“Most of us carry a virus that ages our immune system and shortens our lives. Can we beat it?” begins a feature story in the June 23 issue of New Scientist.
The article (“Insidious virus steals our years”) goes on to explain how this virus – the herpesvirus called human cytomegalovirus (CMV) – does its damage; and previews research in the UK to test antivirals that could “help claw back” CMV’s immune damage and pursue a preventive vaccine. This work is particularly important for people with chronic fatigue syndrome (ME/CFS), many of whom are subject to CMV activations.
50% to 85% of the Population Infected
Half or more of the US, UK and Australian populations carry CMV – most often after infection in early childhood when it generally causes a bout of mild mono-like symptoms – without knowing it. But, like all herpesviruses (e.g., the chickenpox/varicella zoster virus and mononucleosis/Epstein-Barr virus), CMV can lie dormant in the body after the acute infection with the ability to reactivate.
Most people are aware that the chickenpox virus, for example, hides in the nerve fibers and often reactivates as painful, nerve-damaging “shingles” eruptions in older or immune-compromised adults. But until HIV/AIDS came along, researchers assumed CMV was harmless in healthy adults, the New Scientist article explains.
How CMV Decimates Immune Function
The AIDS researchers found that – in people infected with the HIV retrovirus – CMV was active and producing bad, sometimes life-threatening problems. And in investigating CMV, they discovered that it insidiously cripples the immune system as follows:
• Normally, on initial infection with a virus, the immune system trains immune T-cells to remember and recognize the virus in future.
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• However, the CMV virus somehow fools those dedicated T-cells so that they don’t recognize it when it is next encountered.
• So every time the CMV virus reactivates the immune system regards it as a new, previously unknown intruder, and keeps training up more useless T-cells. This is a process that continues until a large portion of all T-cells are essentially ‘disarmed’, leaving none to recognize CMV, and too few to take on other infections effectively.
• The result, according to an 18-year tracking study of 500 older adults led by Prof. Paul Moss at the University of Birmingham in the UK, is that life expectancy in CMV-positive individuals (70% of the group) is shortened by an average of four years.
• In particular, people in his CMV-infected study group were more likely to die from cardiovascular disease, Prof. Moss reported recently at the American Association of Immunologists annual meeting in Boston (“The biology and therapeutic management of the immune response to human cytomegalovirus in health and disease”).
• The CMV-infected group was also characterized by earlier cognitive decline, poorer health in general, and more susceptibility to infections such as influenza.
New Hope – Antiviral Trial and Vaccine Development
Dr. Moss reported on his team’s finding that the number of T-cells able to recognize CMV increased in CMV-infected mice treated with an antiviral drug “used to treat herpesviruses.” Meanwhile, in untreated mice, the number of CMV-dedicated T-cells diminished. Immune resistance also appeared to improve in the treated mice vs the untreated ones.
Now, according to the New Scientist article, Dr. Moss’s team is preparing to run an antiviral therapy trial in a cohort of people over age 65, to see if they can achieve similar improvements in infected humans.
Meanwhile, Dr. Phil Stevenson at the University of Cambridge is pursuing the development of a vaccine against CMV. So far his team has discovered, in intriguing animal studies that made infected cells glow using a protein that gives fireflies their light, that Epstein-Barr virus invades via cells in the nose.
Now Stevenson, et al. believe they’re close to identifying specifically which olfactory cells are involved, and how herpesviruses like EBV and potentially CMV are able to bind to them; and are on the trail of antibodies that could keep the viruses from binding to their target cells (i.e., the basis for a preventive vaccine).