Abstract

HIV-infected individuals show significantly shorter leukocyte telomere length compared with uninfected controls.1–4 This may translate to accelerated cellular aging and immunosenescence in the HIV population. HIV-related factors, such as duration of HIV infection or severity of HIV disease progression, fail to explain the variance in telomere length associated with HIV infection. Although nucleoside reverse transcriptase inhibitors can inhibit human telomerase in vitro,5,6 no associations have been reported between telomere length and exposure to nucleoside reverse transcriptase inhibitors in vivo.7,8 In fact, exposure to combination antiretroviral therapy has been associated with longer telomere length in individuals living with HIV.9,10 In observational studies, smoking, alcohol, higher body mass index, and low income have been previously associated with shorter telomeres in the general population. However, these factors were not significantly associated with telomere length among the HIV-infected participants,4 suggesting that HIV infection masked their negative effects on telomere length. Among HIV-infected individuals, high HIV viral load set point has been independently associated with shorter telomeres in 2 independent studies.4,11 This is consistent with the reported association between shorter telomeres and poorer immunological recovery in persons living with HIV and achieving virological control on combination antiretroviral therapy.12 In addition, a history of hepatitis C virus (HCV) infection has been associated with shorter telomeres in both HIV-infected and uninfected individuals.4,13 A recent study reported that although telomere length in HIV-infected individuals was shorter than that in uninfected persons, the slope of telomere length vs. age was no different, suggesting an acute shortening early on during the course of infection.11 Our aim was to measure telomere length before and immediately after HIV and/or HCV seroconversion and explore whether apparent telomere shortening occurs immediately after HIV/HCV seroconversion, or rather over time throughout the chronic infection period.

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