Infection may cut about five years off an individual’s life span relative to an uninfected person
Research published last month in the 杂志 iScience suggests the viral infection accelerates biological changes in the body associated with normal ageing, and may rapidly cut about five years off an individual’s life span relative to an uninfected person.
“Our work demonstrates that even in the early months and years of living with HIV, the virus has already set into motion an accelerated aging process at the DNA level,” Elizabeth Crabb Breen, study lead-author from the University of California Los Angeles (UCLA) said in a statement.
“This emphasises 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,” Dr Crabb Breen said.
在研究中, scientists assessed stored blood samples from 102 male participants, collected six months or less before they became infected with HIV and again two to three years after infection.
The men were participants in the Multicentre AIDS Cohort Study, an ongoing nationwide study initiated in 1984.
Researchers then compared these test results with those of matching samples from 102 non-infected men of the same age taken over the same time period.
The analysis looked at how HIV affects a process in cells called epigenetic DNA methylation that turns genes on or off in the course of their normal biological changes.
These gene-activity changes are naturally made by cells in response to the influence of the environment, people’s behaviours, or other outside factors such as disease which affect how genes behave.
The study particularly looked at five epigenetic measures of ageing described in previous studies.
Four of these changes are what are known as epigenetic “clocks”, and each of them uses a slightly different approach to estimate biological age acceleration, relative to chronologic age.
The fifth measure, scientists explained, assessed the length of telomeres, which are protective cap-like ends of chromosomes.
Telomeres are known to become progressively shorter with age as cells divide, until they become so short that division is no longer possible.
Researchers found a “significant age acceleration” in each of the four epigenetic clock measurements, randing from 1.9 至 4.8 年.
They also observed telomere shortening over the period beginning just before infection and ending two to three years after, in the absence of highly active antiviral treatment.
相比下, scientists did not see a similar age acceleration in the non-infected participants over the same time interval.
“These longitudinal observations clearly demonstrate an early and substantial impact of HIV infection on the epigenetic aging process, and suggest a role for HIV itself in the earlier onset of clinical aging,” scientists wrote in the study.
Researchers say such a comparison between infected and non-infected people has not been done until now.
“The study reported here is the largest, and the first with matched HIV-uninfected controls, to longitudinally follow individuals over the course of becoming infected with HIV, and to document epigenetic changes consistent with accelerated biological aging,”他们补充说.
“Our access to rare, well-characterised 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,” Beth Jamieson, another author of the study, 说.
引用研究的一些局限性, scientists said the research included only men, adding that the results may not be applicable to women.
They added that the number of non-white participants was small, and the study’s sample size was insufficient to consider later effects of highly active antiviral treatment provided for HIV infection, or to predict clinical outcomes.
Another drawback of the study, 研究人员说, is that there is still no consensus on what constitutes normal ageing or how to define it.
“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,” Dr Jamieson added.