Bidirectional infection and release of Rift Valley fever virus in polarized epithelial cells.
Rift Valley Fever (RVF) virus is an arbovirus and is responsible for large outbreaks of disease predominantly in sub-Saharan Africa. However, several aspects of RVF virus transmission, such as high viremia, multiple vector species, and broad host range, result in a pathogen with high likelihood of geographic spread. RVF virus infection in humans and livestock is characterized by broad dissemination of RVF virus antigens throughout the body. We sought insight into the high pathogenicity and broad tropism of this virus through a characterization of its interaction with polarized epithelial cells. Our results indicate that infection and release of RVF virus in polarized epithelial cells occurs at both apical and basolateral membranes and hence is bidirectional. Furthermore, our results indicate that RVF virus causes disruptions in both the microfilament and the microtubule networks. These disruptions may provide a mechanism for bidirectional release of RVF virions.
D008841:Actin Cytoskeleton / Q000502:physiology; D018938:Caco-2 Cells; D002462:Cell Membrane / Q000821:virology; D016764:Cell Polarity; D004847:Epithelial Cells / Q000821:virology; D006801:Humans; D008562:Membrane Glycoproteins / Q000378:metabolism; D008870:Microtubules / Q000502:physiology; D012296:Rift Valley fever virus / Q000378:metabolism / Q000502:physiology*; D014759:Viral Envelope Proteins / Q000378:metabolism
D008562:Membrane Glycoproteins; D014759:Viral Envelope Proteins