLT3 is a valid therapeutic target in acute myeloid leukemia, AML, one of the most common types of leukemia. The technique, developed by Pacific Biosciences, allows for the rapid and comprehensive detection of gene mutations in patients with AML. The findings, published online on April 15, 2012 in Nature, are a result of collaboration among scientists at the University of California, San Francisco, Pacific Biosciences, Mount Sinai School of Medicine, and other institutions. The discovery may help lead to the development of new drugs to treat AML. "By sequencing the FLT3 gene in AML patients who have relapsed on therapy targeted against FLT3, we have determined that FLT3 is a valid therapeutic target, and this will certainly help us better understand the physiology of this type of leukemia in order to help us develop new therapies in the future," said Andrew Kasarskis, Ph.D., who performed the research with colleagues at Pacific Biosciences prior to becoming Vice Chair of the Department of Genetics and Genomic Sciences at Mount Sinai School of Medicine. "In addition, sequencing hundreds of single molecules of FLT3 allowed us to see drug resistance mutations at low frequency. This increased ability to see resistance will let us identify the problem of the resistance sooner in a patient's clinical course and help us take steps to address it." Historically, DNA sequencing of individual molecules in a mixture has been difficult and time-consuming to achieve. However, Pacific Biosciences' single-molecule real-time sequencer, the PacBio® RS, identified mutations in the sequence reads obtained in a single run even at low levels, on the order of 1 to 3 percent of total sequence reads.