The ectromelia virus virulence factor C15 facilitates early viral spread by inhibiting NK cell contact

Peauroi, Elise; Carro, Stephen D.; Pei, Luxin; Reynoso, Glennys V.; Hickman, Heather D.; Eisenlohr, Laurence C.

doi:10.1016/j.isci.2022.105510

iScience

2022

DOI: 10.1016/j.isci.2022.105510

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The ectromelia virus virulence factor C15 facilitates early viral spread by inhibiting NK cell contact

Elise Peauroi

Stephen D. Carro

Luxin Pei

et al.

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2024

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Cited by 3 publications

References 21 publications

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Subcapsular sinus macrophages maximize germinal center development in non-draining lymph nodes during blood-borne viral infection

Aguilar,

Kalia,

Brisse

et al. 2024

Sci. Immunol.

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Lymph node (LN) germinal centers (GCs) are critical sites for B cell activation and differentiation. GCs develop after specialized CD169 + macrophages residing in LN sinuses filter antigens (Ags) from the lymph and relay these Ags into proximal B cell follicles. Many viruses, however, first reach LNs through the blood during viremia (virus in the blood), rather than through lymph drainage from infected tissue. How LNs capture viral Ag from the blood to allow GC development is not known. Here, we followed Zika virus (ZIKV) dissemination in mice and subsequent GC formation in both infected tissue–draining and non-draining LNs. From the footpad, ZIKV initially disseminated through two LN chains, infecting LN macrophages and leading to GC formation. Despite rapid ZIKV viremia, non-draining LNs were not infected for several days. Non-draining LN infection correlated with virus-induced vascular leakage and neutralization of permeability reduced LN macrophage attrition. Depletion of non-draining LN macrophages significantly decreased GC B cells in these nodes. Thus, although LNs inefficiently captured viral Ag directly from the blood, GC formation in non-draining LNs proceeded similarly to draining LNs through LN sinus CD169 + macrophages. Together, our findings reveal a conserved pathway allowing LN macrophages to activate antiviral B cells in LNs distal from infected tissue after blood-borne viral infection.

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Subcapsular sinus macrophages maximize germinal center development in non-draining lymph nodes during blood-borne viral infection

Aguilar,

Kalia,

Brisse

et al. 2024

Sci. Immunol.

Self Cite

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Poxvirus Immune Evasion

Hernaez,

Alcamí

2024

Annual Review of Immunology

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Poxviruses have evolved a wide array of mechanisms to evade the immune response, and we provide an overview of the different immunomodulatory strategies. Poxviruses prevent the recognition of viral DNA that triggers the immune responses and inhibit signaling pathways within the infected cell. A unique feature of poxviruses is the production of secreted proteins that mimic cytokines and cytokine receptors, acting as decoy receptors to neutralize the activity of cytokines and chemokines. The capacity of these proteins to evade cellular immune responses by inhibiting cytokine activation is complemented by poxviruses’ strategies to block natural killer cells and cytotoxic T cells, often through interfering with antigen presentation pathways. Mechanisms that target complement activation are also encoded by poxviruses. Virus-encoded proteins that target immune molecules and pathways play a major role in immune modulation, and their contribution to viral pathogenesis, facilitating virus replication or preventing immunopathology, is discussed.

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Genomic Sequence of the Threespine Stickleback Iridovirus (TSIV) from Wild Gasterosteus aculeatus in Stormy Lake, Alaska

Yoxsimer,

Offenberg,

Katzer

et al. 2024

Viruses

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The threespine stickleback iridovirus (TSIV), a double-stranded DNA virus, was the first megalocytivirus detected in wild North American fishes. We report a second occurrence of TSIV in threespine stickleback (Gasterosteus aculeatus) from Stormy Lake, Alaska, and assemble a nearly complete genome of TSIV. The 115-kilobase TSIV genome contains 94 open reading frames (ORFs), with 91 that share homology with other known iridoviruses. We identify three ORFs that likely originate from recent lateral gene transfers from a eukaryotic host and one ORF with homology to B22 poxvirus proteins that likely originated from a lateral gene transfer between viruses. Phylogenetic analysis of 24 iridovirus core genes and pairwise sequence identity analysis support TSIV as a divergent sister taxon to other megalocytiviruses and a candidate for a novel species designation. Screening of stickleback collected from Stormy Lake before and after a 2012 rotenone treatment to eliminate invasive fish shows 100% positivity for TSIV in the two years before treatment (95% confidence interval: 89–100% prevalence) and 0% positivity for TSIV in 2024 after treatment (95% confidence interval: 0 to 3.7% prevalence), suggesting that the rotenone treatment and subsequent crash and reestablishment of the stickleback population is associated with loss of TSIV.

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The ectromelia virus virulence factor C15 facilitates early viral spread by inhibiting NK cell contact

Cited by 3 publications

References 21 publications

Subcapsular sinus macrophages maximize germinal center development in non-draining lymph nodes during blood-borne viral infection

Subcapsular sinus macrophages maximize germinal center development in non-draining lymph nodes during blood-borne viral infection

Poxvirus Immune Evasion

Genomic Sequence of the Threespine Stickleback Iridovirus (TSIV) from Wild Gasterosteus aculeatus in Stormy Lake, Alaska

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