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. 2013 Jan;8(1):81-101.
doi: 10.2217/fvl.12.127.

Impact of age on markers of HIV-1 disease

Vanessa Pirrone  1 , David J Libon, Christian Sell, Chad A Lerner, Michael R Nonnemacher, Brian Wigdahl
Affiliations

Impact of age on markers of HIV-1 disease

Vanessa Pirrone et al. Future Virol. 2013 Jan.

Abstract

Aging is a complicated process characterized by a progressive loss of homeostasis, which results in an increased vulnerability to multiple diseases. HIV-1-infected patients demonstrate a premature aging phenotype and develop certain age-related diseases earlier in their lifespan than what is seen in the general population. Age-related comorbidities may include the development of bone disease, metabolic disorders, neurologic impairment and immunosenescence. Age also appears to have an effect on traditional markers of HIV-1 disease progression, including CD4+ T-cell count and viral load. These effects are not only a consequence of HIV-1 infection, but in many cases, are also linked to antiretroviral therapy. This review summarizes the complex interplay between HIV-1 infection and aging, and the impact that aging has on markers of HIV-1 disease.

Keywords: HIV-1; aging; comorbidities; disease progression; neurocognitive impairment.

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Figures

Figure 1
Figure 1. HIV-1 infection initiates a premature aging response
Normal aging-related disease states that are observed in the elderly occur at much younger ages in HIV-1-infected patients. These disease states include enhanced neurologic decline, metabolic/cardiovascular diseases including dyslipidemia, lipodystrophy and diabetes, immune system dysfunction and bone disease. HAART also seems to play a role in premature aging.
Figure 2
Figure 2. Immune regulation in response to aging and HIV-1 infection
As an individual ages, immune competence declines and changes occur in the overall function of the immune system. With aging, the number of terminally differentiated CD8+ T cells increases, while their ability to proliferate decreases and CD28 expression decreases. There are also fewer naive CD8+ T cells. Aging also decreases the number and function of CD4+ T cells. This decrease has also been shown to lead to a decrease in the overall CD4+:CD8+ T-cell ratio. HIV-1 infection itself also induces changes in the overall number and function of CD4+ T cells, increasing the number of terminally differentiated CD8+ T cells and decreasing the ability of CD8+ T cells to proliferate. Even though the number of CD4+ T cells decreases, the number of memory CD4+ T cells increases; however, these memory cells are less able to respond to pathogens. Blood monocytes and tissue macrophages typically have a decreased level of activation in older, uninfected patients. Large increases have also been shown in CD14+/CD16+ receptors on mature monocytes in the elderly. This was similar to what was observed in younger HIV-1-infected patients. Within both the older uninfected population, as well as HIV-1-infected patients, macrophages appeared to have diminished microbicidal capability. However, not all aging-related changes have centered on a loss of function. IL-6 cytokine levels increase with aging, as well as independently with HIV-1 infection. p55- and p75-soluble TNF-α receptor levels also increase. These levels all increase further in HIV-1-infected patients as they age.
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