Infection of human lymphomononuclear cells by SARS-CoV-2

Pontelli, Marjorie Cornejo; Castro, Ítalo A.; Martins, Ronaldo B.; Veras, Flávio P.; Serra, Leonardo La; Nascimento, Daniele C.; Cardoso, Ricardo; Rosales, Roberta; Lima, Thais M.; Souza, Juliano P.; Caetité, Diego B; Lima, Mikhael HF de; Kawahisa, Juliana T E; Giannini, Marcela C; Bonjorno, Letícia Pastorelli; Lopes, Maria IF; Batah, Sabrina Setembre; Siyuan, Li; Assad, Rodrigo Luppino; Almeida, Silvana; Oliveira, Fabíola Reis; Benatti, Maíra Nilson; Pontes, Lorena L F; Santana, Rodrigo de Carvalho; Villar, Fernando C; Martins, Maria Auxiliadora Parreiras; Cunha, Thiago M.; Calado, Rodrigo T.; Alves-Filho, José C.; Zamboni, Dario S.; Fabro, Alexandre Todorovic; Louzada‐Júnior, Paulo; Oliveira, Renê DR de; Cunha, Fernando Q.; Arruda, Eurico

doi:10.1101/2020.07.28.225912

Cited by 72 publications

(83 citation statements)

References 38 publications

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“…ACO1 was over-expressed in COVID-19 versus HC and under-expressed in non-COVID-19 viral infections versus HC, whereas ATL3 entirely oppositely regulated ( Figure 4 ). Viral replication can occur in infected cells due to a hinderance of the function of the immune cells drawn in to kill infected cells; as well, there are reports of SARS-CoV-1 and SARS-CoV-2 directly infecting immune cells themselves ( Gu et al., 2005 ; Hu et al., 2012 ; Pontelli et al., 2020 ). As our data are from whole blood RNA, we cannot conclude precisely which of these mechanisms are responsible for the shifts in these genes' expression; however, prior reports suggest that both genes may be involved in viral replication and immune evasion.…”

Section: Discussionmentioning

confidence: 99%

Transcriptomic similarities and differences in host response between SARS-CoV-2 and other viral infections

Thair¹,

He²,

Hasin-Brumshtein³

et al. 2021

iScience

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Section: Discussionmentioning

confidence: 99%

Transcriptomic similarities and differences in host response between SARS-CoV-2 and other viral infections

Thair¹,

He²,

Hasin-Brumshtein³

et al. 2021

iScience

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“…Nevertheless, it remains to be determined whether PSGL-1 is expressed in SARS coronavirus target cells in the lungs, and, if so, whether its expression can impair viral infection. Interestingly, recent studies suggested that SARS-CoV-2 may also enter and infect human T cells, monocytes, and macrophages, which express high levels of PSGL-1 [ 18 , 19 ]. Infection of T cells by SARS-CoVs could also potentially occur in the scenario of PSGL-1-mediated binding of T cells to inflamed human airway endothelium [ 20 , 21 ].…”

Section: Discussionmentioning

confidence: 99%

PSGL-1 Inhibits the Incorporation of SARS-CoV and SARS-CoV-2 Spike Glycoproteins into Pseudovirions and Impairs Pseudovirus Attachment and Infectivity

Waheed

Hetrick

et al. 2020

Viruses

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P-selectin glycoprotein ligand-1 (PSGL-1) is a cell surface glycoprotein that binds to P-, E-, and L-selectins to mediate the tethering and rolling of immune cells on the surface of the endothelium for cell migration into inflamed tissues. PSGL-1 has been identified as an interferon-γ (INF-γ)-regulated factor that restricts HIV-1 infectivity, and has recently been found to possess broad-spectrum antiviral activities. Here we report that the expression of PSGL-1 in virus-producing cells impairs the incorporation of SARS-CoV and SARS-CoV-2 spike (S) glycoproteins into pseudovirions and blocks pseudovirus attachment and infection of target cells. These findings suggest that PSGL-1 may potentially inhibit coronavirus replication in PSGL-1+ cells

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“…It was shown that the virus has complex interaction with the innate and adaptive immunity and can directly infect the immune cells. Viral particles and SARS-CoV-2 RNA were found in monocytes, CD4 + T cells, CD8 + T-cells, and B-cells 31,32,33 .…”

Section: Discussionmentioning

confidence: 97%

Novel transgenic mice with Cre-dependent co-expression of GFP and human ACE2: a safe tool for study of COVID-19 pathogenesis

Bruter

Korshunova

Kubekina

et al. 2021

Preprint

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Current coronavirus disease (COVID-19) pandemia still belongs to the most serious problems of public health. A growing body of data shows that infection caused by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) is a very complex and multifaceted disease requiring its detailed study to fight with. Nevertheless, there is a row of stumbling blocks in the way of experimental research of COVID-19 determined by the deficiency of appropriate animal models. Herein, we report novel humanized mice with Cre-dependent expression of hACE2, the main entry receptor of SARS-CoV-2. These mice carry hACE2 and GFP transgenes floxed by the STOP-cassette, allowing them to be used as breeders for the creation of animals with the tissue-specific co-expression of hACE2 and GFP. Moreover, inducible expression of hACE2 makes this line biosafe, whereas co-expression with GFP simplifies the detection of transgene-expressing cells. In our study, we tested our line by crossing with Ubi-Cre mice, characterized by tamoxifen-dependent ubiquitous activation of Cre-recombinase. After tamoxifen administration, copy number of the STOP-cassette was decreased and the offspring expressed hACE2 and GFP, confirming the efficiency of our system. We believe that our model can be a useful tool for studying COVID-19 pathogenesis because the selective expression of hACE2 can shed light on the role of different tissues in SARS-CoV-2 associated complications. Obviously, it can also be used for preclinical trials of antiviral drugs and new vaccines.

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Infection of human lymphomononuclear cells by SARS-CoV-2

Cited by 72 publications

References 38 publications

Transcriptomic similarities and differences in host response between SARS-CoV-2 and other viral infections

Transcriptomic similarities and differences in host response between SARS-CoV-2 and other viral infections

PSGL-1 Inhibits the Incorporation of SARS-CoV and SARS-CoV-2 Spike Glycoproteins into Pseudovirions and Impairs Pseudovirus Attachment and Infectivity

Novel transgenic mice with Cre-dependent co-expression of GFP and human ACE2: a safe tool for study of COVID-19 pathogenesis

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