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SARS-CoV-2 uses CD4 to infect T helper lymphocytes. 2023
Natalia S Brunetti, and
Gustavo G Davanzo, and
Diogo de Moraes, and
Allan J R Ferrari, and
Gabriela F Souza, and
Stéfanie Primon Muraro, and
Thiago L Knittel, and
Vinicius O Boldrini, and
Lauar B Monteiro, and
João Victor Virgílio-da-Silva, and
Gerson S Profeta, and
Natália S Wassano, and
Luana Nunes Santos, and
Victor C Carregari, and
Artur H S Dias, and
Flavio P Veras, and
Lucas A Tavares, and
Julia Forato, and
Icaro M S Castro, and
Lícia C Silva-Costa, and
André C Palma, and
Eli Mansour, and
Raisa G Ulaf, and
Ana F Bernardes, and
Thyago A Nunes, and
Luciana C Ribeiro, and
Marcus V Agrela, and
Maria Luiza Moretti, and
Lucas I Buscaratti, and
Fernanda Crunfli, and
Raissa G Ludwig, and
Jaqueline A Gerhardt, and
Natália Munhoz-Alves, and
Ana Maria Marques, and
Renata Sesti-Costa, and
Mariene R Amorim, and
Daniel A Toledo-Teixeira, and
Pierina Lorencini Parise, and
Matheus Cavalheiro Martini, and
Karina Bispos-Dos-Santos, and
Camila L Simeoni, and
Fabiana Granja, and
Virgínia C Silvestrini, and
Eduardo B de Oliveira, and
Vitor M Faca, and
Murilo Carvalho, and
Bianca G Castelucci, and
Alexandre B Pereira, and
Laís D Coimbra, and
Marieli M G Dias, and
Patricia B Rodrigues, and
Arilson Bernardo S P Gomes, and
Fabricio B Pereira, and
Leonilda M B Santos, and
Louis-Marie Bloyet, and
Spencer Stumpf, and
Marjorie C Pontelli, and
Sean Whelan, and
Andrei C Sposito, and
Robson F Carvalho, and
André S Vieira, and
Marco A R Vinolo, and
André Damasio, and
Licio Velloso, and
Ana Carolina M Figueira, and
Luis L P da Silva, and
Thiago Mattar Cunha, and
Helder I Nakaya, and
Henrique Marques-Souza, and
Rafael E Marques, and
Daniel Martins-de-Souza, and
Munir S Skaf, and
Jose Luiz Proenca-Modena, and
Pedro M M Moraes-Vieira, and
Marcelo A Mori, and
Alessandro S Farias
Autoimmune Research Laboratory, Department of Genetics, Microbiology and Immunology, Institute of Biology, University of Campinas (UNICAMP), Campinas, Brazil.
The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the agent of a major global outbreak of respiratory tract disease known as Coronavirus Disease 2019 (COVID-19). SARS-CoV-2 infects mainly lungs and may cause several immune-related complications, such as lymphocytopenia and cytokine storm, which are associated with the severity of the disease and predict mortality. The mechanism by which SARS-CoV-2 infection may result in immune system dysfunction is still not fully understood. Here, we show that SARS-CoV-2 infects human CD4+ T helper cells, but not CD8+ T cells, and is present in blood and bronchoalveolar lavage T helper cells of severe COVID-19 patients. We demonstrated that SARS-CoV-2 spike glycoprotein (S) directly binds to the CD4 molecule, which in turn mediates the entry of SARS- CoV-2 in T helper cells. This leads to impaired CD4 T cell function and may cause cell death. SARS-CoV-2-infected T helper cells express higher levels of IL-10, which is associated with viral persistence and disease severity. Thus, CD4-mediated SARS-CoV-2 infection of T helper cells may contribute to a poor immune response in COVID-19 patients.
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