Characterization of Prototype Foamy Virus Infectivity in Transportin 3 Knockdown Human 293t Cell Line

Hamid, Faysal Bin; Kim, Jinsun; Shin, Cha‐Gyun

doi:10.4014/jmb.1606.06011

Cited by 7 publications

(7 citation statements)

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“…Human embryonic kidney 293T (HEK 293T) cells were maintained in Dubecco's Modified Eagle Medium (DMEM) supplemented with 10% fetal bovine serum (FBS, Gibco, USA) and 1% penicillin/ streptomycin (Invitrogen, USA) [22][23][24][25]. The cells were grown in a humidifying incubator at 37 o C with 5% CO…”

Section: Cells and Reagentsmentioning

confidence: 99%

Hepatitis E Virus Papain-Like Cysteine Protease Inhibits Type I Interferon Induction by Down-Regulating Melanoma Differentiation-Associated Gene 5

Kim

Myoung

2018

Journal of Microbiology and Biotechnology

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Upon viral infection, the host cell recognizes the invasion through a number of pattern recognition receptors. Melanoma differentiation associated gene 5 (MDA5) and retinoic acidinducible gene-I (RIG-I) recognize RNA molecules derived from invading viruses, activating downstream signaling cascades, culminating in the induction of the type I interferon. On the other hand, viruses have evolved to evade type I interferon-mediated inhibition. Hepatitis E virus has been shown to encode a few antagonists of type I interferon and it is not surprising that viruses encode multiple mechanisms of viral evasion. In the present study, we demonstrated that HEV PCP strongly down-regulates MDA5-mediated activation of interferon β induction in a dose-dependent manner. Interestingly, MDA5 protein expression was almost completely abolished. In addition, polyinosinic polycytidylic acid (poly(I:C))-and Sendai virus-mediated activation of type I interferon responses were similarly abrogated in the presence of HEV PCP. Furthermore, HEV PCP down-regulates several molecules that play critical roles in the induction of type I IFN expression. Taken together, these data collectively suggest that HEV-encoded PCP is a strong antagonist of type I interferon.

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Section: Cells and Reagentsmentioning

confidence: 99%

Hepatitis E Virus Papain-Like Cysteine Protease Inhibits Type I Interferon Induction by Down-Regulating Melanoma Differentiation-Associated Gene 5

Kim

Myoung

2018

Journal of Microbiology and Biotechnology

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“…Apart from HIV-1 other retroviruses show TRN-SR2 dependency. Faysal Bin et al for example studied the role of TRN-SR2 in the prototype foamy virus (PFV) life cycle [ 42 ]. TRN-SR2 KD cells significantly reduced the infection of PFV (15–20%) compared to the WT cells.…”

Section: Interplay Between Hiv-1 Integrase (In) and Trn-sr2mentioning

confidence: 99%

Role of Transportin-SR2 in HIV-1 Nuclear Import

Tabasi

Nombela

Janssens

et al. 2021

Viruses

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The HIV replication cycle depends on the interaction of viral proteins with proteins of the host. Unraveling host–pathogen interactions during the infection is of great importance for understanding the pathogenesis and the development of antiviral therapies. To date HIV uncoating and nuclear import are the most debated steps of the HIV-1 replication cycle. Despite numerous studies during past decades, there is still much controversy with respect to the identity and the role of viral and host factors involved in these processes. In this review, we provide a comprehensive overview on the role of transportin-SR2 as a host cell factor during active nuclear transport.

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“…PFV IN possesses a potent nuclear localization signal in its CTD spanning residues 289–371; an amino acid mutation study revealed that some residue positions (308, 313, 318, 324, and 329) notably affect nuclear localization [ 93 ]. TNPO3 is a karyopherin involved in transporting phosphorylated serine/ arginine-rich proteins between the cytoplasm and nucleus, and it is known to be a key factor involved in HIV-1 replication [ 94 , 95 ]. In one study, TNPO3 knockdown reduced PFV production in BHK-21 cells and human 293T cells [ 94 ].…”

Section: Genomic Analysis Of Fv In Dnamentioning

confidence: 99%

Foamy Virus Integrase in Development of Viral Vector for Gene Therapy

Kim

Lee

Shin

2020

J. Microbiol. Biotechnol.

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Since the concept was established in 1972, gene therapy has been studied in concert with the development of molecular biotechnology [1][2][3]. The first successful trial of gene therapy in humans was performed in 1989 [4]. In that protocol, patients with melanoma were treated with a gene-modified, tumor-infiltrating lymphocyte construct modified by retroviral transduction. There were no side effects from 3 weeks to 2 months during the monitoring period. In 2017, the FDA approved the first gene therapy in the USA. This novel, genetically engineered chimeric antigen receptor T-cell therapy was soon followed by approval of RPE65 mutation-induced blindness gene therapy. In approximately the last three decades, viral vectors have been used for over 3,000 clinical tasks, from therapy to regenerative medicine, following more than half of them in phase I [5]. Gene therapy has broad prospects as an effective therapeutic strategy for various diseases, including cancer, as well as monogenic, infectious, cardiovascular, and neurological diseases. In terms of types of viruses, adenoviruses, retroviruses, and lentiviruses have been intensively studied, and adeno-associated virus research began recently [5]. However, viral gene therapy vectors pose safety issues, including direct toxicity and stimulation of the immune response [6][7][8]. Nevertheless, viral vectors have been extensively studied because of their advantages, such as their broad host range, including humans, and high gene transfer rates to host cells.Among them, the Retroviridae family is composed of two virus subfamilies, six genera of Orthoretrovirinae and four genera of Spumaretrovirinae (commonly called spumaviruses or foamy viruses [FVs]). FVs were first mentioned as a contaminant in primary monkey kidney cultures in 1954 [9]. Since 'foamy viral agent' was first isolated in 1955, FV has been found in various mammalians, including humans [10]. FVs are exogenous viruses that induce the specific cytopathic effect (CPE), or 'foamy' appearance in host cells [11]. The FV life cycle is different from other retroviruses. First, FV buds from the endoplasmic reticulum instead of the cytoplasmic membrane. This helps form the FV's unique 'spike surface' morphology [11]. Furthermore, the replication of FV is like that of Hepadnaviridae, which is another family of virus that has reverse transcriptase-encoding gene. Reverse transcription of FV genome occurs not in the early steps like other retroviruses, but also in the late steps of replication [12]. Although FV-infected cells show characteristic large vacuoles in vitro, there have been no reported serial diseases from FV infection in vivo, so FVs have been considered potential gene therapy vectors [10]. Here, we discuss research achievements with foamy virus vectors (FVVs) in gene therapy and specifically focus on the characteristics of FV integrase (IN) and its prospective functions associated with vector research. FVs as Viral Vector CandidatesFVs have a broad range of tissue and cell tropism, and virus infections are g...

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Characterization of Prototype Foamy Virus Infectivity in Transportin 3 Knockdown Human 293t Cell Line

Cited by 7 publications

References 0 publications

Hepatitis E Virus Papain-Like Cysteine Protease Inhibits Type I Interferon Induction by Down-Regulating Melanoma Differentiation-Associated Gene 5

Hepatitis E Virus Papain-Like Cysteine Protease Inhibits Type I Interferon Induction by Down-Regulating Melanoma Differentiation-Associated Gene 5

Role of Transportin-SR2 in HIV-1 Nuclear Import

Foamy Virus Integrase in Development of Viral Vector for Gene Therapy

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