title: Thymic Function Is Most Severely Impaired in Chronic HIV-1 Infection, but Individuals With Faster Disease Progression During Early HIV-1 Infection Expressed Lower Levels of RTEs.
abstract: In HIV disease course, the decline of peripheral CD4 T-cell count correlates with rapid disease progression. The supply of peripheral naive T cells by the thymus requires precursor T-cell proliferation within the thymus. In the setting of HIV-1 infection, when both naive and memory T cells are progressively depleted, the contribution of thymic dysfunction in CD4 depletion needs to be studied. Previous research has shown that thymic function may also be impaired in HIV-1 infection. However, it is inconclusive regarding whether this impairment occurred at the early time or during the chronic phase. In addition, the relationship between thymic dysfunction and disease progression remains unknown. In this study, we examined the thymic function in 65 HIV-infected individuals. Among them, 17 were in acute phase, 15 were in early chronic phase, 15 were in chronic phase with no ART (antiretroviral therapy), and 18 were on ART. We also included 11 uninfected individuals as controls. We measured the peripheral blood levels of T-cell receptor rearrangement excision circles and PTK7 and CD31 expressions for the frequency of circulating recent thymic emigrants. We observed that the 2 indicators of thymic function, sj/β-TREC and PTK7, seemed to be lower in the chronic infection group than those in the acute and early chronic groups. Both indicators returned to the normal level after ART. However, after 1-year follow-up of patients with early HIV-1 infection, rapid progressors (n = 4) had lower PTK7 and CD31 expressions than chronic progressors (n = 6).
authors.affiliation: *Key Laboratory of AIDS Immunology of National Health and Family Planning Commission, Department of Laboratory Medicine, The First Affiliated Hospital, China Medical University, Shenyang, China; †Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, Hangzhou, China; and ‡Department of Clinical Laboratory, Dongying People's Hospital, Dongying, China.
authors.forename: Sijia
authors.initials: S
authors.lastname: He
authors.forename: Zining
authors.initials: Z
authors.lastname: Zhang
authors.forename: Yajing
authors.initials: Y
authors.lastname: Fu
authors.forename: Chaolong
authors.initials: C
authors.lastname: Qin
authors.forename: Sha
authors.initials: S
authors.lastname: Li
authors.forename: Xiaoxu
authors.initials: X
authors.lastname: Han
authors.forename: Junjie
authors.initials: J
authors.lastname: Xu
authors.forename: Jing
authors.initials: J
authors.lastname: Liu
authors.forename: Yongjun
authors.initials: Y
authors.lastname: Jiang
authors.forename: Hong
authors.initials: H
authors.lastname: Shang
mesh_terms: D000328:Adult; D019380:Anti-HIV Agents / Q000627:therapeutic use*; D015496:CD4-Positive T-Lymphocytes / Q000502:physiology*; D002908:Chronic Disease; D015658:HIV Infections / Q000150:complications* / Q000188:drug therapy; D015497:HIV-1; D006801:Humans; D008297:Male; D013950:Thymus Gland / Q000473:pathology*; D019562:Viral Load; D055815:Young Adult
chemical_list: D019380:Anti-HIV Agents