Difference in production of infectious wild-type measles and vaccine viruses in monocyte-derived dendritic cells

Ohgimoto, Kaori; Ohgimoto, Shinji; Ihara, Toshiaki; Mizuta, Hiroyuki; Ishido, Satoshi; Ayata, Minoru; Ogura, Hisashi; Hotta, Hak

doi:10.1016/j.virusres.2006.07.006

Cited by 18 publications

(18 citation statements)

References 28 publications

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“…Previous studies comparing infectious virus production after vaccine and WT infection of moDCs are conflicting. One study showed greater virus production by WT MeV (43), and another study showed similar virus production by vaccine and WT strains (44). In our study, Bilt-infected moDCs produced more virus at 24 h, but by 48 h, Edm-infected cells produced more infectious virus.…”

Section: Discussionsupporting

confidence: 64%

Induction of Dendritic Cell Production of Type I and Type III Interferons by Wild-Type and Vaccine Strains of Measles Virus: Role of Defective Interfering RNAs

Shivakoti

Siwek

Hauer

et al. 2013

J Virol

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The innate immune response to viral infection frequently includes induction of type I interferons (IFN), Measles is a disease caused by measles virus (MeV) and remains a leading cause of childhood mortality, with approximately 164,000 deaths in 2008 (1). Infection is initiated in the respiratory tract and then spreads to the local lymph nodes and through the blood to cause systemic infection and a rash disease (2-6). MeV infection leads to weeks of immune suppression (7-9) that result in increased susceptibility to the secondary infections that are responsible for most measles-related deaths (10). Infection with a live-attenuated MeV vaccine induces protective immunity and does not result in clinically significant immune suppression (11-13).Dendritic cells (DCs) are among the earliest cells infected by MeV (2, 3) and play an important role as a link between innate and adaptive immune responses. DCs recognize pathogen-associated molecular patterns through cell surface and intracellular receptors, such as Toll-like receptors and RNA helicases (14), which can lead to activation of transcription factors and induction of cytokines, such as type I (alpha interferon [IFN-␣] and IFN-␤) and type III (IFN-) interferon (15). DCs also initiate the adaptive immune response by presenting antigen to T cells (16,17).IFNs are an important component of the innate response to virus infection and use primarily JAK-STAT signaling to induce IFN-stimulated genes (ISGs), such as myxovirus resistance gene (Mx) and ISG56, also known as IFIT1. ISGs include genes encoding proteins that inhibit viral replication (15), and viruses have developed many ways to counteract IFN signaling. Two nonstructural proteins of MeV, V and C, regulate the IFN pathway by blocking induction of type I IFN and inhibiting JAK-STAT signaling (18-27).Inhibition of IFN induction has been proposed as a possible contributor to the virulence and immune suppression of wildtype (WT) MeV (28), but studies of MeV induction of IFN have been conflicting. Some studies comparing IFN induction by vaccine and WT strains of MeV report that the vaccine virus induces higher levels of IFN than does the WT virus (29-31), while other studies do not see this difference (27,32,33). The sequences of the V and C protein genes are similar between vaccine and WT strains (23,34,35). In vivo studies have not detected IFN induction during measles (26,36), and in vitro studies have often been confounded by the presence of defective interfering (DI) RNA particles in virus stocks (31,32,35,37). DI RNAs are most frequently produced during virus replication when the multiplicity of infection (MOI) or the passage of the standard virus is high (38). The 5= copy-back form of DI RNA forms a hairpin RNA structure that is the prevalent form produced during paramyxovirus replication and is packaged similarly to the standard virus (39). DI RNA particles are postulated to interfere with the replication of the standard virus by competing for viral proteins in the infected cell (38). However, DI RNA particle...

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Section: Discussionsupporting

confidence: 64%

Induction of Dendritic Cell Production of Type I and Type III Interferons by Wild-Type and Vaccine Strains of Measles Virus: Role of Defective Interfering RNAs

Shivakoti

Siwek

Hauer

et al. 2013

J Virol

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“…However, epithelial cells and unstimulated monocytes do not express signaling lymphocyte activation molecule (SLAM, CD150), the receptor used by wild-type MV [8,9], making this sequence of events unlikely. Moreover, wild-type MV does not readily infect monocytes or epithelial cell lines in vitro [10–12]. CD150 is expressed on subsets of thymocytes, macrophages, dendritic cells (DCs), and activated B- and T-lymphocytes [8,9]; therefore, these cells are the most likely primary target cells for MV infection.…”

Section: Introductionmentioning

confidence: 99%

Predominant Infection of CD150+ Lymphocytes and Dendritic Cells during Measles Virus Infection of Macaques

et al. 2007

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Measles virus (MV) is hypothesized to enter the host by infecting epithelial cells of the respiratory tract, followed by viremia mediated by infected monocytes. However, neither of these cell types express signaling lymphocyte activation molecule (CD150), which has been identified as the receptor for wild-type MV. We have infected rhesus and cynomolgus macaques with a recombinant MV strain expressing enhanced green fluorescent protein (EGFP); thus bringing together the optimal animal model for measles and a virus that can be detected with unprecedented sensitivity. Blood samples and broncho-alveolar lavages were collected every 3 d, and necropsies were performed upon euthanasia 9 or 15 d after infection. EGFP production by MV-infected cells was visualized macroscopically, in both living and sacrificed animals, and microscopically by confocal microscopy and FACS analysis. At the peak of viremia, EGFP fluorescence was detected in skin, respiratory and digestive tract, but most intensely in all lymphoid tissues. B- and T-lymphocytes expressing CD150 were the major target cells for MV infection. Highest percentages (up to 30%) of infected lymphocytes were detected in lymphoid tissues, and the virus preferentially targeted cells with a memory phenotype. Unexpectedly, circulating monocytes did not sustain productive MV infection. In peripheral tissues, large numbers of MV-infected CD11c+ MHC class-II+ myeloid dendritic cells were detected in conjunction with infected T-lymphocytes, suggesting transmission of MV between these cell types. Fluorescent imaging of MV infection in non-human primates demonstrated a crucial role for lymphocytes and dendritic cells in the pathogenesis of measles and measles-associated immunosuppression.

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“…Human peripheral blood lymphocytes (PBL) were prepared as described previously (27). PBL were cultured in RPMI containing 10% FBS supplemented with 2.5 g of PHA-L (Sigma, St. Louis, MO) per ml for 2 days, and then total RNA was isolated from the activated PBL by using an RNeasy mini kit (Qiagen, Hilden, Germany).…”

Section: Methodsmentioning

confidence: 99%

Contribution of Matrix, Fusion, Hemagglutinin, and Large Protein Genes of the CAM-70 Measles Virus Vaccine Strain to Efficient Growth in Chicken Embryonic Fibroblasts

Sharma

Ohgimoto

Kato

et al. 2009

J Virol

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Difference in production of infectious wild-type measles and vaccine viruses in monocyte-derived dendritic cells

Cited by 18 publications

References 28 publications

Induction of Dendritic Cell Production of Type I and Type III Interferons by Wild-Type and Vaccine Strains of Measles Virus: Role of Defective Interfering RNAs

Induction of Dendritic Cell Production of Type I and Type III Interferons by Wild-Type and Vaccine Strains of Measles Virus: Role of Defective Interfering RNAs

Predominant Infection of CD150+ Lymphocytes and Dendritic Cells during Measles Virus Infection of Macaques

Contribution of Matrix, Fusion, Hemagglutinin, and Large Protein Genes of the CAM-70 Measles Virus Vaccine Strain to Efficient Growth in Chicken Embryonic Fibroblasts

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