Work is already underway on vaccines that take a different approach to priming the disease-fighting immune system to protect high-risk groups, including children with sickle cell disease, said the study's corresponding author, Jason Rosch, Ph.D., an assistant member of the St. Jude Infectious Diseases department. "These results will help guide vaccine design going forward," he said.
Sickle cell disease is caused by an inherited mutation in the gene that carries instructions for making hemoglobin. That is the protein red blood cells use to carry oxygen. The mutation leaves red blood cells prone to the sickled shape that gives the disease its name and is also responsible for the episodes of intense pain, organ damage and other problems associated with the life-shortening disease. About 300,000 infants are born with sickle cell disease each year, making it the world's most common genetic disorder.
For this study, scientists compared the genomes of 322 pneumococcal bacteria collected from sickle cell patients between 1994 and 2011 to DNA from 327 strains obtained from individuals without sickle cell disease.
The analysis revealed that over time, the genomes of bacteria isolated from sickle cell patients shrank as genes and the corresponding DNA were discarded or combined. A comparison of the bacterial genomes from individuals with and without sickle cell disease suggested the changes reflected bacterial adaptation to their sickle cell host and contributed to the bacteria's ability to persist despite advances in preventive care.
Using a technique called transposon sequencing (Tn-seq), researchers showed that the bacteria's ability to cause widespread infection in mice with and without sickle cell disease was drama
|Contact: Summer Freeman|
St. Jude Children's Research Hospital