La Piedad Michoacán Mexico Virus V protein antagonizes type I interferon response by binding STAT2 protein and preventing STATs nuclear translocation

Pisanelli, Giuseppe; Laurent-Rolle, Maudry; Manicassamy, Balaji; Belicha-Villanueva, Alan; Morrison, Juliet; Lozano-Dubernard, Bernardo; Castro-Peralta, Felipa; Iovane, G.; Garcı́a-Sastre, Adolfo

doi:10.1016/j.virusres.2015.10.027

Cited by 8 publications

(4 citation statements)

References 75 publications

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“…These binding events inhibit phosphorylation and nuclear translocation of the STATs. In contrast, Rubulavirinae V proteins generally bind STAT1 or STAT2 via the C-terminal region alone ( Nishio et al 2002 , 2005 ; Pisanelli et al 2016 ), and this leads to the targeted degradation of STATs via the proteosomal pathway. This requires the recruitment of additional host proteins, such as DDB1 ( Lin et al 1998 ; Andrejeva et al 2002 ), that enable the polyubiquitination of STATs.…”

Section: Organization and Function Of The Proteins Resulting From Gene Editingmentioning

confidence: 99%

Evolutionary history of cotranscriptional editing in the paramyxoviral phosphoprotein gene

2021

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The phosphoprotein gene of the paramyxoviruses encodes multiple protein products. The P, V, and W proteins are generated by transcriptional slippage. This process results in the insertion of non-templated guanosine nucleosides into the mRNA at a conserved edit site. The P protein is an essential component of the viral RNA polymerase, and is encoded by a faithful copy of the gene in the majority of paramyxoviruses. However, in some cases the non essential V protein is encoded by default and guanosines must be inserted into the mRNA in order to encode P. The number of guanosines inserted into the P gene can be described by a probability distribution which varies between viruses. In this article we review the nature of these distributions, which can be inferred from mRNA sequencing data, and reconstruct the evolutionary history of cotranscriptional editing in the paramyxovirus family. Our model suggests that, throughout known history of the family, the system has switched from a P default to a V default mode four times; complete loss of the editing system has occurred twice, the canonical zinc finger domain of the V protein has been deleted or heavily mutated a further two times, and the W protein has independently evolved a novel function three times. Finally, we review the physical mechanisms of cotranscriptional editing via slippage of the viral RNA polymerase.

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Section: Organization and Function Of The Proteins Resulting From Gene Editingmentioning

confidence: 99%

Evolutionary history of cotranscriptional editing in the paramyxoviral phosphoprotein gene

2021

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“…www.nature.com/scientificreports/ Meanwhile, we have observed that the reduction in monocyte numbers in HIV patients may be associated with compromised immune function. Monocytes, as primary participants in the innate immune system, play a crucial role in antiviral infections through the IFN signaling pathway 54 . Monocytes serve as target cells for HIV-1 infection, and monocytes release inflammatory factors and differentiate upon HIV-1 infection, stimulated by the IFN signaling pathway 55 .…”

Section: Discussionmentioning

confidence: 99%

Identification of the shared hub gene signatures and molecular mechanisms between HIV-1 and pulmonary arterial hypertension

Mai,

Yang,

Xie

et al. 2024

Sci Rep

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The close link between HIV-1 infection and the occurrence of pulmonary arterial hypertension (PAH). However, the underlying molecular mechanisms of their interrelation remain unclear. The microarray data of HIV-1 and PAH were downloaded from GEO database. We utilized WGCNA to identify shared genes between HIV-1 and PAH, followed by conducting GO and pathway enrichment analyses. Subsequently, differentially genes analysis was performed using external validation datasets to further filter hub genes. Immunoinfiltration analysis was performed using CIBERSORT. Finally, hub gene expression was validated using scRNA-seq data. We identified 109 shared genes through WGCNA, primarily enriched in type I interferon (IFN) pathways. By taking the intersection of WGCNA important module genes and DEGs, ISG15 and IFI27 were identified as pivotal hub genes. Immunoinfiltration analysis and scRNA-seq results indicated the significant role of monocytes in the shared molecular mechanisms of HIV-1 and PAH. In summary, our study illustrated the possible mechanism of PAH secondary to HIV-1 and showed that the heightened IFN response in HIV-1 might be a crucial susceptibility factor for PAH, with monocytes being pivotal cells involved in the type I IFN response pathway. This provides potential new insights for further investigating the molecular mechanisms connecting HIV-1 and PAH.

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“…This contrasts with V proteins from other members of the Rubulavirinae subfamily. LPMV-V protein IFN evasion is similar to that of Henipavirus V protein with its selective binding with STAT2 protein, though not with STAT1, and with the inhibition of STATs phosphorylation and subsequent nuclear translocation ( Figure 3 ) [ 133 ].…”

Section: Role Of the P V And W Proteins In Ifn Antagonismmentioning

confidence: 99%

Type I and Type II Interferon Antagonism Strategies Used by Paramyxoviridae: Previous and New Discoveries, in Comparison

Pisanelli

Pagnini

Iovane

et al. 2022

Viruses

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Paramyxoviridae is a viral family within the order of Mononegavirales; they are negative single-strand RNA viruses that can cause significant diseases in both humans and animals. In order to replicate, paramyxoviruses–as any other viruses–have to bypass an important protective mechanism developed by the host’s cells: the defensive line driven by interferon. Once the viruses are recognized, the cells start the production of type I and type III interferons, which leads to the activation of hundreds of genes, many of which encode proteins with the specific function to reduce viral replication. Type II interferon is produced by active immune cells through a different signaling pathway, and activates a diverse range of genes with the same objective to block viral replication. As a result of this selective pressure, viruses have evolved different strategies to avoid the defensive function of interferons. The strategies employed by the different viral species to fight the interferon system include a number of sophisticated mechanisms. Here we analyzed the current status of the various strategies used by paramyxoviruses to subvert type I, II, and III interferon responses.

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La Piedad Michoacán Mexico Virus V protein antagonizes type I interferon response by binding STAT2 protein and preventing STATs nuclear translocation

Cited by 8 publications

References 75 publications

Evolutionary history of cotranscriptional editing in the paramyxoviral phosphoprotein gene

Evolutionary history of cotranscriptional editing in the paramyxoviral phosphoprotein gene

Identification of the shared hub gene signatures and molecular mechanisms between HIV-1 and pulmonary arterial hypertension

Type I and Type II Interferon Antagonism Strategies Used by Paramyxoviridae: Previous and New Discoveries, in Comparison

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