Tests on brain samples from dead people have strengthened claims that Alzheimer’s disease may be caused by the same virus that causes cold sores.

"We think the virus is a very strong risk factor for the disease," says Ruth Itzhaki of the University of Manchester, UK – head of the team leading the investigation.

If confirmed by further research, the finding opens up the possibility of treating Alzheimer’s with acyclovir, a cheap antiviral drug used to treat cold sores, or even vaccinating against it.

One of the hallmarks of the incurable disease is the presence of sticky plaques, which seem to clog up the working of the brain and result in dementia.

Brain maps

The virus that causes cold sores – Herpes simplex type 1 – was found in 90% of plaque samples from six patients who had died of Alzheimer’s disease.

The virus was also found in 80% of the plaques in brain tissue from five "control" patients who didn’t die of Alzheimer’s, although they had far fewer plaques overall than the patients.

However, the most convincing evidence that the virus is linked with the disease came from scans mapping the whereabouts of the virus across the whole brain. These showed that, in the Alzheimer’s patients, 72% of the virus found was in the plaques, compared with just 24% in the non-Alzheimer’s brains.

"It’s very specifically located in the plaques, so it strongly supports the likelihood that the virus is a major cause of plaque formation," says Itzhaki.

In earlier studies, Itzhaki’s team demonstrated that when healthy brain cells are grown in culture and infected with HSV-1, they accumulate the same amyloid beta protein that is found in plaque.

Itzhaki’s team followed that up by showing that amyloid beta plaques formed in the brains of mice deliberately infected with the virus.

Now the new results provide direct evidence that the same happens in the brains of people with Alzheimer’s.

Antiviral attack

Itzhaki found that all six patients had inherited at least one copy of APOE-ε4 – a gene variant previously linked with higher risk of Alzheimer’s.

She speculates that the variant somehow impairs clearance of the amyloid protein from brain cells infected by the virus, or perhaps leads to excessive production of the protein in those cells. "It either enhances the damage, or makes the cells less efficient at repairing it," she says.

"We suggest the virus enters the brain in the elderly as their immune systems decline, and establishes a latent infection from which it is repeatedly reactivated by events such as stress, immunosuppression and brain inflammation," says Itzhaki.

In normal brains, the infection is kept under control, but in patients with the APOE-ε4 gene variant, the virus gets the upper hand, leading to Alzheimer’s.

Already, Itzhaki has followed up her findings to see if antiviral drugs like acyclovir reduce symptoms. "We’ve used the antivirals in infected human cells and found it reduced the burden of beta amyloid," she says. "It was obvious by eye that there were great reductions."

The next step, says Itzhaki, is to raise funds for a clinical trial. "All the evidence we have suggests it would work," she says.

Not everyone is convinced, however. "Although the new research provides some additional evidence supporting a link between the herpes virus and Alzheimer’s disease, there is considerable uncertainty around whether this is a promising avenue of research," says Clive Ballard, director of research at the UK Alzheimer’s Society.

A virus that causes a universal childhood infection is often passed from parent to child at birth, not in the blood but in the

DNA

, according to a new study.

Researchers found that most babies infected with the HHV-6 virus, which causes roseola, had the virus integrated into their chromosomes. Not only that, but either the father or mother also had the virus in the chromosomes, suggesting it was a germline transmission – passed on in egg or sperm.

"This is really a unique mechanism for congenital infections," said Caroline Breese Hall, a pediatrician at the University of Rochester Medical Center in New York who led the study.

Her team is now investigating what this means for the children.

"If you have a chromosome that has got a virus integrated into it, what does it mean? What does it do? Can it activate again? Can it start spewing out virus and cause problems? Can you get an immune response to it?" Hall said.

Fever and rash

The questions are critical because nearly everybody is infected with HHV-6. It is a herpes virus that causes roseola – an infection marked by high fever and the usual vague virus symptoms that may include respiratory or stomach problems.

About 20% of children also have a characteristic sudden rash that appears just as the fever breaks.

Hall’s team studied 250 infants, 85 with HHV-6. Of them, 43 were born with the virus and 42 were infected later.

Most of the babies born with the virus – a congenital infection – had the virus in the chromosome. Hall said the assumption had been that the virus somehow crossed the placenta from mother to child, but in 86% of cases, it was inherited directly in the genetic material.

Just 14% were infected across the placenta.

Tests showed either the mother or the father – but not both – also had HHV-6 in the chromosomes.

"Because we know a parent already had the virus in the chromosome, we know that it didn’t spontaneously wiggle its way in once the baby got it," Hall said.

Woven into DNA

There were several spots where the virus integrated into the DNA, but usually right at the end of the chromosome, where a key structure called the telomere is found. Telomeres protect the chromosome and are involved in aging and immune response.

The virus is everywhere in people who inherit it, Hall said. "In your hair, your nails, your skin, your blood, and at very high titers (levels)," she said.

The babies infected this way did not appear ill but Hall wants to follow them as they grow up to see if they develop normally. They all had antibodies to HHV-6, which is evidence of an immune reaction of some sort.

There is no drug licensed to treat HHV-6 infection.

Other viruses are known to integrate into the DNA and pass on from parent to child, but these so-called human endogenous retroviruses have never been known to cause symptoms or activate an immune response.

They say the difference between herpes and love is that herpes lasts forever. But new research hints at a way to chase the virus from its hiding place and get rid of it for good.

Unlike viruses such as HIV or smallpox that slay nearly every cell they encounter, herpes simplex virus-1 (HSV-1) – the cause of cold sores – is a docile beast. When we’re healthy, HSV-1 snoozes inside our neurons, secluded from drugs and the immune system, where it switches on a single gene called LAT.

When we catch a cold, because the virus can’t distinguish between a mild cold and a deadly fever, the virus flees to the body’s surface, where it infects and kills epithelial cells. "It’s sort of like rats leaving a sinking ship," says Bryan Cullen, a virologist at Duke University in Durham, North Carolina.

Now, by finding clues to how LAT works, Cullen’s team may have found a way to force the virus out of dormancy and onto the skin’s surface, where it’s easier to fight.

Hiding behind mRNA

Researchers suspected that LAT was the key to herpes’ ability to remain dormant inside nerve cells, but no-one knew how it did this. These nerve cells transcribe LAT into messenger RNA (mRNA), but while mRNA can usually be translated into a protein, mRNA from LAT doesn’t code for a protein and the cells usually just chew the mRNA to bits.

To determine the mysterious molecule’s job, Cullen’s team infected mice with HSV-1, and waited for the virus to retreat to nerve cells and go silent. Next, the researchers scoured the cells for traces of sliced RNA that matched that from LAT. Several hits turned out to be microRNAs, a recently-discovered kind of molecule that cells use to dial down the levels of proteins.

Four microRNAs came from cut-up LAT, while the fifth came from a previously unknown chunk of RNA, which suggests LAT isn’t the only viral DNA molecule involved in latency.

Collateral damage

Many microRNAs play a role in maladies such as cancer and heart disease, and some viruses even make microRNAs to stymie cell defences.

But in a twist, HSV-1’s microRNAs latch onto viral mRNA molecules, preventing them from being used as templates for proteins. As a result, the cells are prevented from cranking out two virus proteins (ICP0 and ICP4) essential for escaping dormancy, Cullen’s team found.

It may be possible to coax viruses out of hiding by blocking these microRNAs, and then treating patients with drugs that stamp out herpes in epithelial cells, such as acyclovir. "Every virus that pops out gets killed," Cullen says.

But this approach could prove troublesome because waking a virus seems to sacrifice the infected nerve cell, says virologist Patricia Spear, of Northwestern University in Evanston, Illinois. "You would be inducing replication of virus in the neuron and the question is how many neurons you want to kill off," she says.

Journal reference: Nature, DOI: 10.1038/nature07103

Vaccination has changed little since the time of Louis Pasteur. The method involves deliberately injecting a dead or inactivate organism into a person to stimulate their immune system to produce cells that fight off the fully fledged organism.

However, many infections have resisted all attempts at producing vaccines.
One of these is the herpes simplex virus type 2 (HSV-2), which is usually the cause of genital herpes.

Now Michal Margalith at Vical, a biopharmaceutical company based in San Diego, says he and colleagues have developed an HSV-2 vaccine using the emerging technology of DNA vaccines.

This involves injecting the patient with a circular piece of DNA called a plasmid that programs their cells to produce HSV-2 proteins that trigger an immune response. That should train the vaccinated person’s immune system to fight off the real virus.
The team says that the technique has successfully produced an immune response in mice. However, DNA vaccines are still highly experimental in humans.

The incidence of oral

cancer

due to a virus transmitted during oral

sex

has increased steeply over the last 30 years, according to research in the US. And scientists relate this trend to changes in people’s sexual behaviour.

The number of tongue, mouth and throat cancers due to the sexually transmitted human papilloma virus (HPV), which can also cause cervical cancer in women, rose by about a third from 1973 to 2004, say researchers.

The team led by Maura Gillison at Johns Hopkins University in Baltimore, Maryland, US, studied trends in oral cancers recorded by US National Cancer Institute registries.

Earlier work by this team and others had established a link between certain strains of the common sexually transmitted virus and oral cancer. The latest study, which looked at nearly 46,000 cases, is the first to quantify an increase in mouth and throat cancers due to sexual activity.

‘Vaccinate boys’

"What we do know is that the prevalence of HPV is high, particularly among young people and this shouldn’t be a surprise given that, since the sexual revolution, people have been having more sexual partners," says Lesley Walker, director of cancer information at Cancer Research UK.

The rise was largest among young white males, suggesting this group is more likely to have oral sex at a younger age now than it was 20 years ago, says Gillison’s team. It adds that further research on the role of race and sex, and oral sexual behaviour, is needed.

What is not in doubt, says Gillison, is the need to consider giving boys the HPV vaccine, to protect them from the disease.

A Merck vaccine is currently licensed for use in young women and girls to protect them against the most common cervical cancer-causing strains of HPV. These strains are also thought to cause oral cancer, as well as penile and anal cancer.

"We need to start having a discussion about those cancers other than cervical cancer that may be affected in a positive way by the vaccine," urges Gillison.

Cost concerns

One US campaign group, the Oral Cancer Foundation, is now calling on the US Food and Drug Administration to "move rapidly to approve the vaccination of young boys with the cervical cancer vaccine, to reduce the pool of HPV16 [a particularly aggressive strain]" and protect them from oral cancer.

Walker says however, given the high cost of such a programme, authorities might require more evidence that such a move really would prevent a significant number of male cancers.

Tonsil and throat cancers affect about two in every 100,000 adults in the US and about half a million people around the world each year.

Although, oral cancers linked to HPV infection have risen, the study notes the incidence of oral cancers in parts of the mouth or throat not linked to HPV infection remained constant until 1982, and then started to decline.

Gillison says this is probably due to falling consumption of tobacco and alcohol, which are also linked to the cancers.

Valentine’s Day is one of those western holidays that has spread worldwide, and it means something a bit different everywhere.

In Britain, Valentine’s cards are anonymous, which many North Americans would see as defeating the purpose. Meanwhile in Japan women (only) send men, not cards, but chocolates – different ones for family or colleagues than for sweethearts, and the recipient had better know the difference, and perhaps return the favour a month later on White Day, a Japanese innovation.

But here’s another Valentine’s Day innovation we can all get behind – in fact, there’s no reason to limit it to Valentine’s Day except for the connection to, well, love, or what sometimes passes for it.

A website called inSPOT allows people who have been diagnosed with a sexually transmitted infection to alert recent sex partners, anonymously if they wish, and the site guarantees it won’t divulge who sent what. The theory is that people are a lot more comfortable broaching difficult subjects online.

The e-cards range from tasteful to hilarious, our favourites being "You’re too hot to be out of action", "I got screwed while screwing, you might have too," and "Who? What? When? Where? It doesn’t matter," all followed by, "I got diagnosed with (fill in the blank from the drop-down menu which ranges from syphilis to shigella), you should get tested."

That menu doesn’t include HIV. There’s a separate card for that, which just says, "There’s no easy way to say this…" No joking around there. All the cards allow you to add a short personal message – or not – but I thought the card looked a bit too spammy and deletable without some personal connection.

Not romantic, but a very good idea, as sexual guards are lowered two decades after the first big AIDS scares and STIs are on the rise everywhere. Some of the cards are gay-oriented – the group currently at greatest risk – but the sites include information on STIs for women too.

The site focuses on a handful of cities in the US and Canada – plus Romania – and recipients based there can use the link on the e-card to find a clinic. But you don’t have to be in one of those cities to get, or send, the e-card.

Hey, it’s Valentine’s Day! Go out and get tested for the clap, or worse. Then celebrate a positive by telling the ones you love(d). At least the cards are better than most of the sentimental claptrap (pardon me) that will get sent the more usual way.

As ugly as cold sores look, the virus behind them may be uglier still. New evidence has supported the growing suspicion of a link between the herpes simplex virus-1 (HSV-1) and Alzheimer’s, especially in people who carry a specific gene variant.

The variant, called ApoE4, is present in about half of all people who develop Alzheimer’s, and around 30 per cent of Caucasians carry at least one copy of it. About 80 per cent of elderly people carry HSV-1, so any exacerbating effect could be having a huge impact. The good news is that antiviral drugs could slow Alzheimer’s progression in those with HSV-1.

Ruth Itzhaki and colleagues at the University of Manchester, UK, infected cultures of human brain cells with HSV-1 and found that it caused a dramatic increase in levels of amyloid beta protein – the main constituent of the plaques which form in the brains of people …

Viruses lurking in biological samples could be killed off with an intense pulse of visible light, new research shows.

Scientists in the US say the technique seems to have significant advantages over alternative methods, including use of UV irradiation or microwaves, as it kills viruses more effectively and safely.

The technique destroys a virus with a pulse of light from a low-power laser. The pulse produces mechanical vibrations in the virus shell, or capsid, irreversibly damaging and disintegrating it, and so "deactivating" the virus for good. The technique might be used to kill HIV, as well as hepatitis C, say the researchers involved.

Traditional methods of destroying viruses, such as UV irradiation, can cause mutations, which eventually make the micro-organisms resistant. UV light can also damage the DNA of surrounding healthy cells.

Scientists have also tried using microwaves to kill viruses but this is even less promising since the water in and around a micro-organism strongly absorbs this frequency of light. Most of the energy from the microwave radiation is absorbed by the water and does not even reach the virus itself.

Human cells undamaged

Kong-Thon Tsen of Arizona State University, and colleagues at Johns Hopkins School of Medicine, and the Uniformed Services University of The Health Sciences, all in the US, found that visible light can overcome this problem.

The researchers applied pulses of purple-coloured light lasting just 100 femtoseconds (10^-15 seconds) to viruses called M13 bacteriophages. It takes just a single pulse to destroy the viruses completely, say the researchers.

The "power density" of the laser is just 5 microjoules per square centimetre, which is low enough to leave surrounding human cells and tissue undamaged, but high enough to produce large-amplitude vibrations in a virus’s capsid. It is also too low to cause genetic mutations, meaning the virus will not build up resistant to the treatment over time.

Disinfecting blood

Tsen told New Scientist that the technique could be used to disinfect blood or other biological samples in hospitals.

"In addition, we believe that the method may be especially important in designing novel treatments for blood-borne viral diseases," he said. "For example blood dialysis allows us to irradiate a patient’s blood outside the body and potentially cleanse it of infectious virus particles before reintroducing it into the patient. In this way, we could reduce mortality associated with diseases like hepatitis C and AIDS."

The team now plans to test the efficacy of its technique in killing a wide range of deadly viruses, including HIV and hepatitis C. "We also plan to conduct further tests on the effects of the low-power visible laser on mammalian cells to determine any potential side effects and confirm that it selectively kills viruses," said Tsen.

When earthquakes, hurricanes or volcanic eruptions strike, communications systems are always vulnerable. If they go down, it becomes that much harder to coordinate an emergency response.

Aris Mardirossian of Maryland, US, is proposing a balloon-based communications solution. His emergency communications balloons will automatically inflate and launch when a natural disaster strikes or seems imminent.

The system consists of a set of ground- and air-based monitoring systems that look for signs of a natural disaster. These include the low atmospheric pressures and high winds that indicate a hurricane, the ground movement that accompanies an earthquake, and the noxious gases produced by a volcano. Balloons fitted with communications transmitters – similar to cellphone base stations – are then launched to ensure that communications channels remain open.

Read the full disaster balloons patent application.

ANTISOCIAL behaviour doesn’t just harm society – it may also harm the perpetrators’ health. That’s the message of a 30-year study examining the hidden costs of petty crime to society.

The researchers, who monitored 500 children for 30 years, found that naughty boys who didn’t reform in adulthood suffered worse health than their peers, including many who were equally deprived in childhood. The researchers are now seeking a way of identifying those who are most likely to become persistent offenders, with a view to intervening before it is too late.

"It’s the first study to demonstrate the link between children who engage in antisocial behaviour and deficits in physical health when they grow up," says study leader Candice Odgers of the Institute of Psychiatry at King’s College London. As well as accounting for more than their share of crime in later life, "they also incur hitherto unrecognised medical costs", she says.

Odgers analysed data on more than 500 men in their early 30s from a range of socio-economic backgrounds in Dunedin, New Zealand. The results, published in Archives of General Psychiatry (vol 64, p 476), show that individuals whose bad behaviour began in childhood and persisted into adulthood were twice as likely to be infected with the herpes virus and three times as likely to suffer from chronic bronchitis or gum disease as those who never engaged in bad behaviour.

Although these individuals accounted for just 10 per cent of the sample, they were responsible for 18 per cent of traffic injuries, 29 per cent of the days spent in psychiatric hospitals, 72 per cent of the months spent in jail and 42 per cent of the total months where study members were homeless or taken in by others.

Persistent offenders also had three times the healthy blood level of C-reactive protein, a marker that indicates raised risk of heart attacks or stroke. It is surprising to see this marked risk for heart disease in such young men, Odgers says. "As we follow them to their 50s and 60s, the health burden will likely get even worse."

Her analysis so far suggests that nurture plays a strong role in determining who is most likely to offend, and their subsequent health. For example, 40 per cent of persistent offenders came from families of low economic status, and 23 per cent experienced maltreatment as a child – at least double that in any other group.

Odgers’s study reinforces previous research that early intervention could help. Around a quarter of the sample were badly behaved as children, but reformed at adolescence. Many of them had the same deprived backgrounds as the persistent offenders, yet by the age of 32 they were almost as healthy as the controls.

The key question, says Odgers, is how to identify which boys are most likely to offend in later life. Possible markers include attention deficit hyperactivity disorder – which affected 38 per cent of persistent offenders – and a family history of alcohol addiction. Further analyses are under way to assess the impact of genes.