LOS ANGELES (CNS) - HIV-infected individuals often suffer from
``substantial'' premature aging which can cut nearly five years off a patient's
lifespan, according to new UCLA-led research published today.
The impact of the disease within three years of initial infection can
accelerate biologic changes associated with normal aging relative to
chronologic age, the research found.
``Our work demonstrates that the early months and years of living with
HIV have already set into motion an accelerated aging process at the DNA
level,'' said lead author Elizabeth Crabb Breen, professor emerita in the
Cousins Center for Psychoneuroimmunology, department of psychiatry and
biobehavioral sciences at the David Geffen School of Medicine at UCLA.
``This emphasizes the critical importance of early HIV diagnosis and an awareness of aging-related problems, as well as the value of preventing HIV
infection in the first place,'' she said.
The study has been published in the peer-reviewed journal iScience.
Previous research has suggested that HIV, and antiretroviral therapy
to keep the infection under control, are associated with earlier onset of age-
related conditions such as heart and kidney disease, frailty, and difficulties
with cognition. While this may represent accelerated aging, there is no
consensus on what constitutes normal aging or how to define it, according to
the researchers.
Breen says the study is the first to match individuals who became
infected with patients who remained uninfected for comparison. The research
followed people from before to after their initial HIV infection in order to
trace the biologic changes they undergo over a two- to three-year period.
For the study, researchers examined how HIV affects epigenetic DNA
methylation, a process cells use to turn genes on or off to help support normal physiological changes. Epigenetics refers to changes made in response to the influence of environment, behaviors, and other outside factors, that affect how genes behave without changing the genes themselves.
The researchers examined five epigenetic measures of aging. Four of
them are epigenetic ``clocks,'' each of which uses a slightly different
approach to estimate biologic age acceleration in years relative to chronologic age. The fifth estimates the length of telomeres, protective cap-like parts at the ends of chromosomes that become shorter with age as cells divide until they become so short that cell division is no longer possible.
They examined these epigenetic measures in stored blood samples
collected within six months before, and again two to three years after, HIV
infection in more than 100 participants in the Multicenter AIDS Cohort Study,
and in a matched group of the same number of MACS participants of the same age and over the same time period who remained uninfected with HIV.
The MACS -- now part of the MACS/WIHS Combined Cohort Study, or MWCCS -- is a large-scale nationwide study using demographic factors, habits, disease history, and sexual history among men who have sex with men to examine the natural history of HIV infection and AIDS.
All participants have regular study visits, usually about six months
apart, at which testing for HIV infection is performed, and blood and other
samples are collected and stored for research use.
UCLA researchers say it is one of the few cohort studies in the world
to have biological samples available both before and after documented HIV
infection in the same people.
Infected individuals showed significant epigenetic age acceleration in
each of the four epigenetic ``clocks,'' ranging from 1.9 to 4.8 years, as
well as telomere length shortening from pre- to post-HIV infection in the
absence of highly active antiretroviral treatment.
Similar age acceleration was not seen in uninfected participants over
the same time interval, according to the study.
``Our access to rare, well-characterized, samples allowed us to design
this study in a way that leaves little doubt about the role of HIV in
eliciting biological signatures of early aging,'' said senior author Beth
Jamieson, professor of medicine in the division of hematology/oncology at the
Geffen School.
``Our long-term goal is to determine whether we can use any of these
signatures to predict whether an individual is at increased risk for specific
aging-related disease outcomes, thus exposing new targets for intervention
therapeutics,'' she said.
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