scholarly journals Evidence that Receptor Destruction by the Sendai Virus Hemagglutinin-Neuraminidase Protein Is Responsible for Homologous Interference

2016 ◽  
Vol 90 (17) ◽  
pp. 7640-7646 ◽  
Author(s):  
Hideo Goto ◽  
Keisuke Ohta ◽  
Yusuke Matsumoto ◽  
Natsuko Yumine ◽  
Machiko Nishio
Keyword(s):  
Influenza A ◽  
Direct Evidence ◽  
Sendai Virus ◽  
Sialic Acids ◽  
Persistently Infected ◽  
Viral Interference ◽  
Lectin Blot ◽  
Infected Cells ◽  
Human Parainfluenza Virus ◽  
Sialic Acid Receptor

ABSTRACTReceptor destruction has been considered one of the mechanisms of homologous Sendai virus (SeV) interference. However, direct evidence of receptor destruction upon virus infection and its relevance to interference is missing. To investigate a precise mechanism of homologous interference, we established SeV persistently infected cells. The persistently infected cells inhibited superinfection by homologous SeV but supported replication of human parainfluenza virus 2 (hPIV2) and influenza A virus (IAV). We confirmed that SeV particles could not attach to or penetrate the infected cells and that the hemagglutinin-neuraminidase (HN) protein of SeV was involved in the interference. Lectin blot assays showed that the α2,3-linked sialic acids were specifically reduced in the SeV-infected cells, but the level of α2,6-linked sialic acids had not changed. As infection with IAV removed both α2,3- and α2,6-linked sialic acids, especially α2,3-linked sialic acids, IAV-infected cells inhibited superinfection of SeV. These results provide concrete evidence that destruction of the specific SeV receptor, α2,3-linked sialic acids, is relevant to homologous interference by SeV.IMPORTANCEViral interference is a classically observed phenomenon, but the precise mechanism is not clear. Using SeV interference, we provide concrete evidence that reduction of the α2,3-linked sialic acid receptor by the HN of SeV is closely related with viral interference. Since SeV infection resulted in decrease of only α2,3-linked sialic acids, IAV, which also utilized α2,6-linked sialic acids to initiate infection, superinfected the SeV-infected cells. In contrast, SeV could not superinfect the IAV-infected cells because both α2,3- and α2,6-linked sialic acids were removed. These results indicate that receptor destruction critically contributes to viral interference.

Sendai virus replication in Friend erythroleukemia cells. I. Acutely and persistently infected cells become resistant to virus-induced lysis

1986 ◽  
Vol 4 (2) ◽  
pp. 117-132
Author(s):  
Arrigo Benedetto ◽  
Carla Amici ◽  
Stefania Zaniratti ◽  
Giuliano Elia ◽  
Maria Pia Camporiondo
Keyword(s):  
Virus Replication ◽  
Sendai Virus ◽  
Persistently Infected ◽  
Erythroleukemia Cells ◽  
Infected Cells ◽  
Friend Erythroleukemia Cells

scholarly journals IRF-3 Activation by Sendai Virus Infection Is Required for Cellular Apoptosis and Avoidance of Persistence

2008 ◽  
Vol 82 (7) ◽  
pp. 3500-3508 ◽  
Author(s):  
Kristi Peters ◽  
Saurabh Chattopadhyay ◽  
Ganes C. Sen
Keyword(s):  
Virus Infection ◽  
Persistent Infection ◽  
Cellular Response ◽  
Sendai Virus ◽  
Virus Production ◽  
Viral Gene Expression ◽  
Viral Gene ◽  
Infected Cells ◽  
Jnk Activation ◽  
Human Parainfluenza Virus

ABSTRACT Here, we report that specific manipulations of the cellular response to virus infection can cause prevention of apoptosis and consequent establishment of persistent infection. Infection of several human cell lines with Sendai virus (SeV) or human parainfluenza virus 3, two prototypic paramyxoviruses, caused slow apoptosis, which was markedly accelerated upon blocking the action of phosphatidylinositol 3-kinases (PI3 kinases) in the infected cells. The observed apoptosis required viral gene expression and the action of the caspase 8 pathway. Although virus infection activated PI3 kinase, as indicated by AKT activation, its blockage did not inhibit JNK activation or IRF-3 activation. The action of neither the Jak-STAT pathway nor the NF-κB pathway was required for apoptosis. In contrast, IRF-3 activation was essential, although induction of the proapototic protein TRAIL by IRF-3 was not required. When IRF-3 was absent or its activation by the RIG-I pathway was blocked, SeV established persistent infection, as documented by viral protein production and infectious virus production. Introduction of IRF-3 in the persistently infected cells restored the cells' ability to undergo apoptosis. These results demonstrated that in our model system, IRF-3 controlled the fate of the SeV-infected cells by promoting apoptosis and preventing persistence.

scholarly journals Cytokine and contact-dependent activation of natural killer cells by influenza A or Sendai virus-infected macrophages

2004 ◽  
Vol 85 (8) ◽  
pp. 2357-2364 ◽  
Author(s):  
Jukka Sirén ◽  
Timo Sareneva ◽  
Jaana Pirhonen ◽  
Mari Strengell ◽  
Ville Veckman ◽  
...  
Keyword(s):  
Nk Cells ◽  
Influenza A ◽  
Nk Cell ◽  
Sendai Virus ◽  
Cell Contact ◽  
Cellular Interactions ◽  
Innate Immune Responses ◽  
Infected Cells ◽  
Cells Cultured

NK cells participate in innate immune responses by secreting gamma interferon (IFN-γ) and by destroying virus-infected cells. Here the interaction between influenza A or Sendai virus-infected macrophages and NK cells has been studied. A rapid, cell–cell contact-dependent production of IFN-γ from NK cells cultured with virus-infected macrophages was observed. Expression of the MHC class I-related chain B (MICB) gene, a ligand for NK cell-activating receptor NKG2D, was upregulated in virus-infected macrophages suggesting a role for MICB in the activation of the IFN-γ gene in NK cells. IL12Rβ2, IL18R and T-bet mRNA synthesis was enhanced in NK cells cultured with virus-infected macrophages. Upregulation of these genes was dependent on macrophage-derived IFN-α. In contrast to IL12Rβ2, expression of WSX-1/TCCR, a receptor for IL27, was reduced in NK cells in response to virus-induced IFN-α. In conclusion, these results show that virus-infected macrophages activate NK cells via cytokines and direct cellular interactions and further emphasize the role of IFN-α in the activation of innate immunity.

scholarly journals Nucleocapsid Incorporation into Parainfluenza Virus Is Regulated by Specific Interaction with Matrix Protein

2001 ◽  
Vol 75 (3) ◽  
pp. 1117-1123 ◽  
Author(s):  
Elizabeth C. Coronel ◽  
Toru Takimoto ◽  
K. Gopal Murti ◽  
Natalia Varich ◽  
Allen Portner
Keyword(s):  
Matrix Protein ◽  
Sendai Virus ◽  
Specific Interaction ◽  
Parainfluenza Virus ◽  
Protein Protein Interaction ◽  
Significant Difference ◽  
Infected Cells ◽  
Protein Amino Acids ◽  
Human Parainfluenza Virus

ABSTRACT The paramyxovirus nucleoproteins (NPs) encapsidate the genomic RNA into nucleocapsids, which are then incorporated into virus particles. We determined the protein-protein interaction between NP molecules and the molecular mechanism required for incorporating nucleocapsids into virions in two closely related viruses, human parainfluenza virus type 1 (hPIV1) and Sendai virus (SV). Expression of NP from cDNA resulted in in vivo nucleocapsid formation. Electron micrographs showed no significant difference in the morphological appearance of viral nucleocapsids obtained from lysates of transfected cells expressing SV or hPIVI NP cDNA. Coexpression of NP cDNAs from both viruses resulted in the formation of nucleocapsid composed of a mixture of NP molecules; thus, the NPs of both viruses contained regions that allowed the formation of mixed nucleocapsid. Mixed nucleocapsids were also detected in cells infected with SV and transfected with hPIV1 NP cDNA. However, when NP of SV was donated by infected virus and hPIV1 NP was from transfected cDNA, nucleocapsids composed of NPs solely from SV or solely from hPIVI were also detected. Although almost equal amounts of NP of the two viruses were found in the cytoplasm of cells infected with SV and transfected with hPIV1 NP cDNA, 90% of the NPs in the nucleocapsids of the progeny SV virions were from SV. Thus, nucleocapsids containing heterologous hPIV1 NPs were excluded during the assembly of progeny SV virions. Coexpression of hPIV1 NP and hPIV1 matrix protein (M) in SV-infected cells increased the uptake of nucleocapsids containing hPIV1 NP; thus, M appears to be responsible for the specific incorporation of the nucleocapsid into virions. Using SV-hPIV1 chimera NP cDNAs, we found that the C-terminal domain of the NP protein (amino acids 420 to 466) is responsible for the interaction with M.

scholarly journals Simultaneous expression of H-2-restricted and alloreactive recognition by a cloned line of influenza virus-specific cytotoxic T lymphocytes.

1981 ◽  
Vol 153 (5) ◽  
pp. 1371-1376 ◽  
Author(s):  
T J Braciale ◽  
M E Andrew ◽  
V L Braciale
Keyword(s):  
T Cells ◽  
Influenza Virus ◽  
Influenza A ◽  
Direct Evidence ◽  
Cross Reactivity ◽  
Cytotoxic T Cell ◽  
Cell Level ◽  
Histocompatibility Complex ◽  
Infected Cells ◽  
Theoretical Considerations

Based on theoretical considerations and several types of experimental evidence with heterogeneous cell populations it has been proposed that alloreactive T cells and major histocompatibility complex (MHC)-restricted T cells directed to foreign non-NHC antigens represent overlapping subsets. In this report we provide direct evidence for this hypothesis at the clonal level. We have isolated a cloned continuous influenza virus-specific cytotoxic T cell (CTL) line derived from a single (H-2b X H-2d)F1 CTL precursor which simultaneously exhibits H-2-restricted cytotoxicity of influenza A/Japan/305/57 virus in association with H-2Kd and alloreactive cytotoxicity for H-2Kk alloantigen. Cold target inhibition data demonstrate that both MHC-restricted and alloreactive recognition is mediated by the same cell population. In addition to cross-reactivity at the target cell level, we shown that this cloned CTL line can be specifically stimulated to proliferate either by A/Japan/305/57 virus-infected cells expressing H-2Kd or by uninfected cells of the H-2Kk haplotype.

Sendai virus gene expression in lytically and persistently infected cells

Virology ◽  
1990 ◽  
Vol 177 (1) ◽  
pp. 131-140 ◽  
Author(s):  
H.E. Homann ◽  
P.H. Hofschneider ◽  
W.J. Neubert
Keyword(s):  
Gene Expression ◽  
Sendai Virus ◽  
Persistently Infected ◽  
Virus Gene ◽  
Virus Gene Expression ◽  
Infected Cells

scholarly journals Early Stage of Establishment of Persistent Sendai Virus Infection: Unstable Dynamic Phase and Then Selection of Viruses Which Are Tightly Cell Associated, Temperature Sensitive, and Capable of Establishing Persistent Infection

2004 ◽  
Vol 78 (21) ◽  
pp. 11939-11951 ◽  
Author(s):  
Morihiro Ito ◽  
Taijiro Takeuchi ◽  
Machiko Nishio ◽  
Mitsuo Kawano ◽  
Hiroshi Komada ◽  
...  
Keyword(s):  
Virus Infection ◽  
Cell Lines ◽  
Temperature Sensitivity ◽  
Persistent Infection ◽  
Sendai Virus ◽  
Early Stage ◽  
Persistently Infected ◽  
Dynamic Phase ◽  
M Proteins ◽  
Infected Cells

ABSTRACT We obtained 157 cloned cell lines persistently infected with Sendai virus; these cell lines were generated independently of each other. Infectious viruses could be isolated from 123 of these cloned cell lines by inoculation of culture fluids or infected cells into embryonated eggs. The majority of the viruses carried by cells persistently infected with viruses showed high cytotoxicity and did not have the ability to establish persistent infection. The association of carried virus with cells became stronger and virus isolation correspondingly became more difficult as cells persistently infected with virus were subcultured. Viruses derived from virus-infected cells eventually acquired the ability to establish persistent infection, although the ways in which the viruses acquired this ability varied. The viruses also acquired temperature sensitivity as persistently infected cells were subcultured. First, the hemagglutinin-neuraminidase and M proteins acquired temperature sensitivity, and then the polymerase(s) did so. The M proteins were localized in the nuclei of cells infected with cloned viruses that had the ability to establish persistent infection. Cells infected with viruses capable of establishing persistent infection showed no or slight staining by terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end labeling. Specific amino acid substitutions accumulated in the M protein and the L protein as virus-infected cells were subcultured. This study shows that there is an unstable dynamic phase at an early stage of the establishment of persistent Sendai virus infection (steady state), and then viruses capable of establishing persistent infection are selected.

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