2 beautifull free PDF in Cell http://www.cell.com/
http://download.cell.com/images/edimages/Cell/IEP/Shapira.pdf
A Physical and Regulatory Map of Host-Influenza Interactions Reveals Pathways in H1N1 Infection
SUMMARY
During the course of a viral infection, viral proteins interact with an array of host proteins and pathways.
Here, we present a systematic strategy to elucidate the dynamic interactions between H1N1 influenza and its human host. A combination of yeast two hybrid analysis and genome-wide expression profiling implicated hundreds of human factors in mediating viral-host interactions. These factors were then examined functionally through depletion analyses in
primary lung cells. The resulting data point to potential roles for some unanticipated host and viral proteins in viral infection and the host response, including a network of RNA-binding proteins, components
of WNT signaling, and viral polymerase subunits. This multilayered approach provides a comprehensive and unbiased physical and regulatory model of influenza-host interactions and demonstrates a general strategy for uncovering complex host-pathogen relationships.
another PDF : here : http://download.cell.com/images/edimages/Cell/IEP/Brass.pdf
The IFITM Proteins Mediate Cellular Resistance to Influenza A H1N1 Virus,
West Nile Virus, and Dengue Virus
SUMMARY
Influenza viruses exploit host cell machinery to replicate,
resulting in epidemics of respiratory illness. In turn, the host expresses antiviral restriction factors to defend against infection. To find host cell modifiers of influenza A H1N1 viral infection, we used a functional genomic screen and identified over 120 influenza A virus-dependency factors with roles in endosomal acidification, vesicular trafficking, mitochondrial
metabolism, and RNA splicing.We discovered that the interferon-inducible transmembrane proteins IFITM1, 2, and 3 restrict an early step in influenza
A viral replication. The IFITM proteins confer basal resistance to influenza A virus but are also inducible by interferons type I and II and are critical
for interferon’s virustatic actions. Further characterization revealed that the IFITM proteins inhibit the early replication of flaviviruses, including dengue virus and West Nile virus. Collectively this work identifies a family of antiviral restriction factors that mediate cellular innate immunity to at least three major human pathogens.
http://download.cell.com/images/edimages/Cell/IEP/Shapira.pdf
A Physical and Regulatory Map of Host-Influenza Interactions Reveals Pathways in H1N1 Infection
SUMMARY
During the course of a viral infection, viral proteins interact with an array of host proteins and pathways.
Here, we present a systematic strategy to elucidate the dynamic interactions between H1N1 influenza and its human host. A combination of yeast two hybrid analysis and genome-wide expression profiling implicated hundreds of human factors in mediating viral-host interactions. These factors were then examined functionally through depletion analyses in
primary lung cells. The resulting data point to potential roles for some unanticipated host and viral proteins in viral infection and the host response, including a network of RNA-binding proteins, components
of WNT signaling, and viral polymerase subunits. This multilayered approach provides a comprehensive and unbiased physical and regulatory model of influenza-host interactions and demonstrates a general strategy for uncovering complex host-pathogen relationships.
another PDF : here : http://download.cell.com/images/edimages/Cell/IEP/Brass.pdf
The IFITM Proteins Mediate Cellular Resistance to Influenza A H1N1 Virus,
West Nile Virus, and Dengue Virus
SUMMARY
Influenza viruses exploit host cell machinery to replicate,
resulting in epidemics of respiratory illness. In turn, the host expresses antiviral restriction factors to defend against infection. To find host cell modifiers of influenza A H1N1 viral infection, we used a functional genomic screen and identified over 120 influenza A virus-dependency factors with roles in endosomal acidification, vesicular trafficking, mitochondrial
metabolism, and RNA splicing.We discovered that the interferon-inducible transmembrane proteins IFITM1, 2, and 3 restrict an early step in influenza
A viral replication. The IFITM proteins confer basal resistance to influenza A virus but are also inducible by interferons type I and II and are critical
for interferon’s virustatic actions. Further characterization revealed that the IFITM proteins inhibit the early replication of flaviviruses, including dengue virus and West Nile virus. Collectively this work identifies a family of antiviral restriction factors that mediate cellular innate immunity to at least three major human pathogens.