Tit Bits

 

    HIV: Targeting host genes for therapy

 

    By inactivating any one of five human genes, scientists can prevent HIV from entering and growing in immune cells.


    Antiviral therapies targeting host genes that the virus depends on, rather than targeting the virus itself, are promising because these genes do not mutate as frequently as viruses do. This could avoid the development of drug resistance. Bruce Walker at the Ragon Institute of MGH, MIT and Harvard in Cambridge, Massachusetts, and his colleagues screened the genome of human T cells and identified five genes not essential to cell survival whose inactivation protected cells from HIV infection. Cultured cells lacking these genes resisted HIV infection. The genes encode proteins that facilitate virus entry into human cells, and one that mediates cell aggregation, which allows the virus to spread between cells. The authors say their approach could also be used to find drug targets for other pandemic viruses.

Source: www.nature.com

 

Gut bacterium indirectly causes symptoms by altering fruit fly microbiome

 

     CagA, a protein produced by the bacterium Helicobacter pylori, can alter the population of microbes living in the fruit fly gut, leading to disease symptoms, according to new research published in PLOS Pathogens by Tiffani Jones and Karen Guillemin of the University of Oregon.

 

  Microbes living in the human gut normally help keep people healthy, but disruptions to this microbial community can promote disease. Infections with specific microbial species can disrupt the gut microbiome, but it is unclear how such disruption occurs and whether it promotes disease.

 

  In the new study, Jones and her colleagues used Drosophila fruit flies to test the effects of infection with H. pylori, which can cause gastric cancer in humans. They hypothesized that a protein associated with H. pylori called CagA disrupts the fruit fly gut microbiome and contributes to disease.

 

  To test their hypothesis, the researchers genetically engineered fruit flies to express the CagA protein in their intestines, without being infected by H. pylori. This allowed them to disentangle the specific effects of CagA from the overall effects of H. pylori infection. They found that CagA expression in the fruit fly gut caused excess growth of intestinal cells and promoted immune system responses that are associated with H. pylori infection.

 

 

Source: www.Phys.org



ENVIS CENTRE Newsletter Vol.15, Issue 4, Oct - Dec 2017
 
 
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