Host–Pathogen Interactions in Measles Virus Replication and Anti-Viral Immunity

Jiang, Yanliang; Qin, Yali; Chen, Mingzhou

doi:10.3390/v8110308

Cited by 21 publications

(9 citation statements)

References 122 publications

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“…However, MeV with a C protein knockout was a more efficient inducer of SG formation than wild‐type MeV. It was determined that the intact C protein would lead to a decrease in PKR expression, which would subsequently allow for SG formation (Jiang, Qin, & Chen, 2016). Similar function has been attributed to the influenza NS1 protein and vaccinia virus E3L protein (Khaperskyy, Hatchette, & McCormick, 2012; Simpson‐Holley et al, 2011).…”

Section: Emerging Translation Strategies During Virus–host Interactionmentioning

confidence: 99%

Emerging translation strategies during virus–host interaction

et al. 2020

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Translation control is crucial during virus–host interaction. On one hand, viruses completely rely on the protein synthesis machinery of host cells to propagate and have evolved various mechanisms to redirect the host's ribosomes toward their viral mRNAs. On the other hand, the host rewires its translation program in an attempt to contain and suppress the virus early on during infection; the antiviral program includes specific control on protein synthesis to translate several antiviral mRNAs involved in quenching the infection. As the infection progresses, host translation is in turn inhibited in order to limit viral propagation. We have learnt of very diverse strategies that both parties utilize to gain or retain control over the protein synthesis machinery. Yet novel strategies continue to be discovered, attesting for the importance of mRNA translation in virus–host interaction. This review focuses on recently described translation strategies employed by both hosts and viruses. These discoveries provide additional pieces in the understanding of the complex virus–host translation landscape. This article is categorized under: Translation > Translation Mechanisms Translation > Translation Regulation

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Section: Emerging Translation Strategies During Virus–host Interactionmentioning

confidence: 99%

Emerging translation strategies during virus–host interaction

et al. 2020

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“…The main structural proteins for both viruses are: Nucleoprotein (N), Phosphoprotein (P), Matrix protein (M), Fusion protein (F), and Large Protein (L). The MV genome encodes two non-structural proteins, C and V, [20], while the SeV genome encodes a set of non-structural proteins, collectively referred as C-proteins (C', C, Y1, Y2, V, W) [21]. Viral replication for MV and SeV follows a negative-stranded RNA virus replication model in which genomic RNA (minus strand) is used as a template to create a copy of positive sense RNA, employing the RNA-dependent RNA polymerase embedded in the virion.…”

Section: Cancers 2020 12 X 3 Of 27mentioning

confidence: 99%

Prospects for Using Expression Patterns of Paramyxovirus Receptors as Biomarkers for Oncolytic Virotherapy

Matveeva¹,

Shabalina

2020

Cancers

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The effectiveness of oncolytic virotherapy in cancer treatment depends on several factors, including successful virus delivery to the tumor, ability of the virus to enter the target malignant cell, virus replication, and the release of progeny virions from infected cells. The multi-stage process is influenced by the efficiency with which the virus enters host cells via specific receptors. This review describes natural and artificial receptors for two oncolytic paramyxoviruses, nonpathogenic measles, and Sendai viruses. Cell entry receptors are proteins for measles virus (MV) and sialylated glycans (sialylated glycoproteins or glycolipids/gangliosides) for Sendai virus (SeV). Accumulated published data reviewed here show different levels of expression of cell surface receptors for both viruses in different malignancies. Patients whose tumor cells have low or no expression of receptors for a specific oncolytic virus cannot be successfully treated with the virus. Recent published studies have revealed that an expression signature for immune genes is another important factor that determines the vulnerability of tumor cells to viral infection. In the future, a combination of expression signatures of immune and receptor genes could be used to find a set of oncolytic viruses that are more effective for specific malignancies.

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“…Measles is a highly contagious respiratory infection that is caused by MV – an enveloped ssRNA virus. After MV fuses with the host cell membrane, genome replication occurs in the cytoplasm and the virus is released by budding at the plasma membrane (Jiang et al, 2016). Knockdown of AnxA2 via shRNA in cervical epithelial cells (HeLa) caused reduced MV progeny virus generation 24 h post-infection, but did not affect MV entry and RNA replication (Koga et al, 2018).…”

Section: Annexin A2 In Virus Replication Assembly and Releasementioning

confidence: 99%

Annexin A2 in Virus Infection

2018

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Viral life cycles consist of three main phases: (1) attachment and entry, (2) genome replication and expression, and (3) assembly, maturation, and egress. Each of these steps is intrinsically reliant on host cell factors and processes including cellular receptors, genetic replication machinery, endocytosis and exocytosis, and protein expression. Annexin A2 (AnxA2) is a membrane-associated protein with a wide range of intracellular functions and a recurrent host factor in a variety of viral infections. Spatially, AnxA2 is found in the nucleus and cytoplasm, vesicle-bound, and on the inner and outer leaflet of the plasma membrane. Structurally, AnxA2 exists as a monomer or in complex with S100A10 to form the AnxA2/S100A10 heterotetramer (A2t). Both AnxA2 and A2t have been implicated in a vast array of cellular functions such as endocytosis, exocytosis, membrane domain organization, and translational regulation through RNA binding. Accordingly, many discoveries have been made involving AnxA2 in viral pathogenesis, however, the reported work addressing AnxA2 in virology is highly compartmentalized. Therefore, the purpose of this mini review is to provide information regarding the role of AnxA2 in the lifecycle of multiple epithelial cell-targeting viruses to highlight recurrent themes, identify discrepancies, and reveal potential avenues for future research.

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Host–Pathogen Interactions in Measles Virus Replication and Anti-Viral Immunity

Cited by 21 publications

References 122 publications

Emerging translation strategies during virus–host interaction

Emerging translation strategies during virus–host interaction

Prospects for Using Expression Patterns of Paramyxovirus Receptors as Biomarkers for Oncolytic Virotherapy

Annexin A2 in Virus Infection

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