Exosome-Mediated Delivery of Inducible miR-423-5p Enhances Resistance of MRC-5 Cells to Rabies Virus Infection

Wang, Jingyu; Teng, Yawei; Zhao, Guanshu; Li, Fang; Hou, Ali; Sun, Boxing; Kong, Wei; Gao, Feng; Cai, Linjun; Jiang, Chunlai

doi:10.3390/ijms20071537

Cited by 23 publications

(21 citation statements)

References 47 publications

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“…We found that HTNV increased exosome secretion from the infected-HUVECs, in agreement with previous publications on HTLV, 28 EV71, 10 HIV, 14 and Rabies viruses. 31 We demonstrated that HUVECs could take up exosomes in a time-and dose-dependent way and further tested how exosomes derived from Exo-HV control the fate of recipient cells. We have proved that Exo-HV contain partial viral RNAs other than viral proteins, but cannot transfer productive infection to naïve cells.…”

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confidence: 91%

Exosomal miR‐145‐5p derived from orthohantavirus‐infected endothelial cells inhibits HTNV infection

et al. 2020

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Human infection of orthohantavirus can cause potentially fatal diseases, such as hemorrhagic fever with renal syndrome (HFRS) caused by Hantaan virus (HTNV) in Eurasia. Exosomes are new carriers for information exchange between cells. Cumulative findings suggest that exosomes released from parental infected cells can block or promote viral infection in recipient cells, but the role of exosomes in hantavirus infection is poorly understood. In our study, we identified the exosomes derived from HTNV‐infected human vascular endothelial cells (HUVECs) (Exo‐HV) and found the antiviral properties of Exo‐HV in the uninfected recipient cells. High‐throughput sequencing revealed the distinctly expressed miRNAs transcriptomes in Exo‐HV. MiR‐145‐5p, one of the abundant miRNAs packaged into Exo‐HV, was found to be able to transferred to recipient cells and functioned by directly targeting M RNA of HTNV 76‐118 and inducing type I interferon (IFN‐I) response, thus, blocking the viral replication. Concluding, this study indicated that exosomes released by HTNV‐infected HUVECs were able to transfer active molecules, miR‐145‐5p as a proving sample, to mediate novel anti‐HTNV activity in the neighboring uninfected cells, which will help us to explore new strategies for the treatment of infectious disease utilizing exosomes with miRNA.

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confidence: 91%

Exosomal miR‐145‐5p derived from orthohantavirus‐infected endothelial cells inhibits HTNV infection

et al. 2020

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“…EVs from infected cells are able to activate other cells DENV (Velandia-Romero et al, 2020;Mishra et al, 2019) RNAs inside EVs related to host responses to infection DENV (Martins et al, 2018a), H5N1 (Maemura et al, 2018;Maemura et al, 2020), HBV (Zhao X. et al, 2019), HIV (Bernard et al, 2014), HSV-1 (Han et al, 2016;Huang et al, 2019), influenza (Liu Y. et al, 2019), Rabies (Wang et al, 2019a), RSV (Chahar et al, 2018), West Nile (Slonchak et al, 2019) EVs from infected cells can trigger the secretion of proinflammatory molecules in other cells HIV (Sampey et al, 2016;Mukhamedova et al, 2019), H5N1 (Maemura et al, 2018;Maemura et al, 2020), HBV (Zhao X. et al, 2019), RSV (Chahar et al, 2018) EVs involved in IFN-mediated responses DENV (Martins et al, 2018), HBV (Yao et al, 2019;Zhao X. et al, 2019), HCV (Dreux et al, 2012;Okamoto et al, 2014), HIV-1 (Khatua et al, 2009), HSV-1 (Huang et al, 2019), influenza EVs that can restrict viral replication Rabies (Wang et al, 2019a), HBV (Zhao X. et al, 2019), HIV (Ouattara et al, 2018), Induction of massive inflammatory responses/vascular permeability DENV (Sung et al, 2019) EVs can block/impair viral propagation Enterovirus (Chen et al, 2015), Influenza (Liu Y. et al, 2019), HIV-1 (Khatua et al, 2009), HSV-1 (Han et al, 2016;Deschamps and Kalamvoki, 2018;Huang et al, 2019), Rabies…”

Section: Mechanism Virusmentioning

confidence: 99%

“…Cells infected with herpes simplex virus (HSV-1) produce EVs packed with miR-H28 and miR-H29, which are able to restrict viral transmission to uninfected cells through the induction of IFN-gamma production (Huang et al, 2019). Other mechanisms of EV-mediated viral inhibition can also occur, as observed for MRC-5 cells infected with rabies, that show increased production of EVs containing miR-423-5p, which inhibits RABV replication in neighboring recipient cells (Wang et al, 2019a). Exosomes from the microenvironment and biofluids can also modulate viral infection, as shown for seminal EVs, which seems to have a protective effect against HIV infection.…”

Section: Mechanism Virusmentioning

confidence: 99%

Extracellular Vesicles in Viral Infections: Two Sides of the Same Coin?

Martins

Alves

2020

Front. Cell. Infect. Microbiol.

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Extracellular vesicles are small membrane structures containing proteins and nucleic acids that are gaining a lot of attention lately. They are produced by most cells and can be detected in several body fluids, having a huge potential in therapeutic and diagnostic approaches. EVs produced by infected cells usually have a molecular signature that is very distinct from healthy cells. For intracellular pathogens like viruses, EVs can have an even more complex function, since the viral biogenesis pathway can overlap with EV pathways in several ways, generating a continuum of particles, like naked virions, EVs containing infective viral genomes and quasi-enveloped viruses, besides the classical complete viral particles that are secreted to the extracellular space. Those particles can act in recipient cells in different ways. Besides being directly infective, they also can prime neighbor cells rendering them more susceptible to infection, block antiviral responses and deliver isolated viral molecules. On the other hand, they can trigger antiviral responses and cytokine secretion even in uninfected cells near the infection site, helping to fight the infection and protect other cells from the virus. This protective response can also backfire, when a massive inflammation facilitated by those EVs can be responsible for bad clinical outcomes. EVs can help or harm the antiviral response, and sometimes both mechanisms are observed in infections by the same virus. Since those pathways are intrinsically interlinked, understand the role of EVs during viral infections is crucial to comprehend viral mechanisms and respond better to emerging viral diseases.

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“…Gene knockout mutants have also been developed to improve safety be preventing generation of virus progeny, this includes matrix (M) or phosphoprotein (P) deficient strains [ 140 , 141 , 142 ]. Alternative methods to improve safety either substitute the virus for a harmless pseudotyped adenovirus or vaccinia virus expressing the RABV G-protein, or remove the virus entirely by means of DNA vaccines expressing G protein [ 143 , 144 , 145 ].…”

Section: Factors Behind the Success/failure Of An Nsv Vaccinementioning

confidence: 99%

Investigating the Interaction between Negative Strand RNA Viruses and Their Hosts for Enhanced Vaccine Development and Production

et al. 2021

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The current pandemic has highlighted the ever-increasing risk of human to human spread of zoonotic pathogens. A number of medically-relevant zoonotic pathogens are negative-strand RNA viruses (NSVs). NSVs are derived from different virus families. Examples like Ebola are known for causing severe symptoms and high mortality rates. Some, like influenza, are known for their ease of person-to-person transmission and lack of pre-existing immunity, enabling rapid spread across many countries around the globe. Containment of outbreaks of NSVs can be difficult owing to their unpredictability and the absence of effective control measures, such as vaccines and antiviral therapeutics. In addition, there remains a lack of essential knowledge of the host–pathogen response that are induced by NSVs, particularly of the immune responses that provide protection. Vaccines are the most effective method for preventing infectious diseases. In fact, in the event of a pandemic, appropriate vaccine design and speed of vaccine supply is the most critical factor in protecting the population, as vaccination is the only sustainable defense. Vaccines need to be safe, efficient, and cost-effective, which is influenced by our understanding of the host–pathogen interface. Additionally, some of the major challenges of vaccines are the establishment of a long-lasting immunity offering cross protection to emerging strains. Although many NSVs are controlled through immunisations, for some, vaccine design has failed or efficacy has proven unreliable. The key behind designing a successful vaccine is understanding the host–pathogen interaction and the host immune response towards NSVs. In this paper, we review the recent research in vaccine design against NSVs and explore the immune responses induced by these viruses. The generation of a robust and integrated approach to development capability and vaccine manufacture can collaboratively support the management of outbreaking NSV disease health risks.

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Exosome-Mediated Delivery of Inducible miR-423-5p Enhances Resistance of MRC-5 Cells to Rabies Virus Infection

Cited by 23 publications

References 47 publications

Exosomal miR‐145‐5p derived from orthohantavirus‐infected endothelial cells inhibits HTNV infection

Exosomal miR‐145‐5p derived from orthohantavirus‐infected endothelial cells inhibits HTNV infection

Extracellular Vesicles in Viral Infections: Two Sides of the Same Coin?

Investigating the Interaction between Negative Strand RNA Viruses and Their Hosts for Enhanced Vaccine Development and Production

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