|
| |
BREAK
THROUGHS IN HEALTH SECTOR |
| |
Dr.
Rajesh S Gokhale, National Institute of Immunology,
New Delhi |
| |
| |
| |
| Resisting
Rotaviral diarrhea |
| |
|
Rotaviral
diarrhoea contributes to 40% of the total
dehydrating diarrhoea disease in young
children, causing 150,000 deaths per year
in India.
The
first rotaviral diarrhoea vaccine specific
to India has now completed the first phase
of human clinical trial. Two candidate
vaccines 116E and I1321 were developed
under the Indo-US Vaccine Program. 116E
was developed by Dr. M K Bhan and Dr.Pratima
Ray |
|
|
|
(All
India Institute of Medical Sciences, New Delhi) &
Dr. Nita Bhandari (Society of Applied Studies, New Delhi)
in collaboration withDr. Roger I Glass, Center for Disease
Control and Prevention, Atlanta, USA. I1321was developed
by Dr. C.Durga Rao (Indian Institute of Science, Banglaore)
in collaboration with Dr. Harry Greenberg (Stanford
University, USA).
|
| |
|
According
to results of recent infant trials both
candidate vaccines have been deemed
safe and well tolerated. Vaccine take
was reported in 74% of the recipients
of candidate vaccine 116E wile in case
of I1321 the same was 40%. M/s. Bharat
Biotech International Ltd., Hyderabad
has produced a prototype vaccine of
116E, the most promising candidate under
GMP conditions. This will be followed
by larger clinical trials. A double-blind,
randomized placebo, controlled dose,
escalating phase Ib/IIa study has been
planned to evaluate the safety and immun-
|
|
|
|
ogenicity
of live attenuated rotavirus vaccine 116E in healthy,
non-malnourished infants, 8-20 weeks of age. |
| |
| New
pathway for combating Tuberculosis |
| |
Tuberculosis
affects more than one third of the world's population
and is a leading cause of morbidity and mortality
across the globe. When Mycobacterium tuberculosis
infects humans, it takes refuge in immune cells called
macrophages. To survive, mycobacterium requires iron
for sustenance. As free iron is not readily found
in an intra cellular environment, most bacteria manufacture
and secrete chemical compounds called siderophores
that scavenge iron from the environment. Although
siderophores were discovered over fifty years ago,
the genes involved in adding the long lipid chain
anchor that enables M. tuberculosis to do so more
efficiently remained a mystery till now.
Mycobacteria evolve siderophores with lipid-chain
tails that enable them to exploit the macrophage's
lipid-trafficking system to capture iron more efficiently.
Instead of using siderophores that diffuse freely,
mycobacteria anchor siderophores to lipid membranes
by means of a long fatty acid tail. After these siderophores
bind to iron within the macrophage, the lipid tail
makes the iron sticky enough to permit delivery to
the very compartment in macrophages where the mycobacterium
are lurking.

A
team led by Dr. Rajesh S Gokhale from the National Institute
of Immunology, New Delhi has identified five key genes
that enable M.Tuberculosis to acquire the iron it needs
for sustaining and promoting infection. They identified
the location of four genes that produce the lipid tail.
Since the gene required for the synthesis of siderophore
core called mbt-1 functions the same way, the new locus
and genes were named mbt-2 and mbt K, mbt L, mbt M and
mbt N. Targeting these genes is a good strategy for
preventing tuberculosis and other mycobacterial infections,
because some of these genes are conserved across a number
of related bacterial families, and are promising targets
for drugs to treat tuberculosis and other bacterial
diseases.
|
| |
|
| |
|
|
|