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7.346 Virus-host Interactions in Infectious Diseases (MIT) 7.346 Virus-host Interactions in Infectious Diseases (MIT)

Description

Co-evolution and adaptation between viruses and humans are often portrayed as a zero-sum biological arms race. Viruses enter host cells equipped with an array of mechanisms to evade the host defense responses and replicate. The rapid rate of mutation of viruses permits evolution of various methodologies for infection, which in turn drive development of non-specific but highly effective host mechanisms to restrict infection. This class will discuss the varied solutions each side has developed as a means for survival. We will use examples drawn from human disease-causing pathogens that contribute seriously to the global health burden, including HIV, influenza and dengue virus. Primary research papers will be discussed to help students learn to pose scientific questions and design and conduct Co-evolution and adaptation between viruses and humans are often portrayed as a zero-sum biological arms race. Viruses enter host cells equipped with an array of mechanisms to evade the host defense responses and replicate. The rapid rate of mutation of viruses permits evolution of various methodologies for infection, which in turn drive development of non-specific but highly effective host mechanisms to restrict infection. This class will discuss the varied solutions each side has developed as a means for survival. We will use examples drawn from human disease-causing pathogens that contribute seriously to the global health burden, including HIV, influenza and dengue virus. Primary research papers will be discussed to help students learn to pose scientific questions and design and conduct

Subjects

virus | virus | host | host | infection | infection | protein-protein interactions | protein-protein interactions | host mimicry | host mimicry | intra-cellular trafficking | intra-cellular trafficking | host-cell machinery | host-cell machinery | signaling pathways | signaling pathways | antiviral proteins | antiviral proteins | HIV | HIV | influenza | influenza | dengue virus | dengue virus | biotechnology | biotechnology | vaccine development | vaccine development | host sensors | host sensors | IFN production | IFN production | Secreted IFN | Secreted IFN | filoviruses | filoviruses | hCMV | hCMV | IFITM proteins | IFITM proteins

License

Content within individual OCW courses is (c) by the individual authors unless otherwise noted. MIT OpenCourseWare materials are licensed by the Massachusetts Institute of Technology under a Creative Commons License (Attribution-NonCommercial-ShareAlike). For further information see http://ocw.mit.edu/terms/index.htm

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7.342 To Divide or Not To Divide: Control of Cell Cycle and Growth by Extracellular Cues (MIT) 7.342 To Divide or Not To Divide: Control of Cell Cycle and Growth by Extracellular Cues (MIT)

Description

Cells, regardless of whether they are in an organ in the human body or a component of a bacterial colony, can sense the chemical composition of the environment, the presence of neighboring cells, and even the types of their neighboring cells. Depending on the identity of a cell and the information it receives from its environment, it can grow (increase in size), proliferate (make more cells), become quiescent (stop growing and dividing), differentiate (make different types of cells), or die. How cells achieve the astonishing feat of appropriately sensing and responding to their environment has been a major question in biology. In this course we will read and critically discuss the primary scientific literature with the goal of highlighting the basic principles of cell growth, adaptation, a Cells, regardless of whether they are in an organ in the human body or a component of a bacterial colony, can sense the chemical composition of the environment, the presence of neighboring cells, and even the types of their neighboring cells. Depending on the identity of a cell and the information it receives from its environment, it can grow (increase in size), proliferate (make more cells), become quiescent (stop growing and dividing), differentiate (make different types of cells), or die. How cells achieve the astonishing feat of appropriately sensing and responding to their environment has been a major question in biology. In this course we will read and critically discuss the primary scientific literature with the goal of highlighting the basic principles of cell growth, adaptation, a

Subjects

Cell growth | Cell growth | cell cycle | cell cycle | bacteria | bacteria | cell signaling | cell signaling | yeast | yeast | Genetic regulation | Genetic regulation | signaling pathways | signaling pathways | RAS | RAS | TOR (Target Of Rapamycin) | TOR (Target Of Rapamycin) | sporulation | sporulation | IME1 | IME1 | biofilms | biofilms

License

Content within individual OCW courses is (c) by the individual authors unless otherwise noted. MIT OpenCourseWare materials are licensed by the Massachusetts Institute of Technology under a Creative Commons License (Attribution-NonCommercial-ShareAlike). For further information see http://ocw.mit.edu/terms/index.htm

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7.346 Virus-host Interactions in Infectious Diseases (MIT)

Description

Co-evolution and adaptation between viruses and humans are often portrayed as a zero-sum biological arms race. Viruses enter host cells equipped with an array of mechanisms to evade the host defense responses and replicate. The rapid rate of mutation of viruses permits evolution of various methodologies for infection, which in turn drive development of non-specific but highly effective host mechanisms to restrict infection. This class will discuss the varied solutions each side has developed as a means for survival. We will use examples drawn from human disease-causing pathogens that contribute seriously to the global health burden, including HIV, influenza and dengue virus. Primary research papers will be discussed to help students learn to pose scientific questions and design and conduct

Subjects

virus | host | infection | protein-protein interactions | host mimicry | intra-cellular trafficking | host-cell machinery | signaling pathways | antiviral proteins | HIV | influenza | dengue virus | biotechnology | vaccine development | host sensors | IFN production | Secreted IFN | filoviruses | hCMV | IFITM proteins

License

Content within individual OCW courses is (c) by the individual authors unless otherwise noted. MIT OpenCourseWare materials are licensed by the Massachusetts Institute of Technology under a Creative Commons License (Attribution-NonCommercial-ShareAlike). For further information see https://ocw.mit.edu/terms/index.htm

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https://ocw.mit.edu/rss/all/mit-allcourses.xml

Attribution

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7.342 To Divide or Not To Divide: Control of Cell Cycle and Growth by Extracellular Cues (MIT)

Description

Cells, regardless of whether they are in an organ in the human body or a component of a bacterial colony, can sense the chemical composition of the environment, the presence of neighboring cells, and even the types of their neighboring cells. Depending on the identity of a cell and the information it receives from its environment, it can grow (increase in size), proliferate (make more cells), become quiescent (stop growing and dividing), differentiate (make different types of cells), or die. How cells achieve the astonishing feat of appropriately sensing and responding to their environment has been a major question in biology. In this course we will read and critically discuss the primary scientific literature with the goal of highlighting the basic principles of cell growth, adaptation, a

Subjects

Cell growth | cell cycle | bacteria | cell signaling | yeast | Genetic regulation | signaling pathways | RAS | TOR (Target Of Rapamycin) | sporulation | IME1 | biofilms

License

Content within individual OCW courses is (c) by the individual authors unless otherwise noted. MIT OpenCourseWare materials are licensed by the Massachusetts Institute of Technology under a Creative Commons License (Attribution-NonCommercial-ShareAlike). For further information see https://ocw.mit.edu/terms/index.htm

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https://ocw.mit.edu/rss/all/mit-allcourses.xml

Attribution

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