Vaccinia Virus Infection Inhibits Skin Dendritic Cell Migration to Draining Lymph Node

Aggio, Juliana Bernardi; Krmeská, Veronika; Ferguson, Brian J.; Wowk, Pryscilla Fanini; Rothfuchs, Antonio Gigliotti

doi:10.1101/2020.02.17.952374

Cited by 3 publications

(3 citation statements)

References 39 publications

(49 reference statements)

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“…skin infection suggested that dendritic cell migration from the skin to draining lymph nodes is impaired on VACV 56 . The relocation of the virus from the skin to the lymphatics might also be supported by other mechanisms such as direct lymphatic vessel access, as observed in skin infection models of Zika virus 57 .…”

Section: ();mentioning

confidence: 99%

Monkeypox: disease epidemiology, host immunity and clinical interventions

et al. 2022

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Monkeypox virus (MPXV), which causes disease in humans, has for many years been restricted to the African continent, with only a handful of sporadic cases in other parts of the world. However, unprecedented outbreaks of monkeypox in non-endemic regions have recently taken the world by surprise. In less than 4 months, the number of detected MPXV infections has soared to more than 48,000 cases, recording a total of 13 deaths. In this Review, we discuss the clinical, epidemiological and immunological features of MPXV infections. We also highlight important research questions and new opportunities to tackle the ongoing monkeypox outbreak.

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Section: ();mentioning

confidence: 99%

Monkeypox: disease epidemiology, host immunity and clinical interventions

et al. 2022

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“…Since numerous nascent viruses are wrapped inside the cell, VICM is a good choice for the virus to avoid immune system defense such as antibody neutralization. In addition, VACV infection can impair the migratory capacity of skin dendritic cells from the infection sites to draining lymph node 37 , which is also a potential way of immune escape for the vaccinia. Besides (which was not certified by peer review) is the author/funder.…”

Section: Discussionmentioning

confidence: 99%

Vaccinia virus induces EMT-like transformation and RhoA-mediated mesenchymal migration

Liu

Wang

et al. 2023

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The emerging outbreak of monkeypox is closely associated with the viral infection and spreading, threatening global public health. Virus-induced cell migration facilitates viral transmission. However, high-resolution dynamics and mechanisms underlying this type of cell migration remain unclear. Here, we investigate the motility of cells infected by vaccinia virus (VACV), a close relative of monkeypox, through combining multi-omics analyses and high-resolution live-cell imaging. We find that, upon VACV infection, the epithelial cells undergo EMT-like transformation, during which they lose intercellular junctions and acquire the migratory capacity to promote viral spreading. After transformation, VACV-induced mesenchymal migration is highly dependent on the actin cytoskeleton and RhoA signaling, which is responsible for the depolymerization of robust actin stress fibers, the leading-edge protrusion formation, and the rear-edge recontraction. Our study reveals how poxviruses alter the epithelial phenotype and regulate RhoA signaling to induce fast migration, providing a unique perspective to understand the pathogenesis of poxviruses.

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“…Future experiments will be required to understand the role of infected DCs at later timepoints. Recent studies with the poxvirus vaccinia (VACV) have demonstrated that the immune system can halt viral spread after cutaneous viral replication by shutting off lymphatic transport of virus or by preventing DC trafficking to the LN (Aggio et al, 2021;Churchill et al, 2022). If these skin immune-defense mechanisms also occur during ZIKV infection, viral replication in the skin might not directly translate to infectious virus in the blood.…”

Section: Discussionmentioning

confidence: 99%

Zika virus spreads through infection of lymph node-resident macrophages

Reynoso

Gordon

Kalia

et al. 2022

Preprint

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Zika virus (ZIKV) is an arthopod-vectored flavivirus that disseminates from the infection site into peripheral tissues, where it can elicit virus-induced pathology. To move through the body, ZIKV is thought to exploit the mobility of myeloid cells, in particular monocytes and dendritic cells. However, multiple distinct steps during viral spread culminate in peripheral tissue infection, and the timing and mechanisms underlying mobile immune cell shuttling of virus remain unclear. To understand the very early steps in ZIKV dissemination from the skin, we kinetically and spatially mapped ZIKV-infected lymph nodes (LNs), an intermediary stop en route to the blood. Contrary to dogma, migratory immune cells were not required for large quantities of virus to reach the LN or blood. Instead, ZIKV rapidly infected a subset of immobile macrophages in the LN, which shed virus through the lymphatic pathway into the blood. Importantly, infection of LN macrophages alone was sufficient to initiate viremia. Together, our studies indicate that sessile macrophages that live and die in the LN contribute to initial ZIKV spread to the blood. These data build a more complete picture of ZIKV movement through the body and identify an alternate anatomical site for potential antiviral intervention.

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Vaccinia Virus Infection Inhibits Skin Dendritic Cell Migration to Draining Lymph Node

Cited by 3 publications

References 39 publications

Monkeypox: disease epidemiology, host immunity and clinical interventions

Monkeypox: disease epidemiology, host immunity and clinical interventions

Vaccinia virus induces EMT-like transformation and RhoA-mediated mesenchymal migration

Zika virus spreads through infection of lymph node-resident macrophages

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