We all know about the deadly pathogens, but a new study reveals just how easy it is to create them.
The bacteria that cause the superbugs, or MRSA, are so abundant in our environment that scientists have been unable to stop them from spreading.
But a new genetic tool called “epigenetics” might be able to wipe them out entirely.
That could mean scientists can now kill off the bacteria without killing off our own bodies.
This new approach is based on a gene called Cas9, which makes the bacteria’s DNA double.
Cas9 is a key component of the genome of every bacteria, and it’s the gene that allows bacteria to replicate.
Researchers have long known that some of the strains of bacteria that make up the superbug species, including MRSA and methicillin-resistant Staphylococcus aureus, also have copies of this gene.
But these genes were not known to be able or willing to produce Cas9.
Now, a team led by Harvard Medical School microbiologist Michael E. Zaslavs of Harvard Medical Schools Division of Infectious Diseases has used genetic engineering to create a strain of MRSA that does not make Cas9 but instead copies its own gene.
“We’re very close to producing Cas9-free MRSA,” said Erika Sargent of the University of Arizona.
In other words, you won’t need to use a cocktail of antibiotics.
Scientists can now target Cas9 and its genes directly.
And the gene can be used to modify the bacteria to make it resistant to other antibiotics.
Researchers in India, Denmark, and the United Kingdom are developing a synthetic version of Cas9 that could also be used in clinical settings.
The goal is to produce a synthetic drug that would make the superbup less likely to become resistant.
But that’s just the beginning.
“This is not the end of the journey,” said Dr. Zislavs.
“Our goal is just to eliminate the need for antibiotics.”
So far, the researchers have tested Cas9 in human cells, and they’ve found it to work well.
But the next step is to test it in bacteria in the lab.
The researchers are working on creating a synthetic Cas9 gene that can be inserted into the genome.
Once that gene is inserted into cells, the gene’s activity is recorded.
If the gene is turned off, the activity drops.
Dr. Sarget said they’ve been able to block the activity of the Cas9 molecule by using fluorescent tags.
But in order to make the Cas 9 gene more active, researchers need to inject it into the cell culture.
This could be done with a gene that encodes a protein called Cas3, which encodes Cas9’s other two genes.
That protein could be injected directly into the cells of cells.
Once the Cas3 gene is injected, the Cas gene would be turned off.
Then the Cas protein would be released from the cell, and Cas9 activity would be recorded.
That’s how the researchers were able to produce the Cas1 gene, which also encodes the Cas7 gene.
The Cas1 and Cas7 genes are turned off by the Cas2 gene.
That means if the researchers inject the Cas6 gene into the culture, it would be able turn the Cas5 gene off.
So the researchers wanted to see if the Cas 6 gene would also be able.
To test that, they injected Cas6 into the bacteria cells.
They found that the Cas 7 gene was turned off too, but the Cas 5 gene was activated.
Dr Sargets team then injected Cas9 into the mice that were infected with MRSA.
Once they injected the antibiotic, the MRSA cells grew very slowly, and only one cell, called a MDA-MB-231, emerged.
“What we saw was that the MRSE was a superorganism that had no capacity to survive the antibiotic,” said Professor M.K. Gupta, of the Centre for Infection and Immunity, at Harvard Medical College.
“The MDA cells were dying very rapidly.”
So the MRME cells were able survive the antibiotics, but they weren’t able to reproduce.
“If the antibiotic was given for 24 hours and the MRMSEs didn’t survive the 24 hours, we would see a rapid decline in the number of cells that survived the antibiotic treatment,” Gupta said.
But if the antibiotic did survive the entire 24-hour treatment, they were able.
So Dr. Gupta and his team were able also to see how well the MRSSA bacteria reproduced.
They wanted to know whether the MRSSB cells survived the 24-hours, and so they injected a different antibiotic into them.
They were able in some cases to get some of them to reproduce, but there were still many MRSSBs.
And these MRSSAs had an entirely different set of genes from the MRSH cells.
“When you inject the antibiotic in these cells, they’re dying very slowly,” Gupta explained.
“And when you