Recovery of a Sendai virus variant with temperature-sensitive hemolytic activity from persistently infected cells from mouse brain

1978 ◽  
Vol 58 (2) ◽  
pp. 81-93 ◽  
Author(s):  
Arlene R. Collins ◽  
T. D. Flanagan
Keyword(s):  
Mouse Brain ◽  
Hemolytic Activity ◽  
Sendai Virus ◽  
Temperature Sensitive ◽  
Virus Variant ◽  
Persistently Infected ◽  
Infected Cells

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 Nontransmissible Virus-Like Particle Formation by F-Deficient Sendai Virus Is Temperature Sensitive and Reduced by Mutations in M and HN Proteins

2003 ◽  
Vol 77 (5) ◽  
pp. 3238-3246 ◽  
Author(s):  
Makoto Inoue ◽  
Yumiko Tokusumi ◽  
Hiroshi Ban ◽  
Takumi Kanaya ◽  
Tsuyoshi Tokusumi ◽  
...  
Keyword(s):  
Gene Expression ◽  
Sendai Virus ◽  
M Protein ◽  
Temperature Sensitive ◽  
Amino Acid Substitutions ◽  
Wild Type ◽  
Sensitive Mutant ◽  
Temperature Sensitive Mutant ◽  
Virus Like Particle ◽  
Infected Cells

ABSTRACT The formation of nontransmissible virus-like particles (NTVLP) by cells infected with F-deficient Sendai virus (SeV/ΔF) was found to be temperature sensitive. Analysis by hemagglutination assays and Western blotting demonstrated that the formation of NTVLP at 38°C was about 1/100 of that at 32°C, whereas this temperature-sensitive difference was only moderate in the case of F-possessing wild-type SeV. In order to reduce the NTVLP formation with the aim of improving SeV for use as a vector for gene therapy, amino acid substitutions found in temperature-sensitive mutant SeVs were introduced into the M (G69E, T116A, and A183S) and HN (A262T, G264R, and K461G) proteins of SeV/ΔF to generate SeV/MtsHNtsΔF. The use of these mutations allows vector production at low temperature (32°C) and therapeutic use at body temperature (37°C) with diminished NTVLP formation. As expected, the formation of NTVLP by SeV/MtsHNtsΔF at 37°C was decreased to about 1/10 of that by SeV/ΔF, whereas the suppression of NTVLP formation did not cause either enhanced cytotoxicity or reduced gene expression of the vector. The vectors showed differences with respect to the subcellular distribution of M protein in the infected cells. Clear and accumulated immunocytochemical signals of M protein on the cell surface were not observed in cells infected by SeV/ΔF at an incompatible temperature, 38°C, or in those infected by SeV/MtsHNtsΔF at 37 or 38°C. The absence of F protein in SeV/ΔF and the additional mutations in M and HN in SeV/MtsHNtsΔF probably weaken the ability to transport M protein to the plasma membrane, leading to the diminished formation of NTVLP.

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.

scholarly journals Temperature-sensitive virus derived from BHK cells persistently infected with HVJ (Sendai virus).

1975 ◽  
Vol 15 (1) ◽  
pp. 55-63 ◽  
Author(s):  
Y Kimura ◽  
Y Ito ◽  
K Shimokata ◽  
Y Nishiyama ◽  
I Nagata
Keyword(s):  
Sendai Virus ◽  
Temperature Sensitive ◽  
Persistently Infected ◽  
Bhk Cells

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.

Infective substructures of measles virus from acutely and persistently infected cells.

1979 ◽  
Vol 32 (1) ◽  
pp. 329-333 ◽  
Author(s):  
S Rozenblatt ◽  
T Koch ◽  
O Pinhasi ◽  
S Bratosin
Keyword(s):  
Measles Virus ◽  
Persistently Infected ◽  
Infected Cells
Sign in / Sign up

Export Citation Format

Share Document