Our studies revealed that HIM-6 dissociated the 5′-flap strand from 5′-flap DNAs. A 5′-flap structure has been suggested as an intermediate in the processing of Okazaki fragments produced by replication or long-patch base excision repair. Biochemical studies showed that human WRN and BLM interact with flap endonuclease-1 to stimulate flap endonuclease activity. The C. elegans homolog of human FEN-1, CRN-1, can also cleave 5′-flap structured DNA. Thus, we predict that HIM-6 coordinates with CRN-1 and assists in processing flap structured DNA. We also determined that HIM-6 was capable of unwinding double-stranded 3-way junction DNA that mimics replication forks to produce partial-duplex products. With the polarity of HIM-6, it may translocate along the leading strand to separate the two template strands ahead of the fork structure. CeWRN-1 and WRN have also been shown to unwind 3-way junctions in that way. Although biochemical studies of human BLM and DmBLM at 3way junctions have not been reported, human BLM was recently shown to function in normal replication fork progression in vivo. Our data showing that HIM-6 unwinds the 3-way junction toward the replication fork suggests that HIM-6 may participate in replication fork progression. Taken together, our results revealed HIM-6 as a DNA helicase with roles in processing recombination Fingolimod company intermediates. Thus, it will be interesting to uncover in vitro activities of HIM-6 with other interacting proteins to address how HIM-6 is involved in HR in C. elegans. Since its introduction to the United States in 1999, West Nile virus, a mosquito-borne flavivirus classified as an NIAID Category B Priority Pathogen, has emerged as a leading cause of viral encephalitis, with more than 5,000 cases including nearly 250 deaths in 2012. WNV is an enveloped positive stranded RNA virus and is closely related to other human pathogens including dengue, yellow fever, Japanese encephalitis and tick-borne encephalitis viruses. Currently there are no therapeutic drugs or vaccines for WNV approved for human use. The fatality rate is approximately 10% for hospitalized WNV cases and up to 70% of the survivors of WNV-encephalitis experience persistent neurological deficits for several months. The pathogenesis of WNV in humans is not well characterized but WNV infection in mice mimics human WNV disease, thus making it a good model to understand the mechanisms that cause WNV disease. WNV infection triggers effective innate immune responses, which collectively mediate virus clearance from the periphery and control its dissemination in the brain, however in subset of patients WNV enters the central nervous system . Therefore, WNV neuropathogenesis is mainly dependent on the ability of the virus to enter the brain and replicate within resident cells including neurons and astrocytes. Increased leukocyte infiltration, specifically CD8 + T cells are critical for clearing virus infection from the CNS, although migrating inflammatory monocytes and T cells also contribute to neuropathology by potentiating inflammation.