As ERAD tuning components, such as SEL1L and nonlipidated LC3, appear to contribute to viral infection, these cellular pathways represent novel candidate drug targets to combat positive-strand RNA viruses.Ĭopyright © 2014, American Society for Microbiology. In this Gem, we briefly summarize the current knowledge on ERAD tuning pathways and how they might be hijacked for viral genome replication. Recent reports highlight the analogies between mouse hepatitis virus-, equine arteritis virus-, and Japanese encephalitis virus-induced replication platforms and ER-associated degradation (ERAD) tuning vesicles (or EDEMosomes) that display nonlipidated LC3 at their cytosolic face and segregate the ERAD factors EDEM1, OS-9, and SEL1L from the ER lumen. We have used one- and two-particle microrheology, employing m-sized beads and laser interferometric displacement detection, to study the rheological properties of entangled solutions of the filamentous fd virus. De-pending on the relative size and shape of the conning geome-try various two-dimensional (2D) equilibrium congurations of fd-viruses with spatially non-trivial orientational texture were observed. However, the absence of conventional ER and secretory pathway markers in virus-induced ER-derived membranes has for a long time hampered a thorough understanding of their biogenesis. iments, fd-viruses 0:88 mm long and 6:6 nm thick were con-ned to wedge2, rectangular3 and annular4 geometries. Second, unlike squiggly DNA, fd virus is a stiff, rod-like molecule. First, fd viruses are all identical clones of each other. For example, Nidovirales and Flaviviridae subvert the membrane of the endoplasmic reticulum (ER) for their replication. Two things make the virus an ideal candidate for study with nanpores. An essential step during the intracellular life cycle of many positive-strand RNA viruses is the rearrangement of host cell membranes to generate membrane-bound replication platforms.
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