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      Mutation in West Nile Virus Structural Protein prM during Human Infection

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          Abstract

          A mutation leading to substitution of a key amino acid in the prM protein of West Nile virus (WNV) occurred during persistent infection of an immunocompetent patient. WNV RNA persisted in the patient’s urine and serum in the presence of low-level neutralizing antibodies. This case demonstrates active replication of WNV during persistent infection.

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          Rapid detection of west nile virus from human clinical specimens, field-collected mosquitoes, and avian samples by a TaqMan reverse transcriptase-PCR assay.

          R S Lanciotti, A. J. Kerst, R. Nasci … (2000)
          The authors report on the development and application of a rapid TaqMan assay for the detection of West Nile (WN) virus in a variety of human clinical specimens and field-collected specimens. Oligonucleotide primers and FAM- and TAMRA-labeled WN virus-specific probes were designed by using the nucleotide sequence of the New York 1999 WN virus isolate. The TaqMan assay was compared to a traditional reverse transcriptase (RT)-PCR assay and to virus isolation in Vero cells with a large number ( approximately 500) of specimens obtained from humans (serum, cerebrospinal fluid, and brain tissue), field-collected mosquitoes, and avian tissue samples. The TaqMan assay was specific for WN virus and demonstrated a greater sensitivity than the traditional RT-PCR method and correctly identified WN virus in 100% of the culture-positive mosquito pools and 98% of the culture-positive avian tissue samples. The assay should be of utility in the diagnostic laboratory to complement existing human diagnostic testing and as a tool to conduct WN virus surveillance in the United States.
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            West Nile virus discriminates between DC-SIGN and DC-SIGNR for cellular attachment and infection.

            D Sanchez, R W Doms, Bach-Yen Nguyen … (2006)
            The C-type lectins DC-SIGN and DC-SIGNR bind mannose-rich glycans with high affinity. In vitro, cells expressing these attachment factors efficiently capture, and are infected by, a diverse array of appropriately glycosylated pathogens, including dengue virus. In this study, we investigated whether these lectins could enhance cellular infection by West Nile virus (WNV), a mosquito-borne flavivirus related to dengue virus. We discovered that DC-SIGNR promoted WNV infection much more efficiently than did DC-SIGN, particularly when the virus was grown in human cell types. The presence of a single N-linked glycosylation site on either the prM or E glycoprotein of WNV was sufficient to allow DC-SIGNR-mediated infection, demonstrating that uncleaved prM protein present on a flavivirus virion can influence viral tropism under certain circumstances. Preferential utilization of DC-SIGNR was a specific property conferred by the WNV envelope glycoproteins. Chimeras between DC-SIGN and DC-SIGNR demonstrated that the ability of DC-SIGNR to promote WNV infection maps to its carbohydrate recognition domain. WNV virions and subviral particles bound to DC-SIGNR with much greater affinity than DC-SIGN. We believe this is the first report of a pathogen interacting more efficiently with DC-SIGNR than with DC-SIGN. Our results should lead to the discovery of new mechanisms by which these well-studied lectins discriminate among ligands.
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              Virus and antibody dynamics in acute west nile virus infection.

              Jordan Kamel, Jeffrey Linnen, Steven Kleinman … (2008)
              The dynamics of the early stages of West Nile virus (WNV) infection can be assessed by follow-up studies of viremic blood donors. A total of 245 donors with WNV viremia were followed up weekly for 4 weeks and then monthly for up to 6 additional months or until seroconversion. Plasma samples were tested for WNV RNA by transcription-mediated amplification (TMA) and for WNV-specific IgM and IgG antibodies. RNA persistence was investigated by 6 replicate TMA tests; samples that were viremic for >40 days were tested for WNV-neutralizing activity. Follow up of 35 additional viremic donors for up to 404 days was conducted to evaluate persistence of WNV-specific antibody. The median time from RNA detection to IgM seroconversion was 3.9 days; to IgG seroconversion, 7.7 days; to RNA negativity by single-replicate TMA, 13.2 days; and to RNA negativity by 6-replicate TMA, 6.1 additional days after results of single-replicate TMA are negative. For 4 donors in whom RNA persisted for >40 days after the index donation, all samples obtained after this threshold were also positive for WNV IgG and neutralizing activity. The mean times to IgM and IgA negativity were 156 and 220 days, respectively. IgM and IgG develop rapidly after viremia and before RNA levels become undetectable, which occurred a mean of 13.2 days after the index donation among donors in this study. WNV RNA detection by replicate TMA rarely persists for >40 days after the index donation and is accompanied by WNV-specific neutralizing antibody, consistent with an absence of WNV transmission via transfusion of seropositive blood components.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Emerg Infect Dis
                Journal ID (iso-abbrev): Emerging Infect. Dis
                Journal ID (publisher-id): EID
                Title: Emerging Infectious Diseases
                Publisher: Centers for Disease Control and Prevention
                ISSN (Print): 1080-6040
                ISSN (Electronic): 1080-6059
                Publication date (Print): September 2016
                Volume: 22
                Issue: 9
                Pages: 1647-1649
                Affiliations
                [1]Sheba Medical Center, Tel-Hashomer, Israel (Y. Lustig, M. Hindiyeh, N. Keller, E. Mendelson);
                [2]Centers for Disease Control and Prevention, Fort Collins, Colorado, USA (R.S. Lanciotti);
                [3]School of Public Health, Sackler Faculty of Medicine, Tel-Aviv University, Tel Aviv, Israel (M. Hindiyeh, E. Mendelson);
                [4]Faculty of Health Sciences, Ben-Gurion University of the Negev, Be'er sheva, Israel (R. Milo);
                [5]Barzilai Medical Center, Ashkelon, Israel (R. Milo, S. Mayan)
                Author notes
                Address for correspondence: Yaniv Lustig, National Zoonotic Reference Laboratory, Central Virology Laboratory, Ministry of Health, Sheba Medical Center, Ramat-Gan, Israel; email: Yaniv.lustig@ 123456sheba.health.gov.il
                Article
                Publisher ID: 16-0132
                DOI: 10.3201/eid2209.160132
                PMC ID: 4994336
                PubMed ID: 27322782
                SO-VID: 48656d08-f957-41f9-a9c1-9e0bc24aa656
                History
                Categories
                Subject: Dispatch
                Subject: Dispatch
                Subject: Mutation in West Nile Virus Structural Protein prM during Human Infection

                ScienceOpen disciplines: Infectious disease & Microbiology
                Keywords: west nile virus,wnv,persistent infection,wnv mutation,prm protein,viruses,human infection
                Data availability:
                ScienceOpen disciplines: Infectious disease & Microbiology
                Keywords: west nile virus, wnv, persistent infection, wnv mutation, prm protein, viruses, human infection

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