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Viral infection paralyses protein synthesis in infected animals

24/06/2010

Scientists from the Department of Molecular Biology at the UAM and "Severo Ochoa" Centre of Molecular Biology (CSIC-UAM) describe for the first time how viral infection paralyses protein synthesis in the cells of the infected animals, which reveals the extraordinary capacity of certain viruses to manipulate the cellular translation machinery for their own benefit, at the same time preventing the host from synthesising proteins with antiviral activity.

Although the phenomenon of cellular translation inhibition (or shut-off) induced by viral infections has been known since the 1960s, its significance in the viral infection of animals (in vivo infection) had not been demonstrated through experiments.

Up to now, there had been methodological difficulties which prevented the accurate measurement of protein synthesis in the tissue cells of animals infected with a virus. For this project, an experimental methodology has been developed which enables protein synthesis in the infected cell to be estimated and that of the virus itself in the tissues of the animals.

Using recombinant Sindbis virus (virus with ARN genome from the Alfavirus family), the researchers detected the inactivation of cellular translation factor eIF2 in the neurones in the brains of infected rats, which promotes the instantaneous paralysis of the protein synthesis (translation) of said neurones. In these conditions, the virus is able to synthesise its own proteins thanks to the use of a translation initiation mechanism in its ARN messengers which does not require the activity of the translation factor eIF2.

This finding, published by René Toribio and Iván Ventoso in the journal Proc. Natl. Acad. Sci. USA, provides keys to a better understanding of parasite-host interactions and shows the efficacy and relative simplicity with which the virus manipulates the translation of the host. The study also proposes an experimental approximation which could be used in the study of shut-off in other viruses that infect animals.

 

Although the phenomenon of cellular translation inhibition (or shut-off) induced by viral infections has been known since the 1960s, its significance in the viral infection of animals (in vivo infection) had not been demonstrated through experiments.

Up to now, there had been methodological difficulties which prevented the accurate measurement of protein synthesis in the tissue cells of animals infected with a virus. For this project, an experimental methodology has been developed which enables protein synthesis in the infected cell to be estimated and that of the virus itself in the tissues of the animals.

Using recombinant Sindbis virus (virus with ARN genome from the Alfavirus family), the researchers detected the inactivation of cellular translation factor eIF2 in the neurones in the brains of infected rats, which promotes the instantaneous paralysis of the protein synthesis (translation) of said neurones. In these conditions, the virus is able to synthesise its own proteins thanks to the use of a translation initiation mechanism in its ARN messengers which does not require the activity of the translation factor eIF2.

This finding, published by René Toribio and Iván Ventoso in the journal Proc. Natl. Acad. Sci. USA, provides keys to a better understanding of parasite-host interactions and shows the efficacy and relative simplicity with which the virus manipulates the translation of the host. The study also proposes an experimental approximation which could be used in the study of shut-off in other viruses that infect animals.

 

Although the phenomenon of cellular translation inhibition (or shut-off) induced by viral infections has been known since the 1960s, its significance in the viral infection of animals (in vivo infection) had not been demonstrated through experiments.

Up to now, there had been methodological difficulties which prevented the accurate measurement of protein synthesis in the tissue cells of animals infected with a virus. For this project, an experimental methodology has been developed which enables protein synthesis in the infected cell to be estimated and that of the virus itself in the tissues of the animals.

Using recombinant Sindbis virus (virus with ARN genome from the Alfavirus family), the researchers detected the inactivation of cellular translation factor eIF2 in the neurones in the brains of infected rats, which promotes the instantaneous paralysis of the protein synthesis (translation) of said neurones. In these conditions, the virus is able to synthesise its own proteins thanks to the use of a translation initiation mechanism in its ARN messengers which does not require the activity of the translation factor eIF2.

This finding, published by René Toribio and Iván Ventoso in the journal Proc. Natl. Acad. Sci. USA, provides keys to a better understanding of parasite-host interactions and shows the efficacy and relative simplicity with which the virus manipulates the translation of the host. The study also proposes an experimental approximation which could be used in the study of shut-off in other viruses that infect animals.

 

Although the phenomenon of cellular translation inhibition (or shut-off) induced by viral infections has been known since the 1960s, its significance in the viral infection of animals (in vivo infection) had not been demonstrated through experiments.

Up to now, there had been methodological difficulties which prevented the accurate measurement of protein synthesis in the tissue cells of animals infected with a virus. For this project, an experimental methodology has been developed which enables protein synthesis in the infected cell to be estimated and that of the virus itself in the tissues of the animals.

Using recombinant Sindbis virus (virus with ARN genome from the Alfavirus family), the researchers detected the inactivation of cellular translation factor eIF2 in the neurones in the brains of infected rats, which promotes the instantaneous paralysis of the protein synthesis (translation) of said neurones. In these conditions, the virus is able to synthesise its own proteins thanks to the use of a translation initiation mechanism in its ARN messengers which does not require the activity of the translation factor eIF2.

This finding, published by René Toribio and Iván Ventoso in the journal Proc. Natl. Acad. Sci. USA, provides keys to a better understanding of parasite-host interactions and shows the efficacy and relative simplicity with which the virus manipulates the translation of the host. The study also proposes an experimental approximation which could be used in the study of shut-off in other viruses that infect animals.

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