'New drugs to prevent tuberculosis in the offing'

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LONDON: Researchers have identified a novel regulatory mechanism, which when deactivated, results
in
the death of
tuberculosis pathogen, an advance that could pave
the way for
new
drugs
to
prevent
the life-threatening disease.

According
to
the World Health Organization (WHO),
tuberculosis claimed over 1.3 million lives
in 2016, said researchers from
the University of Leicester
in
the UK.

The causative agent of
tuberculosis, Mycobacterium
tuberculosis, is a highly successful pathogen which can survive and grow
in humans for decades, according
to
the study published
in
the journal Cell Reports.

M
tuberculosis is a slow growing bacterium with a very thick and complex cell wall that is resistant
tomany common antibiotics, requiring
the development of
new
drugs and approaches
in order
to stop
thedeadly disease.

"M
tuberculosis is a nasty pathogen which is very difficult
to treat because of its unique biology," said Galina Mukamolova from
the University of Leicester.

"However, our research revealed weakness and vulnerable sides of this pathogen. We have shown that inactivation of just one protein can result
in dramatic consequences.

"We can interfere into
the very sophisticated mechanism for regulation of cell wall biosynthesis described
in our study
in order
to kill M
tuberculosis," Mukamolova said.

The team examined a protein called protein kinase B (PknB) found
in M
tuberculosis and found
thereasons why it is necessary for growth
in
the pathogen.

PknB has been known for many years and extensively studied by many scientific groups.

Previously, scientists showed that it was somehow involved
in regulation of cell wall biosynthesis, however
the precise mechanism was not clear.

"We have shown that CwlM, another protein required for M
tuberculosis growth, is
the main protein which is phosphorylated by PknB," said Mukamolova.


"This function makes PknB indispensable for
the growth of M
tuberculosis. We found that two forms of CwlM (phosphorylated and non-phosphorylated) coexist
in growing bacteria
in different cellular compartments and may regulate different arms of
the same process," Mukamolova said.


The research suggests that inactivation of CwlM, for example by using novel
drugs, would result
indeath and lysis of M
tuberculosis, researchers said.


This is an excellent target for
new drug development, which is particularly important because of
tuberculosis' rising resistance
to existing
drugs, they said.

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