MOST of us could gain extra years of life by ridding ourselves of a virus we don't even realise we are carrying - if new efforts to tackle the stealthy parasite bear fruit.
Between 50 and 80 per cent of people living in the UK, US and Australia are infected by cytomegalovirus, or CMV - a herpes virus closely related to the one that causes chickenpox. In some African countries, the figure is thought to be even higher.
CMV can lead to brain damage and hearing loss in newborns, but was long assumed to be harmless in healthy adults, says Allison Aiello, an epidemiologist at the University of Michigan in Ann Arbor. "Then HIV came along."
When people are infected with CMV and HIV, they can develop all sorts of nasty complications, such as CMV retinitis, which causes blindness. As researchers investigated further, they realised that the damaging effects of CMV were caused by its unique effect on the immune system.
Your body responds to any infection by training a small number of immune cells to recognise and remember the pathogen in future. CMV somehow cheats the system.
When the virus next attacks you, the immune T-cells trained to remember the virus do not work as they should. Instead, the body trains up a fresh batch of T-cells to recognise CMV, eating into your limited supply of untrained cells.
Over time, around 40 per cent of T-cells may be trained specifically to attack CMV, leaving fewer to tackle other possible infections.
A slew of research shows that this continual using up of untrained T-cells ages the immune system. The latest study suggests that this takes its toll on life expectancy.
For 18 years, Paul Moss at the University of Birmingham, UK, and his colleagues followed the health of more than 500 people over the age of 65. Around 70 per cent of the people were infected with CMV.
"We saw a four-year reduction in lifespan in the CMV-positive group," says Moss, who presented the findings at the American Association of Immunologists' annual meeting in Boston, last month.
To put that figure in perspective, Aiello says: "Smoking and drinking can take that much time off your life."
Those infected with CMV were more likely to die from cardiovascular disease, says Moss. The virus has also been linked to accelerated cognitive decline and poorer physical health generally - and it may leave the body more susceptible to other infections, such as flu.
Now the good news: Moss's team reckons that long-term treatment with antiviral drugs could help claw back those years.
His team infected 6-week-old mice with CMV and, once the rodents were 6 months old and the virus was established, they treated some of them with a drug used to treat herpes viruses.
While the number of untrained immune cells dwindled in the untreated mice, numbers remained high in the mice given antivirals.
"We were able to completely reverse this particular effect of CMV," says Moss. What's more, the treated mice appeared more resilient to being infected with flu further down the line, and lost less weight during that infection than their untreated counterparts. Moss presented this study in Boston, too.
He will soon begin trialling the antivirals in people over 65. "If we can strengthen the immune systems of older people, we will hopefully see a reduction in the incidence of flu infection, as well as reduced morbidity and mortality," he says.
Any treatment, however, might require people to take the drugs for months, if not years. What would be better, says Phil Stevenson at the University of Cambridge, would be to prevent infection in the first place by developing a vaccine.
"For CMV, the thing you want to stop is the primary infection," he says. Finding a way to block the entry of the virus will be tricky, though, partly because no one is sure exactly how CMV infects people.
The same problem applies to Epstein-Barr virus (EBV) - a related virus that can cause glandular fever and cancer.
A 30-year-long research programme to generate a vaccine for it failed, says Stevenson, because it began with an assumption that EBV first infects the body through the immune system's B-cells. This was where the virus was spotted in people presenting with symptoms.
To investigate whether the virus may be infecting other cells first, Stevenson's team turned to a mouse model.
They were able to make the virus glow by adding a gene for a light-emitting protein found in fireflies.
When Stevenson studied the mice a day after they had been infected, he found that the cells in their noses were the ones glowing (Journal of General Virology, DOI: 10.1099/vir.0.006569-0).
Posts
No comments:
Post a Comment