Why are older people with human immunodeficiency virus more prone to age-related diseases?
Groundbreaking new drugs and treatments have impacted older people living with human immunodeficiency virus (PLWH). Thanks to combinations of drugs that are used to keep HIV infections under control, called combination antiretroviral therapy (cART), PLWH live longer because they suffer from fewer random infections and fewer cancers resulting from AIDS. While patients have gained years, their health remains precarious. There has been an increase in the number of age-related conditions these patients suffer, such as coronary artery disease, chronic obstructive pulmonary disease, and non-AIDS-defining cancers. Is there a connection between age and and HIV that causes these diseases to take hold?
This question sparked the interest of researchers eager to understand how these patients age and the precise nature of this heightened aging process. In particular, researchers want to understand if these age-related conditions are actually accelerated in PLWH or merely made more prominent.
As described in an article in Aging, Volume 9, Issue 3, entitled “Longitudinal study of surrogate aging measures during human immunodeficiency virus seroconversion,” researchers sought to identify the timing of an aging trigger along the course of HIV infection. Researchers found that the telomere length, a region of a chromosome that generally gets shorter as we age and is a surrogate marker of cellular aging, is shorter in patients with human immunodeficiency virus compared with HIV-uninfected individuals. But when they added in age as a factor, they found no difference between the two groups. This might suggest that abrupt shortening does indeed occur early on in the course of the disease, possibly at the period of intense immunosuppression related to acute HIV infection and prior to the institution of cART.
Critical time between the onset of HIV and start of cART therapy
This study has important scientific and clinical ramifications for persons living with human immunodeficiency virus (PLWH) who have survived to old ages. By observing changes to cells that occur in people with human immunodeficiency virus in their old age, researchers gather important clues into the susceptibility of these patients to age-related conditions. The goal is to shorten or prevent the onset of telomere shortening during the onset period of human immunodeficiency virus. Intercepting this process at this critical time period may be one strategy that can improve outcomes in an aging HIV-infected population.
The researchers initially looked at the aging biomarkers of a surrogate, lab-controlled representative group of intravenous drug users before and after acquiring HIV. They sought to identify when age acceleration might occur in HIV and to describe potential key biologic pathways that are disturbed during the period when HIV is first detected in the blood. Their research verified, for the first time, that there were changes in the biomarkers for aging shortly after HIV infection, suggesting that the time period shortly after HIV onset may be critical in the aging process of patients with HIV.
Given that this is a time where profound changes occur in the immune system, with rapid destruction of immune system boosting cells (CD4 T cells) and proliferation of cancer-killing cells (CD8 T cells), targeting this time period with immediate cART initiation may be one therapeutic intervention that can reduce downstream aging complications. This theory warrants further prospective study and may be of vital importance in a population whose demographics are quickly aging.