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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.

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