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4 results on '"Chawdury A"'

1. Targeting Viral Proteostasis Limits Influenza Virus, HIV, and Dengue Virus Infection (vol 44, pg 46, 2016)

Author

Heaton, Nicholas S, Moshkina, Natasha, Fenouil, Romain, Gardner, Thomas J, Aguirre, Sebastian, Shah, Priya S, Zhao, Nan, Manganaro, Lara, Hultquist, Judd F, Noel, Justine, Sachs, David, Hamilton, Jennifer, Leon, Paul E, Chawdury, Amit, Tripathi, Shashank, Melegari, Camilla, Campisi, Laura, Hai, Rong, Metreveli, Giorgi, Gamarnik, Andrea V, Garcia-Sastre, Adolfo, Greenbaum, Benjamin, Simon, Viviana, Fernandez-Sesma, Ana, Krogan, Nevan J, Mulder, Lubbertus CF, van Bakel, Harm, Tortorella, Domenico, Taunton, Jack, Palese, Peter, and Marazzi, Ivan

Subjects
Immunology
Published
2016

2. Targeting Viral Proteostasis Limits Influenza Virus, HIV, and Dengue Virus Infection

Author

Heaton, Nicholas S, Moshkina, Natasha, Fenouil, Romain, Gardner, Thomas J, Aguirre, Sebastian, Shah, Priya S, Zhao, Nan, Manganaro, Lara, Hultquist, Judd F, Noel, Justine, Sachs, David, Hamilton, Jennifer, Leon, Paul E, Chawdury, Amit, Tripathi, Shashank, Melegari, Camilla, Campisi, Laura, Hai, Rong, Metreveli, Giorgi, Gamarnik, Andrea V, García-Sastre, Adolfo, Greenbaum, Benjamin, Simon, Viviana, Fernandez-Sesma, Ana, Krogan, Nevan J, Mulder, Lubbertus CF, van Bakel, Harm, Tortorella, Domenico, Taunton, Jack, Palese, Peter, and Marazzi, Ivan

Subjects
Immunology
Published
2016

3. Targeting Viral Proteostasis Limits Influenza Virus, HIV, and Dengue Virus Infection

Author

Heaton, Nicholas S, Moshkina, Natasha, Fenouil, Romain, Gardner, Thomas J, Aguirre, Sebastian, Shah, Priya S, Zhao, Nan, Manganaro, Lara, Hultquist, Judd F, Noel, Justine, Sachs, David, Hamilton, Jennifer, Leon, Paul E, Chawdury, Amit, Tripathi, Shashank, Melegari, Camilla, Campisi, Laura, Hai, Rong, Metreveli, Giorgi, Gamarnik, Andrea V, García-Sastre, Adolfo, Greenbaum, Benjamin, Simon, Viviana, Fernandez-Sesma, Ana, Krogan, Nevan J, Mulder, Lubbertus CF, van Bakel, Harm, Tortorella, Domenico, Taunton, Jack, Palese, Peter, and Marazzi, Ivan

Subjects
Medical Microbiology, Biomedical and Clinical Sciences, Clinical Sciences, Immunology, Emerging Infectious Diseases, Biodefense, Vector-Borne Diseases, Sexually Transmitted Infections, Pneumonia & Influenza, Infectious Diseases, Influenza, Aetiology, 2.1 Biological and endogenous factors, 2.2 Factors relating to the physical environment, Infection, Good Health and Well Being, Dengue Virus, HIV, Host-Parasite Interactions, Humans, Immunoprecipitation, Influenza A virus, Mass Spectrometry, Models, Theoretical, Protein Folding, Proteomics, Virus Replication
Abstract

Viruses are obligate parasites and thus require the machinery of the host cell to replicate. Inhibition of host factors co-opted during active infection is a strategy hosts use to suppress viral replication and a potential pan-antiviral therapy. To define the cellular proteins and processes required for a virus during infection is thus crucial to understanding the mechanisms of virally induced disease. In this report, we generated fully infectious tagged influenza viruses and used infection-based proteomics to identify pivotal arms of cellular signaling required for influenza virus growth and infectivity. Using mathematical modeling and genetic and pharmacologic approaches, we revealed that modulation of Sec61-mediated cotranslational translocation selectively impaired glycoprotein proteostasis of influenza as well as HIV and dengue viruses and led to inhibition of viral growth and infectivity. Thus, by studying virus-human protein-protein interactions in the context of active replication, we have identified targetable host factors for broad-spectrum antiviral therapies.

Published
2016

4. Targeting Viral Proteostasis Limits Influenza Virus, HIV, and Dengue Virus Infection.

Author

Heaton, Nicholas S, Moshkina, Natasha, Fenouil, Romain, Gardner, Thomas J, Aguirre, Sebastian, Shah, Priya S, Zhao, Nan, Manganaro, Lara, Hultquist, Judd F, Noel, Justine, Sachs, David, Hamilton, Jennifer, Leon, Paul E, Chawdury, Amit, Tripathi, Shashank, Melegari, Camilla, Campisi, Laura, Hai, Rong, Metreveli, Giorgi, Gamarnik, Andrea V, García-Sastre, Adolfo, Greenbaum, Benjamin, Simon, Viviana, Fernandez-Sesma, Ana, Krogan, Nevan J, Mulder, Lubbertus CF, van Bakel, Harm, Tortorella, Domenico, Taunton, Jack, Palese, Peter, and Marazzi, Ivan

Subjects
Humans, Dengue Virus, Influenza A virus, HIV, Immunoprecipitation, Proteomics, Virus Replication, Protein Folding, Models, Theoretical, Mass Spectrometry, Host-Parasite Interactions, Immunology
Abstract

Viruses are obligate parasites and thus require the machinery of the host cell to replicate. Inhibition of host factors co-opted during active infection is a strategy hosts use to suppress viral replication and a potential pan-antiviral therapy. To define the cellular proteins and processes required for a virus during infection is thus crucial to understanding the mechanisms of virally induced disease. In this report, we generated fully infectious tagged influenza viruses and used infection-based proteomics to identify pivotal arms of cellular signaling required for influenza virus growth and infectivity. Using mathematical modeling and genetic and pharmacologic approaches, we revealed that modulation of Sec61-mediated cotranslational translocation selectively impaired glycoprotein proteostasis of influenza as well as HIV and dengue viruses and led to inhibition of viral growth and infectivity. Thus, by studying virus-human protein-protein interactions in the context of active replication, we have identified targetable host factors for broad-spectrum antiviral therapies.

Published
2016

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