Virological Synapse for Cell-Cell Spread of Viruses

Garcia, Eduardo; Piguet, Vincent

doi:10.1007/978-0-387-46957-7_22

Cited by 2 publications

(2 citation statements)

References 104 publications

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“…Attachment is followed by endocytosis, storage and viral dissemination through the exosome pathway, or through an "infectious synapse" between uninfected mature DCs harboring HIV-1 and uninfected target cells with retention of the virus on the DC surface and transmission to target cell through adhesion protein interactions. DCs were reported to take up SARS-CoV-1 via the DC-SIGN-receptor and transfer the virus to uninfected target cells through direct cell-to-cell transmission, suggesting that the CoVs family of viruses may also infect T cells "in trans" via VS (91,92). DC-SING and DC-SING receptor (DC-SINR) enhance SARS-CoV-1 and SARS-CoV-2 S protein-driven transinfection (93,94), and there is evidence that DC-SINGR expression is induced in alveolar macrophages by IL-4 and IL-13 upon infection by other viruses (95).…”

Section: Dendritic Cellsmentioning

confidence: 99%

“…Since the levels of these cytokines increase in the early phases of SARS-CoV-2 infection, they could also be involved in macrophage infectivity at lymph node sites. Lymphopenia, in COVID-19, in addition to innate response (60) may also occur via transmission via DC-T cell VS, T cell-T cell VS and even macrophage-T cell VS infection with SARS-CoV-2, in a manner similar to that of HIV-1 transmission (92,94). It is of interest to note that HIV-1 taken up via DC-SIGN remains infectious for prolonged periods of time, protected possibly by trafficking through non-lysosomal endosomes and infecting T cells through DC-mediated viral transmission (89).…”

Section: Dendritic Cellsmentioning

confidence: 99%

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SARS-CoV-2 and HIV-1: So Different yet so Alike. Immune Response at the Cellular and Molecular Level

Demoliou¹,

Papaneophytou²,

Nicolaidou³

2022

Int. J. Med. Sci.

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In the past half century, humanity has experienced two devastating pandemics; the HIV-1 pandemic and the recent pandemic caused by SARS-CoV-2. Both emerged as zoonotic pathogens. Interestingly, SARS-CoV-2 has rapidly migrated all over the world in less than two years, much as HIV-1 did almost 40 years ago. Despite these two RNA viruses being different in their mode of transmission as well as the symptoms they generate, recent evidence suggests that they cause similar immune responses. In this mini review, we compare the molecular basis for CD4 + T cell lymphopenia and other effects on the immune system induced by SARS-CoV-2 and HIV-1 infections. We considered features of the host immune response that are shared with HIV-1 and could account for the lymphopenia and other immune effects observed in COVID-19. The information provided herein, may cast the virus-induced lymphopenia and cytokine storm associated with the acute SARS-CoV-2 infection and pathogenesis in a different light for further research on host immune responses. It can also provide opportunities for the identification of novel therapeutic targets for COVID-19. Furthermore, we provide some basic information to enable a comparative framework for considering the overlapping sets of immune responses caused by HIV-1 and SARS-CoV-2.

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Section: Dendritic Cellsmentioning

confidence: 99%

Section: Dendritic Cellsmentioning

confidence: 99%

SARS-CoV-2 and HIV-1: So Different yet so Alike. Immune Response at the Cellular and Molecular Level

Demoliou¹,

Papaneophytou²,

Nicolaidou³

2022

Int. J. Med. Sci.

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Virus interactions with the actin cytoskeleton—what we know and do not know about SARS-CoV-2

et al. 2022

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The actin cytoskeleton and actin-dependent molecular and cellular events are responsible for the organization of eukaryotic cells and their functions. Viruses, including severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), depend on host cell organelles and molecular components for cell entry and propagation. Thus, it is not surprising that they also interact at many levels with the actin cytoskeleton of the host. There have been many studies on how different viruses reconfigure and manipulate the actin cytoskeleton of the host during successive steps of their life cycle. However, we know relatively little about the interactions of SARS-CoV-2 with the actin cytoskeleton. Here, we describe how the actin cytoskeleton is involved in the strategies used by different viruses for entry, assembly, and egress from the host cell. We emphasize what is known and unknown about SARS-CoV-2 in this regard. This review should encourage further investigation of the interactions of SARS-CoV-2 with cellular components, which will eventually be helpful for developing novel antiviral therapies for mitigating the severity of COVID-19.

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Virological Synapse for Cell-Cell Spread of Viruses

Cited by 2 publications

References 104 publications

SARS-CoV-2 and HIV-1: So Different yet so Alike. Immune Response at the Cellular and Molecular Level

SARS-CoV-2 and HIV-1: So Different yet so Alike. Immune Response at the Cellular and Molecular Level

Virus interactions with the actin cytoskeleton—what we know and do not know about SARS-CoV-2

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