TRIM22. A Multitasking Antiviral Factor

Pagani, Isabel; Poli, Guido; Vicenzi, Elisa

doi:10.3390/cells10081864

Cited by 29 publications

(22 citation statements)

References 127 publications

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“…TRIM22 expression may be induced by interferon and its 5′ anking region gene contains two homologous sequences of IFN-stimulated response elements, which bind to IFN regulatory factor 1 in response to types I and II IFN stimulation and induce TRIM22 expression [22]. In addition to interferon, TRIM22 expression is also regulated by viruses and viral antigens [23]. As a member of the TRIM family, TRIM22 regulates viral infection through various mechanisms.…”

Section: Discussionmentioning

confidence: 99%

Mechanism of autophagy induced by activation of the AMPK/ERK/mTOR signaling pathway after TRIM22-mediated DENV-2 infection of HUVECs

Gou

et al. 2022

Preprint

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Background Dengue virus type 2 (DENV-2) was used to infect primary human umbilical vein endothelial cells (HUVECs) to examine autophagy induced by activation of the adenosine monophosphate-activated protein kinase (AMPK)/extracellular signal-regulated kinase (ERK)/mammalian target of rapamycin (mTOR) signaling pathway following tripartite motif-containing 22 (TRIM22)-mediated DENV-2 infection to further reveal the underlying pathogenic mechanism of DENV-2 infection. Methods Quantitative real-time polymerase chain reaction (qRT-PCR) was used to screen putative interference targets of TRIM22 and determine the knockdown efficiency. The effect of TRIM22 knockdown on HUVEC proliferation was determined using the CCK8 assay. Following TRIM22 knockdown, transmission electron microscopy (TEM) was used to determine the ultrastructure of HUVEC autophagosomes and expression of HUVEC autophagy and AMPK pathway-related genes were measured by qRT-PCR. Moreover, HUVEC autophagy and AMPK pathway-related protein expression levels were determined by western blot analysis. Cell cycle and apoptosis were assessed by flow cytometry (FCM) and the autophagosome structure of the HUVECs was observed by TEM. Results Western blot results indicated that TRIM22 protein expression levels increased significantly 36 h after DENV-2 infection, which was consistent with the proteomics prediction. The CCK8 assay revealed that HUVEC proliferation was reduced following TRIM22 knockdown (P < 0.001). The TEM results indicated that HUVEC autolysosomes increased and autophagy was inhibited after TRIM22 knockdown. The qRT-PCR results revealed that after TRIM22 knockdown, the expression levels of antithymocyte globulin 7 (ATG7), antithymocyte globulin 5 (ATG5), Beclin1, ERK, and mTOR genes decreased (P < 0.01); however, the expression of AMPK genes (P < 0.05) and P62 genes (P < 0.001) increased. FCM revealed that following TRIM22 knockdown, the percentage of HUVECs in the G2 phase increased (P < 0.001) along with cell apoptosis. The effect of TRIM22 overexpression on HUVEC autophagy induced by DENV-2 infection and AMPK pathways decreased after adding an autophagy inhibitor. Conclusions In HUVECs, TRIM22 protein positively regulates autophagy and may affect autophagy through the AMPK/ERK/mTOR signaling pathway. Autophagy is induced by activation of the AMPK/ERK/mTOR signaling pathway following TRIM22-mediated DENV-2 infection of HUVECs.

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Section: Discussionmentioning

confidence: 99%

Mechanism of autophagy induced by activation of the AMPK/ERK/mTOR signaling pathway after TRIM22-mediated DENV-2 infection of HUVECs

Gou

et al. 2022

Preprint

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“…TRIM22, also known as Staf50, is an ISG whose expression is profoundly upregulated by IFN stimulation of different cell types [ 47 ]. Our group described it as the key factor differentiating U937 cell clones with a restrictive phenotype in terms of supporting HIV-1 replication (“Minus clones”) in comparison to those fully permissive clones (“Plus clones”) [ 48 ].…”

Section: Exploiting M1 Polarization To Generate a Model Of Reversible...mentioning

confidence: 99%

Host Restriction Factors Modulating HIV Latency and Replication in Macrophages

Pagani¹,

Demela²,

Ghezzi³

et al. 2022

IJMS

Self Cite

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In addition to CD4+ T lymphocytes, myeloid cells and, particularly, differentiated macrophages are targets of human immunodeficiency virus type-1 (HIV-1) infection via the interaction of gp120Env with CD4 and CCR5 or CXCR4. Both T cells and macrophages support virus replication, although with substantial differences. In contrast to activated CD4+ T lymphocytes, HIV-1 replication in macrophages occurs in nondividing cells and it is characterized by the virtual absence of cytopathicity both in vitro and in vivo. These general features should be considered in evaluating the role of cell-associated restriction factors aiming at preventing or curtailing virus replication in macrophages and T cells, particularly in the context of designing strategies to tackle the viral reservoir in infected individuals receiving combination antiretroviral therapy. In this regard, we will here also discuss a model of reversible HIV-1 latency in primary human macrophages and the role of host factors determining the restriction or reactivation of virus replication in these cells.

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“…Interestingly, this restriction was observed in chronically infected T cell lines in response to arsenic/interferon therapy [ 45 ]. Other TRIM family members remain to be investigated such as TRIM22 for example, which acts as restriction factor for many viruses including HIV [ 65 ], with only one viral antagonist identified [ 66 ]. Therefore, TRIM proteins might be promising candidates when searching for cellular factors able to restrict HTLV-1 replication.…”

Section: Activity Of Known Hiv Restriction Factors On Htlv-1 Replicationmentioning

confidence: 99%

Is the HTLV-1 Retrovirus Targeted by Host Restriction Factors?

Carcone

Journo

Dutartre

2022

Viruses

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Human T cell leukemia virus type 1 (HTLV-1), the etiological agent of adult T cell leukemia/lymphoma (ATLL) and of HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP), was identified a few years before Human Immunodeficiency Virus (HIV). However, forty years later, our comprehension of HTLV-1 immune detection and the host immune responses to HTLV-1 is far more limited than for HIV. In addition to innate and adaptive immune responses that rely on specialized cells of the immune system, host cells may also express a range of antiviral factors that inhibit viral replication at different stages of the cycle, in a cell-autonomous manner. Multiple antiviral factors allowing such an intrinsic immunity have been primarily and extensively described in the context HIV infection. Here, we provide an overview of whether known HIV restriction factors might act on HTLV-1 replication. Interestingly, many of them do not exert any antiviral activity against HTLV-1, and we discuss viral replication cycle specificities that could account for these differences. Finally, we highlight future research directions that could help to identify antiviral factors specific to HTLV-1.

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TRIM22. A Multitasking Antiviral Factor

Cited by 29 publications

References 127 publications

Mechanism of autophagy induced by activation of the AMPK/ERK/mTOR signaling pathway after TRIM22-mediated DENV-2 infection of HUVECs

Mechanism of autophagy induced by activation of the AMPK/ERK/mTOR signaling pathway after TRIM22-mediated DENV-2 infection of HUVECs

Host Restriction Factors Modulating HIV Latency and Replication in Macrophages

Is the HTLV-1 Retrovirus Targeted by Host Restriction Factors?

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