Impact of HIV-1 genetic diversity on disease progression: a prospective cohort study in Guangxi

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Abstract

The high proportion of AIDS cases and mortality rates in Guangxi underscores the urgency to investigate the influence of HIV-1 genetic diversity on disease progression in this region. Newly diagnosed HIV-1 patients were enrolled from January 2016 to December 2021, and the follow-up work and detection of CD4+T lymphocytes were carried out every six months until December 2022. Multivariate logistic regression was used to analyze the factors affecting pre-treatment CD4+T lymphocyte counts, while local weighted regression models (LOESS) and generalized estimating equation models (GEE) were conducted to assess factors influencing CD4+T Lymphocyte Recovery. Cox regression analysis was utilized to examine the impact of subtypes on survival risk. Additionally, HIV-1 env sequences were utilized for predicting CXCR4 and CCR5 receptors. The study encompassed 1867 individuals with pol sequences and 281 with env sequences. Our findings indicate that age over 30, divorced/widowed, peasant, heterosexual infection, CRF01_AE, long-term infection, and Pre-treatment Viral load >10000 copies/ml were factors associated with higher risk for pre-treatment CD4+T lymphocyte decline. Specifically, male gender, age over 30, heterosexual infection (HETs), long-term infection, CRF01_AE, and Pre-treatment CD4 T cell counts below 350/µL were identified as risk factors impeding CD4+T lymphocyte recovery. Pre-treatment CD4+T lymphocyte counts and recovery in individuals infected with CRF01_AE were lower compared to CRF07_BC and CRF55_01B. Additionally, CRF01_AE and CRF08_BC subtypes exhibited higher mortality rates than CRF07_BC, CRF55_01B, and other subtypes. Notably, CRF01_AE demonstrated the highest percentage of CXCR4 affinity ratios. This research unveils the intricate influence of HIV-1 gene diversity on CD4+T lymphocyte dynamics and clinical outcomes. It highlights the multifaceted nature of HIV infection in Guangxi, providing novel insights into subtype-specific disease progression among HIV-infected individuals in this region.

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Most cited references 26

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Incomplete peripheral CD4+ cell count restoration in HIV-infected patients receiving long-term antiretroviral treatment.

Colleen Kelley, Christina Kitchen, Peter W. Hunt … (2009)

Although antiretroviral therapy has the ability to fully restore a normal CD4(+) cell count (>500 cells/mm(3)) in most patients, it is not yet clear whether all patients can achieve normalization of their CD4(+) cell count, in part because no study has followed up patients for >7 years. Three hundred sixty-six patients from 5 clinical cohorts who maintained a plasma human immunodeficiency virus (HIV) RNA level 1000 copies/mL for at least 4 years after initiation of antiretroviral therapy were included. Changes in CD4(+) cell count were evaluated using mixed-effects modeling, spline-smoothing regression, and Kaplan-Meier techniques. The majority (83%) of the patients were men. The median CD4(+) cell count at the time of therapy initiation was 201 cells/mm(3) (interquartile range, 72-344 cells/mm(3)), and the median age was 47 years. The median follow-up period was 7.5 years (interquartile range, 5.5-9.7 years). CD4(+) cell counts continued to increase throughout the follow-up period, albeit slowly after year 4. Although almost all patients (95%) who started therapy with a CD4(+) cell count 300 cells/mm(3) were able to attain a CD4(+) cell count 500 cells/mm(3), 44% of patients who started therapy with a CD4(+) cell count 500 cells/mm(3) over a mean duration of follow-up of 7.5 years; many did not reach this threshold by year 10. Twenty-four percent of individuals with a CD4(+) cell count <500 cells/mm(3) at year 4 had evidence of a CD4(+) cell count plateau after year 4. The frequency of detectable viremia ("blips") after year 4 was not associated with the magnitude of the CD4(+) cell count change. A substantial proportion of patients who delay therapy until their CD4(+) cell count decreases to <200 cells/mm(3) do not achieve a normal CD4(+) cell count, even after a decade of otherwise effective antiretroviral therapy. Although the majority of patients have evidence of slow increases in their CD4(+) cell count over time, many do not. These individuals may have an elevated risk of non-AIDS-related morbidity and mortality.

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Prognostic value of HIV-1 syncytium-inducing phenotype for rate of CD4+ cell depletion and progression to AIDS.

M Tersmette, José Coutinho, I Keet … (1993)

To investigate the relation between detection of syncytium-inducing (SI), human immunodeficiency virus type 1 (HIV-1) variants, rate of CD4+ cell decline, and clinical progression. Prospective study during a 2.5-year follow-up period; cohort study with pairwise matched controls. The Amsterdam cohort study on the course of HIV-1 infection in homosexual men. Asymptomatic HIV-1 infected men (n = 225) were tested for the presence of SI variants and were studied prospectively for CD4+ cell decline and clinical progression. In addition, 45 men with a defined moment of appearance of SI variants and 45 matched controls without SI variants were compared for CD4+ cell decline. Syncytium-inducing variants were detected by cocultivation of peripheral blood mononuclear cells with the MT-2 T-cell line. During a 30-month period, 70.8% of the men with SI variants progressed to AIDS, compared with 15.8% of men without SI variants at entry (P < 0.0001). Multivariable Cox proportional hazard analysis, controlling for CD4+ cell count and HIV-p24 antigenemia, showed a relative hazard for SI variants of 6.7 (95% Cl, 3.5 to 12.7). In the matched control study, before the appearance of SI variants, CD4+ cell counts of 45 men with SI variants and their controls were compared. Syncytium-inducing variants emerged at a mean CD4+ cell count of 0.48 x 10(9)/L(Cl, 0.42 to 0.54), coinciding with the onset of a threefold increased rate of CD4+ cell decline. Men developing AIDS with SI variants had decreased CD4+ cell counts (0.08 x 10(9)/L; 95% Cl, 0.05 to 0.12) at the time of diagnosis compared with persons progressing to AIDS without SI variants (0.25 x 10(9)/L 95% Cl, 0.15 to 0.41) (P = 0.0035]. The HIV-1 biological phenotype is a practical, binary marker for progression to AIDS, which is independent of decreased CD4+ cell counts and antigenemia. Appearance of SI variants, occurring 2 years before progression to AIDS on the average, is predictive for a significantly increased rate of CD4+ cell decline.

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Author and article information

Contributors

Xianwu Pang: URI : https://loop.frontiersin.org/people/1003078Role: Role: Role: Role: Role: Role: Role: Role: Role:

Jinghua Huang: Role: Role: Role: Role:

Kailing Tang: Role: Role: Role: Role:

Jie Ma: Role: Role: Role: Role:

Ningye Fang: Role: Role: Role: Role:

Haomin Xie: Role: Role: Role:

Qin He: Role: Role: Role:

Qiuying Zhu: Role: Role: Role: Role:

Guanghua Lan: URI : https://loop.frontiersin.org/people/1946148Role: Role: Role: Role: Role:

Shujia Liang: URI : https://loop.frontiersin.org/people/266483Role: Role: Role: Role: Role:

Journal

Journal ID (nlm-ta): Front Cell Infect Microbiol

Journal ID (iso-abbrev): Front Cell Infect Microbiol

Journal ID (publisher-id): Front. Cell. Infect. Microbiol.

Title: Frontiers in Cellular and Infection Microbiology

Publisher: Frontiers Media S.A.

ISSN (Electronic): 2235-2988

Publication date (Electronic): 27 June 2024

Publication date Collection: 2024

Volume: 14

Electronic Location Identifier: 1415123

Affiliations

[1] Guangxi Key Laboratory of Major Infectious Disease Prevention Control and Biosafety Emergency Response, Guangxi Key Laboratory of AIDS Prevention Control and Translation, Guangxi Zhuang Autonomous Region Center for Disease Control and Prevention , Nanning, China

Author notes

Edited by: Moises Leon Juarez, Instituto Nacional de Perinatología (INPER), Mexico

Reviewed by: Monica Viveros-Rogel, National Institute of Medical Sciences and Nutrition Salvador Zubirán, Mexico

Leonor Huerta, National Autonomous University of Mexico, Mexico

*Correspondence: Shujia Liang, liangshujia@ 123456126.com

†These authors have contributed equally to this work

Article

DOI: 10.3389/fcimb.2024.1415123

PMC ID: 11236547

PubMed ID: 38994006

SO-VID: 4b9a420b-d98b-447e-874c-8bf63abf03c8

License:

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

History

Date received : 10 April 2024

Date accepted : 31 May 2024

Page count

Figures: 4, Tables: 2, Equations: 0, References: 26, Pages: 10, Words: 4627

Funding

The author(s) declare financial support was received for the research, authorship, and/or publication of this article. The study was supported by grants from the National Natural Science Foundation of China (82160636), the Natural Science Foundation of Guangxi (2024GXNSFAA010306), the Guangxi Key Laboratory of AIDS Prevention Control and Translation [ZZH2020010], the Guangxi Key Laboratory of Major Infectious Disease Prevention and Control and Biosafety Emergency Response (21–220-12), the Guangxi Bagui Honor Scholarship, and the Guangxi Key Research and Development Program (Guike AB22035027).

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section-in-acceptance Virus and Host

ScienceOpen disciplines: Infectious disease & Microbiology

Keywords: hiv-1,subtype,genetic diversity,disease progression,cd4+t lymphocyte

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ScienceOpen disciplines: Infectious disease & Microbiology

Keywords: hiv-1, subtype, genetic diversity, disease progression, cd4+t lymphocyte

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Impact of HIV-1 genetic diversity on disease progression: a prospective cohort study in Guangxi

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Most cited references 26

Incomplete peripheral CD4+ cell count restoration in HIV-infected patients receiving long-term antiretroviral treatment.

A new classification for HIV-1.

Prognostic value of HIV-1 syncytium-inducing phenotype for rate of CD4+ cell depletion and progression to AIDS.

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