Immune Response Gaps Linked to SARS-CoV-2 Infection: Cellular Exhaustion, Senescence, or Both?
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Published:2022-11-08
Issue:22
Volume:23
Page:13734
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ISSN:1422-0067
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Container-title:International Journal of Molecular Sciences
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language:en
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Short-container-title:IJMS
Author:
Barbosa Leonardo Vinicius, Prá Daniele Margarita Marani, Nagashima SeigoORCID, Pereira Marcos Roberto CurcioORCID, Stocco Rebecca BenicioORCID, da Silva Francys de Luca Fernandes, Cruz Milena Rueda, Dallagassa Djessyka, Stupak Thiago João, da Rosa Götz George Willian XavierORCID, Nasimoto Georgia Garofani, Cracco Luiz Augusto FanhaniORCID, Silva Isabela BustoORCID, de Moura Karen Fernandes, Deus Marina de CastroORCID, Martins Ana Paula Camargo, Spitzenbergen Beatriz Akemi Kondo Van, Amaral Andréa Novais MorenoORCID, de Paula Caroline Busatta VazORCID, Machado-Souza CleberORCID, de Noronha LuciaORCID
Abstract
The COVID-19 pandemic, promoted by the SARS-CoV-2 respiratory virus, has resulted in widespread global morbidity and mortality. The immune response against this pathogen has shown a thin line between protective effects and pathological reactions resulting from the massive release of cytokines and poor viral clearance. The latter is possibly caused by exhaustion, senescence, or both of TCD8+ cells and reduced activity of natural killer (NK) cells. The imbalance between innate and adaptive responses during the early stages of infection caused by SARS-CoV-2 contributes to the ineffective control of viral spread. The present study evaluated the tissue immunoexpression of the tissue biomarkers (Arginase-1, CCR4, CD3, CD4, CD8, CD20, CD57, CD68, CD138, IL-4, INF-α, INF-γ, iNOS, PD-1, Perforin and Sphingosine-1) to understand the cellular immune response triggered in patients who died of COVID-19. We evaluated twenty-four paraffin-embedded lung tissue samples from patients who died of COVID-19 (COVID-19 group) and compared them with ten lung tissue samples from patients who died of H1N1pdm09 (H1N1 group) with the immunohistochemical markers mentioned above. In addition, polymorphisms in the Perforin gene were genotyped through Real-Time PCR. Significantly increased tissue immunoexpression of Arginase, CD4, CD68, CD138, Perforin, Sphingosine-1, and IL-4 markers were observed in the COVID-19 group. A significantly lower immunoexpression of CD8 and CD57 was also found in this group. It is suggested that patients who died from COVID-19 had a poor cellular response concerning viral clearance and adaptive response going through tissue repair.
Funder
National Council for Scientific and Technological Development BRDE-PUCPR
Subject
Inorganic Chemistry,Organic Chemistry,Physical and Theoretical Chemistry,Computer Science Applications,Spectroscopy,Molecular Biology,General Medicine,Catalysis
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