Details

Autor(en) / Beteiligte

• Borlido Farias, Guilherme
• Badura, Robert
• M Conceição, Carolina
• Gomes, André
• Godinho-Santos, Ana
• Laia, Joel
• Rosmaninho, Pedro
• Santos, Diana
• Mota da Silva, Maria Catarina
• Almeida, Afonso
• Fernandes, Susana
• Trombetta, Amelia Chiara
• Sousa, Ana E.

Titel

Acute HIV-1 and SARS-CoV-2 infections Share Slan+ Monocyte Depletion - evidence from an hyperacute HIV-1 case report

Ist Teil von

• Viruses, 2021-09, Vol.13 (9), p.1805

Ort / Verlag

Basel: MDPI

Erscheinungsjahr

2021

Quelle

EZB Free E-Journals

Beschreibungen/Notizen

• © 2021 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). Monocytes are key modulators in acute viral infections, determining both inflammation and development of specific B- and T-cell responses. Recently, these cells were shown to be associated to different SARS-CoV-2 infection outcome. However, their role in acute HIV-1 infection remains unclear. We had the opportunity to evaluate the mononuclear cell compartment in an early hyper-acute HIV-1 patient in comparison with an untreated chronic HIV-1 and a cohort of SARS-CoV-2 infected patients, by high dimensional flow cytometry using an unsupervised approach. A distinct polarization of the monocyte phenotype was observed in the two viral infections, with maintenance of pro-inflammatory M1-like profile in HIV-1, in contrast to the M2-like immunosuppressive shift in SARS-CoV-2. Noticeably, both acute infections had reduced CD14low/-CD16+ non-classical monocytes, with depletion of the population expressing Slan (6-sulfo LacNac), which is thought to contribute to immune surveillance through pro-inflammatory properties. This depletion indicates a potential role of these cells in acute viral infection, which has not previously been explored. The inflammatory state accompanied by the depletion of Slan+ monocytes may provide new insights on the critical events that determine the rate of viral set-point in acute HIV-1 infection and subsequent impact on transmission and reservoir establishment. This work was funded by the following grants from Fundação para a Ciência e a Tecnologia (FCT), Portugal, through “Apoio Especial Research4COVID-19”, project numbers 125 to S.M.F. and 803 to A.C.T. Fellowships funded by FCT (Doctorates4COVID-19, 2020.10202.BD), and Janssen-Cilag Farmacêutica were received by A.M.C.G. and G.B.F., respectively.