Disease relevance of SLEV1

• Immunity to JEV and SLEV was protective against clinical encephalitis and death after challenge with WNV [1].
• Prior immunization of hamsters with three heterologous flaviviruses (Japanese encephalitis virus [JEV] SA14-2-8 vaccine, wild-type St. Louis encephalitis virus [SLEV], and Yellow fever virus [YFV] 17D vaccine) reduces the severity of subsequent West Nile virus (WNV) infection [1].
• The 5'-terminal sequences obtained for the SLEV and WNV RNAs were compared with published sequences for yellow fever virus (YFV), Murray Valley encephalitis virus (MVEV), and dengue virus [2].
• Importantly, when these two antigens were tested against a human serum panel from patients having recent WNV or Powassan virus infections, the SLEV VLPs were less likely than SMB antigen to detect flavivirus cross-reactive IgM antibodies [3].
• SLEV induced cytopathic effects in K562 cells, a human mononuclear cell line, and in Neuro 2a cells, a mouse neuroblastoma cell line [4].

High impact information on SLEV1

• Evidence for a susceptibility gene, SLEV1, on chromosome 17p13 in families with vitiligo-related systemic lupus erythematosus [5].
• Louis encephalitis virus transmission in Indian River County, Florida. We derive an empiric relationship between modeled land surface wetness and levels of SLEV transmission in humans [6].
• Louis encephalitis virus (SLEV), and dengue virus type 2 (DENV-2) reported earlier, we recently constructed the DENV-1, -3, and -4 VLP expression plasmids [7].
• The optimal time for performing the fluorescent focus assay (FFA) on Vero cells was 24h for WNV, and 48h for SLEV and the four DENV serotypes [8].
• A serological survey for yellow fever virus (YFV), dengue 2 virus (DENV-2), and St Louis encephalitis virus (SLEV) was undertaken using a seroneutralization technique in 27 wild forest mammal species (574 individuals) in French Guiana [9].

Biological context of SLEV1

• The expression plasmid pCB8SJ2, containing the premembrane and envelope structural protein-encoding regions of SLEV, was constructed to express secreted extracellular virus-like particles (VLPs) from CHO cells [3].
• SLEV-infected K562 and Neuro 2a cells underwent apoptotic cell death, whereas neither the cells inoculated with UV-inactivated virus nor the mock-infected cells developed cytopathic effects [4].
• These findings suggest that up-regulation of bax mRNA is correlated with cytopathic effects in SLEV-infected K562 cells [4].
• The complete nucleotide sequence of the envelope gene of this isolate was directly sequenced from the amplified products and compared with other Brazilian and American SLEV strains [10].
• Louis encephalitis virus (SLEV) from a febrile human case suspected to be dengue, in São Pedro, São Paulo State. A MAC-ELISA done on the patient's acute and convalescent sera was inconclusive and hemagglutination inhibition test detected IgG antibody for flaviviruses [11].

Anatomical context of SLEV1

• A rise in the expression of the pro-apoptotic bax gene was detected specifically in the SLEV-infected K562 cells [4].
• To validate this algorithm, we tested 1,418 serum and cerebrospinal fluid (CSF) samples from confirmed WNV and SLEV infections collected during the WNV epidemic of 2002 in the United States. WNV P/N-to-SLEV P/N ratios (W/S ratios) were calculated and used to identify the infecting virus [12].

Analytical, diagnostic and therapeutic context of SLEV1

• An optimized IgG antibody capture ELISA (GAC-ELISA) with both WNV and SLEV VLPs was developed to circumvent the frequently observed higher background in the antigen-capture IgG-ELISA (ACG-ELISA) [3].
• Results of BLAST search indicated that this sequence shares 93% nucleotide similarity with the sequence of SLEV (strain-MSI.7), confirmed by RT-PCR performed with SLEV specific primers [11].

References