Health and Medical News and Resources

General interest items edited by Janice Flahiff

How bacteria behind serious childhood disease evolve to evade vaccines (& related article about bad immunity genes)

Vaccines

Vaccines (Photo credit: www78)

How bacteria behind serious childhood disease evolve to evade vaccines

From the 29 January 2012 Science Daily article

 Genetics has provided surprising insights into why vaccines used in both the UK and US to combat serious childhood infections can eventually fail. The study, recently published in Nature Genetics, which investigates how bacteria change their disguise to evade the vaccines, has implications for how future vaccines can be made more effective…

n spite of the success of the vaccine programmes, some pneumococcal strains managed to continue to cause disease by camouflaging themselves from the vaccine. In research funded by the Wellcome Trust, scientists at the University of Oxford and at the Centers for Disease Control and Prevention in Atlanta studied what happened after the introduction of this vaccine in the US. They used the latest genomic techniques combined with epidemiology to understand how different serotypes of the pneumococcus bacteria evolve to replace those targeted by the initial vaccine.

The researchers found bacteria that had evaded the vaccine by swapping the region of the genome responsible for making the polysaccharide coating with the same region from a different serotype, not targeted by the vaccine. This effectively disguised the bacteria, making it invisible to the vaccine….

Why bad immunity genes survive -Utah study implicates arms race between genes and germs

 IMAGE: This electron microscope image shows yellow particles of a mouse leukemia virus named Friend virus emerging or “budding ” out of an infected white blood cell known as a T-cell. By…

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SALT LAKE CITY, Feb. 6, 2012 – University of Utah biologists found new evidence why mice, people and other vertebrate animals carry thousands of varieties of genes to make immune-system proteins named MHCs – even though some of those genes make us susceptible to infections and to autoimmune diseases.

“Major histocompatibility complex” (MHC) proteins are found on the surface of most cells in vertebrate animals. They distinguish self from foreign, and trigger an immune response against foreign invaders. MHCs recognize invading germs, reject or accept transplanted organs and play a role in helping us smell compatible mates.

“This study explains why there are so many versions of the MHC genes, and why the ones that cause susceptibility to diseases are being maintained and not eliminated,” says biology Professor Wayne Potts. “They are involved in a never-ending arms race that causes them, at any point in time, to be good against some infections but bad against other infections and autoimmune diseases.”

By allowing a disease virus to evolve rapidly in mice, the study produced new experimental evidence for the arms race between genes and germs – known technically as “antagonistic coevolution.” The findings will be published online the week of Feb. 6, 2012, in the journal Proceedings of the National Academy of Sciences.

Potts, the senior author, ran the study with first author and former doctoral student Jason Kubinak, now a postdoctoral fellow in pathology. Other co-authors were biology doctoral student James Ruff, biology undergraduate C. Whitney Hyzer and Patricia Slev, a clinical assistant professor of pathology. The research was funded by the National Science Foundation and the National Institute of Allergy and Infectious Diseases.

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February 9, 2012 - Posted by | Medical and Health Research News, Public Health | , , , , , ,

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