4.6 Article

Intra-Patient Evolution of HIV-2 Molecular Properties

Journal

VIRUSES-BASEL
Volume 14, Issue 11, Pages -

Publisher

MDPI
DOI: 10.3390/v14112447

Keywords

HIV-1; HIV-2; evolution; disease progression; PNGS; coreceptor; molecular properties

Categories

Funding

  1. Department for Research Cooperation (SAREC) at the Swedish International Development Agency (Sida)
  2. Swedish Research Council [350-20126628, 2016-01417, 2020-06262, 2016-02285, 2019-01439, 321-2012-3274, 2019-05235, 2020-02344]
  3. Swedish Society of Medical Research [SA-2016]
  4. Swedish Research Council [2020-06262, 2019-01439, 2016-02285, 2020-02344, 2019-05235] Funding Source: Swedish Research Council
  5. Vinnova [2019-05235] Funding Source: Vinnova

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This study investigated the evolution of molecular properties of HIV-2 Env regions during the asymptomatic phase of the infection. It found that the rate of change in potential N-linked glycosylation sites and diversity differed between faster and slower progressors.
Limited data are available on the pathogenesis of HIV-2, and the evolution of Env molecular properties during disease progression is not fully elucidated. We investigated the intra-patient evolution of molecular properties of HIV-2 Env regions (V1-C3) during the asymptomatic, treatment-naive phase of the infection in 16 study participants, stratified into faster or slower progressors. Most notably, the rate of change in the number of potential N-linked glycosylation sites (PNGS) within the Env (V1-C3) regions differed between progressor groups. With declining CD4(+) T-cell levels, slower progressors showed, on average, a decrease in the number of PNGSs, while faster progressors showed no significant change. Furthermore, diversity increased significantly with time in faster progressors, whereas no such change was observed in slower progressors. No differences were identified between the progressor groups in the evolution of length or charge of the analyzed Env regions. Predicted virus CXCR4 use was rare and did not emerge as a dominating viral population during the studied disease course (median 7.9 years, interquartile range [IQR]: 5.2-14.0) in either progressor groups. Further work building on our observations may explain molecular hallmarks of HIV-2 disease progression and differences in pathogenesis between HIV-1 and HIV-2.

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