Recruitment of the TSG101/ESCRT-I Machinery in Host Cells by Influenza Virus: Implications for Broad-Spectrum Therapy

Diaz, Leyla; Cassella, Josephine; Bonavia, Aurelio; Duan, Roxanne; Santos, David; Fesseha, Zena; Goldblatt, Michael; Kinch, Michael S.

doi:10.1016/j.antiviral.2009.02.175

Cited by 2 publications

(2 citation statements)

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“…The M1 protein encoded by Influenza A virus contains a putative late domain motif, YKRL, and interacts with the UEV domain of Tsg101 (Diaz et al, 2009). M1 could facilitate influenza budding similar to the well-established interaction of HIV Gag or Ebola VP-40 with Tsg101.…”

Section: Discussionmentioning

confidence: 99%

Type I Interferon Imposes a TSG101/ISG15 Checkpoint at the Golgi for Glycoprotein Trafficking during Influenza Virus Infection

Sanyal

Ashour

Maruyama

et al. 2013

Cell Host & Microbe

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Summary Several enveloped viruses exploit host pathways, such as the cellular endosomal sorting complex required for transport (ESCRT) machinery, for their assembly and release. The influenza A virus (IAV) matrix protein binds to the ESCRT-I complex, although the involvement of early ESCRT proteins such as Tsg101 in IAV trafficking remains to be established. We find that Tsg101 can facilitate IAV trafficking but this is effectively restricted by the interferon (IFN) stimulated protein ISG15. Cytosol from type I IFN-treated cells abolished IAV haemagglutinin (HA) transport to the cell surface in infected semi-intact cells. This inhibition required Tsg101 and could be relieved with deISGylases. Tsg101 is itself ISGylated in IFN-treated cells. Upon infection, intact Tsg101-deficient cells obtained by CRISPR/Cas9 genome editing were defective in surface display of HA and for infectious virion release. These data support the IFN-induced generation of a Tsg101/ISG15-dependent checkpoint in the secretory pathway that compromises influenza virus release.

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Section: Discussionmentioning

confidence: 99%

Type I Interferon Imposes a TSG101/ISG15 Checkpoint at the Golgi for Glycoprotein Trafficking during Influenza Virus Infection

Sanyal

Ashour

Maruyama

et al. 2013

Cell Host & Microbe

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show abstract

“…For example, by modulating endosomal sorting machinery, such as Tsg101 or host factors from the endosomal sorting complex required for transport (ESCRT) pathway, the production of multiple viruses may be interrupted. Enveloped viruses including HIV-1 and Ebola hijack these factors to facilitate viral budding, and studies have implicated a role for tumor susceptibility gene 101 in the replication of multiple seasonal influenza viruses (e.g., H1N1, H2N2 and H3N1), as well as highly pathogenic avian influenza H5N1 virus [31]. Thus, the use of systems biology approaches for antiviral research would translate into effective therapeutics, with the potential to provide the greatest preventive measure against impending pandemic threats.…”

Section: New Horizon For Drug Developmentmentioning

confidence: 99%

Is Systems Biology the Key to Preventing the Next Pandemic?

et al. 2009

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Sporadic outbreaks of epizootics including SARS coronavirus and H5N1 avian influenza remind us of the potential for communicable diseases to quickly spread into worldwide epidemics. To confront emerging viral threats, nations have implemented strategies to prepare for pandemics and to control virus spread. Despite improved surveillance and quarantine measures, we find ourselves in the midst of a H1N1 influenza pandemic. Effective therapeutics and vaccines are essential to protect against current and future pandemics. The best route to effective therapeutics and vaccines is through a detailed and global view of virus-host interactions that can be achieved using a systems biology approach. Here, we provide our perspective on the role of systems biology in deepening our understanding of virus-host interactions and in improving drug and vaccine development.

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Recruitment of the TSG101/ESCRT-I Machinery in Host Cells by Influenza Virus: Implications for Broad-Spectrum Therapy

Cited by 2 publications

References 0 publications

Type I Interferon Imposes a TSG101/ISG15 Checkpoint at the Golgi for Glycoprotein Trafficking during Influenza Virus Infection

Type I Interferon Imposes a TSG101/ISG15 Checkpoint at the Golgi for Glycoprotein Trafficking during Influenza Virus Infection

Is Systems Biology the Key to Preventing the Next Pandemic?

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