September 2018
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www.theasianindependent.co.uk<br />
HEALTH<br />
<strong>September</strong> <strong>2018</strong><br />
15<br />
New way to attack<br />
herpes virus discovered<br />
by scientists<br />
into a human cell. Instead, it carries<br />
its viral DNA into the cell virus. To confirm their find-<br />
and continue creating a new<br />
along with proteins called PP71. ings, the team created a synthetic<br />
version of the virus that<br />
After entering the cell, it releases<br />
these PP71 proteins, which allowed them to adjust the levels<br />
of the IE1 proteins using<br />
enables the viral DNA to replicate<br />
and the infection to spread. small molecules. With this<br />
Normally, when a virus<br />
enters your cell, that cell<br />
blocks the virus's DNA and<br />
prevents it from performing<br />
any actions. A team of scientists<br />
have uncovered the mechanism<br />
that allows the herpes<br />
virus to replicate. Their study<br />
could open new therapeutic<br />
avenues to treat not only<br />
cytomegalovirus but other<br />
viruses as well.<br />
Human cytomegalovirus is a<br />
leading cause of birth defects<br />
and transplant failures. As it's<br />
evolved over time, this virus<br />
from the herpes family has<br />
found a way to bypass the<br />
body's defense mechanisms that<br />
usually guard against viral<br />
infections. Until now, scientists<br />
couldn't understand how it manages<br />
to do so. Normally, when a<br />
virus enters your cell, that cell<br />
blocks the virus's DNA and prevents<br />
it from performing any<br />
actions. The virus must overcome<br />
this barrier to effectively<br />
multiply. To get around this<br />
obstacle, cytomegalovirus doesn't<br />
simply inject its own DNA<br />
The researchers found that,<br />
while PP71 is still present in<br />
the cell, it activates another<br />
protein known as IE1. This<br />
happens within the first few<br />
hours of the virus entering the<br />
cell, allowing the IE1 protein<br />
to take over after PP71 dies<br />
technique, they could let the<br />
virus infect the cell while controlling<br />
how quickly the IE1<br />
protein would break down in<br />
the cell. The first author of the<br />
new study Noam Vardi said,<br />
"We noticed that when the IE1<br />
protein degrades slowly, as it<br />
normally does, the virus can<br />
replicate very efficiently. But if<br />
the protein breaks down faster,<br />
the virus can't multiply as well.<br />
So, we confirmed that the virus<br />
needs the IE1 protein to successfully<br />
replicate."<br />
This study could have broad<br />
implications for the scientific<br />
community, which has been<br />
struggling to determine how<br />
cells maintain their identity<br />
over time. During development,<br />
for instance, stem cells choose a<br />
path based on the proteins that<br />
surround them. But even after<br />
these initial proteins disappear,<br />
the specialized cells don't<br />
change. So, stem cells that turn<br />
into neurons during development<br />
continue to be neurons<br />
long after those proteins are<br />
gone. The new study could lead<br />
to a new therapeutic target to<br />
attack cytomegalovirus and<br />
other herpesviruses, such as<br />
Epstein-Barr virus that causes<br />
mononucleosis and herpes<br />
simplex virus 1 and 2 that produce<br />
most cold sores and genital<br />
herpes.<br />
'New drugs may help<br />
smokers kick the butt'<br />
Scientists say they have<br />
developed over a dozen drugs<br />
which may help smokers reduce<br />
their consumption of tobacco, if<br />
not quit altogether. The<br />
researchers from the<br />
Washington State University in<br />
the US created the substances<br />
with the potential to curb smokers'<br />
desire for nicotine by slowing<br />
how it is broken down in the<br />
body. The finding, published in<br />
the Journal of Medicinal<br />
Chemistry, targets a liver<br />
enzyme, called CYP2A6, which<br />
metabolises nicotine. Nicotine<br />
triggers the release of dopamine<br />
and serotonin, two pleasure<br />
causing chemicals produced by<br />
the body. However, as it gets<br />
metabolised, users can experience<br />
withdrawal symptoms like<br />
tingling in the hands and feet,<br />
sweating, anxiety and irritability.<br />
This is the feeling that the<br />
researchers are targeting, said<br />
Travis Denton, an assistant professor<br />
at the Washington State<br />
University. Denton and Philip<br />
Lazarus, a professor of pharmaceutical<br />
sciences, designed<br />
dozens of molecules that bind<br />
to CYP2A6 and inhibit its ability<br />
to metabolise nicotine.<br />
"If you inhibit CYP2A6, it<br />
should not bother your overall<br />
health," said Lazarus. "If we<br />
could specifically target this<br />
enzyme, people should be fine,<br />
and it will possibly help them<br />
stop smoking or at least<br />
decrease their amount of smoking,"<br />
he said. The researchers<br />
have tested their candidate<br />
drugs to make sure they do not<br />
disrupt other major enzymes<br />
that help the body metabolise<br />
other substances.<br />
This helped narrow the number<br />
of potential drugs down to<br />
18. Once the US Food and<br />
Drug Administration (FDA)<br />
verifies a drug's safety,<br />
clinical trials would begin to<br />
see how it works in a human,<br />
researchers said.<br />
Brain tumours may occur<br />
in children with common<br />
genetic SYNDROME<br />
Parents, please take note. The frequency of<br />
brain tumours has been underestimated in children<br />
with the common genetic syndrome-neurofibromatosis<br />
type 1 (NF1), a new study has<br />
found. According to the researchers, this disorder<br />
is characterised by birthmarks on the skin and<br />
benign nerve tumours that develop in or on the<br />
skin. Brain tumours are<br />
also known to occur in<br />
children and adults<br />
with NF1. They estimated<br />
that only 15-20<br />
per cent of kids with<br />
NF1 develop brain<br />
tumours. But the<br />
study, published in the<br />
journal Neurology:<br />
Clinical Practice,<br />
found that the frequency<br />
of brain tumours in<br />
this population was<br />
more than three times<br />
higher.<br />
"I'm not delivering<br />
the message anymore<br />
that brain tumours are rare in NF1. This study<br />
has changed how I decide which children need<br />
more surveillance and when to let the neurooncologists<br />
know that we may have a problem,"<br />
said senior author David H. Gutmann from the<br />
Washington University School of Medicine.<br />
Brain Magnetic Resonance Imaging (MRI) scans<br />
of children with NF1 characteristically show<br />
bright spots that are absent in the scans of unaffected<br />
children. Unlike tumours, they are generally<br />
thought to disappear in teenage years, the<br />
researchers said. Since brain tumours can be confused<br />
with harmless bright spots, it has never<br />
been clear whether finding these abnormalities<br />
via MRI should be a<br />
cause for concern, they<br />
added. For the study, the<br />
team developed a set of<br />
criteria to distinguish<br />
tumours from other<br />
bright spots. The<br />
researchers then<br />
analysed scans from 68<br />
NF1 patients and 46<br />
children without NF1<br />
for comparison.<br />
All but four (94 per<br />
cent) of the children<br />
with NF1 had bright<br />
spots, and none of the<br />
children without NF1<br />
did. Further, in 57 per<br />
cent of the children with bright spots, at least one<br />
of the spots was deemed likely to be a tumour,<br />
the research team found. Applying the new criteria<br />
to MRI scans will help physicians identify<br />
probable tumours, but that does not mean that all<br />
children with NF1 should be scanned regularly,<br />
the researchers cautioned.