Inhibitors of the interferon response increase the replication of gorilla simian foamy viruses

Couteaudier, Mathilde; Calzada-Fraile, Diego; Montange, Thomas; Gessain, Antoine; Buseyne, Florence

doi:10.1016/j.virol.2019.11.019

Cited by 7 publications

(10 citation statements)

References 50 publications

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“…Our own results also supported the inhibition of various FVs by IFN-β, but not by the ISG product MX2 [124]. Additionally, a new study suggested that pharmacological inhibitors of the IFN-I response enhance the replication of primary gorilla SFVs [125]. Very recently, using a myeloid cell model, the innate sensing pathways involved in FV infection were described [88].…”

Section: Innate Immune Sensing Of Foamy Virusessupporting

confidence: 76%

Foamy Viruses, Bet, and APOBEC3 Restriction

Vasudevan

Becker

Luedde

et al. 2021

Viruses

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Non-human primates (NHP) are an important source of viruses that can spillover to humans and, after adaptation, spread through the host population. Whereas HIV-1 and HTLV-1 emerged as retroviral pathogens in humans, a unique class of retroviruses called foamy viruses (FV) with zoonotic potential are occasionally detected in bushmeat hunters or zookeepers. Various FVs are endemic in numerous mammalian natural hosts, such as primates, felines, bovines, and equines, and other animals, but not in humans. They are apathogenic, and significant differences exist between the viral life cycles of FV and other retroviruses. Importantly, FVs replicate in the presence of many well-defined retroviral restriction factors such as TRIM5α, BST2 (Tetherin), MX2, and APOBEC3 (A3). While the interaction of A3s with HIV-1 is well studied, the escape mechanisms of FVs from restriction by A3 is much less explored. Here we review the current knowledge of FV biology, host restriction factors, and FV–host interactions with an emphasis on the consequences of FV regulatory protein Bet binding to A3s and outline crucial open questions for future studies.

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Section: Innate Immune Sensing Of Foamy Virusessupporting

confidence: 76%

Foamy Viruses, Bet, and APOBEC3 Restriction

Vasudevan

Becker

Luedde

et al. 2021

Viruses

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“…Two cell lines, one epithelial (BHK-21) and one fibroblastic (HT1080), with the highest susceptibility to primary zoonotic gorilla SFV were used as virus-transmitter cells [ 49 ]. They were infected at a low moi for a short period of time to minimize viral particle release associated with CPE.…”

Section: Resultsmentioning

confidence: 99%

“…Transmitter cells (BHK-21 or HT1080) were seeded (10 5 cells/25 cm 2 flasks) and infected the following day at a multiplicity of infection (moi) of 0.05. Ruxolitinib (5 μM) was added to gorilla SFV -infected cultures [ 49 ]. At 72 h post-infection, SFV-infected cells were seeded in 96-well plates (5 x 10 3 /well) in triplicates.…”

Section: Methodsmentioning

confidence: 99%

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Plasma antibodies from humans infected with zoonotic simian foamy virus do not inhibit cell-to-cell transmission of the virus despite binding to the surface of infected cells

et al. 2022

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Zoonotic simian foamy viruses (SFV) establish lifelong infection in their human hosts. Despite repeated transmission of SFV from nonhuman primates to humans, neither transmission between human hosts nor severe clinical manifestations have been reported. We aim to study the immune responses elicited by chronic infection with this retrovirus and previously reported that SFV-infected individuals generate potent neutralizing antibodies that block cell infection by viral particles. Here, we assessed whether human plasma antibodies block SFV cell-to-cell transmission and present the first description of cell-to-cell spreading of zoonotic gorilla SFV. We set-up a microtitration assay to quantify the ability of plasma samples from 20 Central African individuals infected with gorilla SFV and 9 uninfected controls to block cell-associated transmission of zoonotic gorilla SFV strains. We used flow-based cell cytometry and fluorescence microscopy to study envelope protein (Env) localization and the capacity of plasma antibodies to bind to infected cells. We visualized the cell-to-cell spread of SFV by real-time live imaging of a GFP-expressing prototype foamy virus (CI-PFV) strain. None of the samples neutralized cell-associated SFV infection, despite the inhibition of cell-free virus. We detected gorilla SFV Env in the perinuclear region, cytoplasmic vesicles and at the cell surface. We found that plasma antibodies bind to Env located at the surface of cells infected with primary gorilla SFV strains. Extracellular labeling of SFV proteins by human plasma samples showed patchy staining at the base of the cell and dense continuous staining at the cell apex, as well as staining in the intercellular connections that formed when previously connected cells separated from each other. In conclusion, SFV-specific antibodies from infected humans do not block cell-to-cell transmission, at least in vitro, despite their capacity to bind to the surface of infected cells. Trial registration: Clinical trial registration: www.clinicaltrials.gov, https://clinicaltrials.gov/ct2/show/NCT03225794/.

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“…In line with FV envelope (Env)-HS-PG interactions playing an important role in the early phases of FV replication is the observation that cationic polymers like polybrene or protamine sulfate, which are commonly used to enhance cell-free infection of many viruses, do not enhance or even slightly inhibit prototype FV (PFV) Env-mediated infection of target cells. 21 , 22 , 23 , 24 , 25 , 26 …”

Section: Introductionmentioning

confidence: 99%