HIV Accelerates Aging
A call for investigation
by Jules Levin
This CROI focused more on aging than any previous conference, but this serious concern is not receiving adequate attention from our research community. Preliminary research is demonstrating that HIV-positive individuals are aging more quickly than HIV-negative individuals and that the HIV virus, itself, is a major culprit in causing this. As a result, we have been seeing increases in non-AIDS-related co-morbidities and consequent deaths—is there a risk this could explode soon?
We have known for a while that immune activation is caused by HIV; this revs up the immune system to deal with HIV but, at the same time, wears it down. So, as we get older, the immune system is weaker than that in HIV-negative individuals, and this can reduce our ability to fight off cancers, diabetes, and diseases of the kidneys, heart, brain, and bones.
Also, HIV gets into parts of the body soon after initial infection. Apparently, highly active antiretroviral therapy (HAART) improves, but does not reverse, immune activation. We are uncertain how this affects the infected person 30 years into the future, although it appears that it causes premature aging and a weakened immune system. Numerous studies conducted in the past two years find that inflammation and premature aging of T-cells appear to be caused by HIV. The SMART Study, among others, finds that inflammation increases when patients take antiretroviral therapy (ART) treatment interruptions, and that the prevalence of non-AIDS-related co-morbidities and consequent deaths increases due to the inflammation resulting from treatment interruptions.
These findings are not new to HIV. For years, the published literature has been full of articles and research finding that inflammation is associated with co-morbidities like cognitive impairment, diabetes, heart disease, and kidney disease. Hepatitis C is also associated with causing kidney disease and perhaps cognitive impairment. On a particularly troubling note, two studies at CROI found that the brains of HIV-positive individuals had characteristics of HIV-negative individuals 15-20 years older. And metabolic abnormalities, including elevated triglycerides and diabetes, were associated with brain damage.
Researchers have become aware of such concerns only over the past year, but we hope that now they will respond by quickly conducting the right research to help us address the concerns. What is the issue? Isn’t it okay for HIV-positive individuals to get older just like everyone else, even if they do age faster? After all, we can’t have the fountain of youth, some people say. Nonsense.
The point is that HIV accelerates aging, and the consequences of this acceleration in HIV-positive individuals are troublesome, if not dire. About 20% of HIV-positive individuals are over 50 years old, a percentage that has increased by 25% in the past few years, and this trend is on the upswing, so perhaps in several years, as many as 40% will be over 50.
Obviously, this is likely to create a tremendous burden on patients but, less obvious, is that it will create a tremendous burden on the HIV care system in the U.S., which is already tremendously overburdened. We have not spent very much money in recent years to improve the HIV care system and it is straining at the seams. The economic demands of providing services related to the aging population have been overlooked. One study at CROI reported that the cognitive impairment rate among patients over 60 years old was 50%. Bone studies report 50% osteopenia rates and 5-20% osteoporosis rates at the stunningly young age of an average in the mid-40s. Osteoporosis is associated with increased frailty and mortality. A recent study has reported that HIV-positive individuals are much more “frail” than HIV-negative individuals. This can also lead to premature morbidity and mortality concerns.
This is arguably the number one issue for HIV-positive individuals in care in the Western world, but it will occur for the developing world as well, and perhaps be considerably worse for them. This problem cannot be ignored, but so far, it is not getting adequate attention. For years, we have all been giddy about the success of HAART, but the luster may be wearing off now and we might be facing, within a few years, more serious problems, as we age, than we’ve imagined thus far.
On a personal level, HIV-positive individuals should start a dialogue with their clinician about this problem, if they haven’t already. Screening and monitoring can be used to evaluate the development of co-morbidities. A bone DEXA is performed quickly, is inexpensive, and can detect bone loss, for which taking calcium and vitamin D supplements might help. Simple blood tests can monitor lipids, sugar, the kidneys, and the cardiovascular system. Blood tests for inflammation markers are easily available (hsCRP, IL-6, etc.). Monitoring, prevention, and timely treatment are crucial to stave off these complications.
In the meantime, the HIV research community cannot ignore the problem. I hope they will not! We need timely and good research to look for the mechanism of action by which HIV causes immune activation, senescence (aging), and inflammation; and we need to find treatment interventions now.
Jules Levin is the founder and director of the National AIDS Treatment Advocacy Project (NATAP), which educates individuals about HIV and hepatitis treatments, and advocates on behalf of people living with HIV/AIDS and HCV. See accompanying article, “Aging with HIV” by Victor Valcour, M.D. on page 37. Visit www.natap.org.
