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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Critical roles for both STAT1-dependent and STAT1-independent pathways in the control of primary dengue virus infection in mice.

Dengue virus (DEN), a flavivirus, causes dengue fever and dengue hemorrhagic fever/dengue shock syndrome, the most common mosquito-borne viral illnesses in humans worldwide. In this study, using STAT1(-/-) mice bearing two different mutant stat1 alleles in the 129/Sv/Ev background, we demonstrate that IFNR-dependent control of primary DEN infection involves both STAT1-dependent and STAT1-independent mechanisms. The STAT1 pathway is necessary for clearing the initial viral load, whereas the STAT1-independent pathway controls later viral burden and prevents DEN disease in mice. The STAT1-independent responses in mice with primary DEN infection included the early activation of B and NK cells as well as the up-regulation of MHC class I molecules on macrophages and dendritic cells. Infection of bone marrow-derived dendritic cell cultures with either DEN or Sindbis virus, another positive-strand RNA virus, confirmed the early vs late natures of the STAT1-dependent and STAT1-independent pathways. Collectively, these data begin to define the nature of the STAT1-dependent vs the STAT1-independent pathway in vivo.[1]

References

  1. Critical roles for both STAT1-dependent and STAT1-independent pathways in the control of primary dengue virus infection in mice. Shresta, S., Sharar, K.L., Prigozhin, D.M., Snider, H.M., Beatty, P.R., Harris, E. J. Immunol. (2005) [Pubmed]
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