Publications by authors named "R P Galao"

The role of myeloid cells in the pathogenesis of SARS-CoV-2 is well established, in particular as drivers of cytokine production and systemic inflammation characteristic of severe COVID-19. However, the potential for myeloid cells to act as bona fide targets of productive SARS-CoV-2 infection, and the specifics of entry, remain unclear. Using a panel of anti-SARS-CoV-2 monoclonal antibodies (mAbs) we performed a detailed assessment of antibody-mediated infection of monocytes/macrophages.

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Rapid and accessible testing was paramount in the management of the COVID-19 pandemic. Our university established KCL TEST: a SARS-CoV-2 asymptomatic testing programme that enabled sensitive and accessible PCR testing of SARS-CoV-2 RNA in saliva. Here, we describe our learnings and provide our blueprint for launching diagnostic laboratories, particularly in low-resource settings.

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Article Synopsis
  • Researchers studied two siblings with inherited PD-1 deficiency who died from autoimmune issues, including autoimmune pneumonitis and type 1 diabetes (T1D).
  • The current report focuses on two new siblings with neonatal-onset T1D linked to a specific mutation in the PD-L1 gene, resulting in a dysfunctional PD-L1 protein.
  • Despite lacking functional PD-L1, the new siblings exhibited normal immune cell development, suggesting that while both PD-1 and PD-L1 are important for preventing early T1D, PD-L1 deficiency does not cause the same severe autoimmune dysregulation seen in PD-1 deficiency.
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The appearance of new dominant variants of concern (VOC) of severe acute respiratory syndrome coronavirus type 2 (SARS-CoV-2) threatens the global response to the coronavirus disease 2019 (COVID-19) pandemic. Of these, the alpha variant (also known as B.1.

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Ebola virus (EBOV) causes highly pathogenic disease in primates. Through screening a library of human interferon-stimulated genes (ISGs), we identified TRIM25 as a potent inhibitor of EBOV transcription-and-replication-competent virus-like particle (trVLP) propagation. TRIM25 overexpression inhibited the accumulation of viral genomic and messenger RNAs independently of the RNA sensor RIG-I or secondary proinflammatory gene expression.

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