Studies on the early antigens induced by vaccinia virus

Ueda, Yoshiaki; Tagaya, Isamu; Amano, Hiroko; Ito, Michio

doi:10.1016/0042-6822(72)90535-1

Cited by 30 publications

(25 citation statements)

References 11 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The development of early virus-specific antigens after vaccinia virus infection has already been described [22]. We could observe specific surface immunofluorescence in infected L-929 or mastocytoma P-815-X2 cells, beginning 2 h after infection, using human anti-vaccinia hyperimmune sera.…”

Section: Infection Conditionsmentioning

confidence: 63%

“…The infected cells could be used 2 h after infection, but often higher percentage of specific cell cytolysis by immune lymphocytes could be obtained with cells infected for a longer period. Twelve hour infected cells were usually utilized as targets.The development of early virus-specific antigens after vaccinia virus infection has already been described [22]. We could observe specific surface immunofluorescence in infected L-929 or mastocytoma P-815-X2 cells, beginning 2 h after infection, using human anti-vaccinia hyperimmune sera.…”

mentioning

confidence: 63%

See 1 more Smart Citation

Target cell‐dependent T cell‐mediated lysis of vaccinia virus‐infected cells

Koszinowski¹,

Thomssen²

1975

Eur J Immunol

View full text Add to dashboard Cite

Cell-mediated lysis of virus-infected cells 245are at work f o r cellular antigens also. This confirms their im- Elimination of B cells was performed by incubation with goat antiserum to mouse Ig (Gibco, BCL 1039). The serum was absorbed with C3H mouse thymocytes until there was no more cytotoxicity against thymocytes. 15 x 1 O6 cells were incubated in 0.2 ml of antiserum 30 min in 37 "C, washed and incubated again with an equal volume of guinea pig complement absorbed with mouse liver powder. T cell eliminationAnti-@ serum from AKR mice was kindly provided by Dr.Rollinghoff, Mainz. 1 5 x l o 6 spleen cells were incubated in 0.2 ml anti-@ serum for 30 min at 37 "C. Controls were run with normal mouse serum. The cells were washed and resuspended in 0.2 ml guinea pig complement absorbed with mouse liver powder and agarose [ 201. After incubation for 30 min at 37 "C the cells were washed and resuspended to the desired concentration. The viability of the cells was tested by the trypan blue exclusion test. Anti-vaccinia serumHyperimmune serum was obtained from sensitized rabbits injected intracutaneously with 5 ml 1 O6 TCIDso/ml followed 6-10 weeks later by booster intravenous injections of the same dosage. Syngeneic hyperimmune serum was obtained from mice after three intraperitoneal injections of 2 ml 1 O6 TCIDso/ml given at two week intervals. The animals were bled one week after the last injection. Normal serum was obtained from noninfected animals. All sera were inactivated and stored at -70 "C. Target cellsL-929 cells, kindly provided by Dr. Lehmann-Grube, Hamburg, were grown as monolayers in MEM containing 10 % FCS and 100 pg/ml of penicillin and streptomycin in Roux bottles. Mastocytoma P-8 15-X2 suspension cultures were grown in 10 cm Petri dishes containing Dulbecco's fortified Eagle's medium (Grand Island Biological Co.) with 10 % FCS and antibiotics, on a rocker platform (Bellco Glass Co, Vineland, N.Y.) in a humidified 8 % C02-atmosphere. Infection of target cellsMonolayers of L-929 cells were trypsinized, suspended in fresh medium and plated in 0.1 ml volumes in sterile flat bottom microtest plates (Greiner, Nurtingen N o 220 ART)t o reach a final concentration of 5 x 1 O4 cells/well. Five hours later the medium was removed and the cells were incubated with 0.2 ml virus suspension containing 5 x 1 O5 TCIDso/ 0.2 ml medium. Two hours later all the supernatants were discarded and fresh medium was added. Suspensions of mastocytoma P-815-X2 cells were infected by incubating the cells in a medium containing 10 TCIDSO of virus per mastocytoma cell under constant rocking. After 2 h the cells were washed and resuspended in fresh medium. Eur. J. Immunol. 1975.5: 245-251Cell-mediated lysis of virus-infected cells 247Five times 1 O6 infected o r noninfected mastocytoma cells were suspended in 0.2 ml medium and 100 yCi "Cr (sodiumchromat, Amersham, Buchler, Braunschweig N o CJSlP. spec. activity 100-200 mCi/mg Cr) was added. After 2 h incubation the cells were washed three times, resuspended to the required concent...

show abstract

Section: Infection Conditionsmentioning

confidence: 63%

mentioning

confidence: 63%

Target cell‐dependent T cell‐mediated lysis of vaccinia virus‐infected cells

Koszinowski¹,

Thomssen²

1975

Eur J Immunol

View full text Add to dashboard Cite

show abstract

“…Vaccinia virus B18R was reported to be localized to the surface of infected cells (26,27). The observation that M135R has a functional signal sequence as well as a transmembrane domain but was not secreted prompted us to assess the localization of M135R.…”

Section: Resultsmentioning

confidence: 99%

M135R Is a Novel Cell Surface Virulence Factor of Myxoma Virus

Barrett

Sypula

Wang

et al. 2007

J Virol

View full text Add to dashboard Cite

Myxoma virus (MV) encodes a cell surface protein (M135R) that is predicted to mimic the host alpha/beta interferon receptor (IFN-␣/␤-R) and thus prevent IFN-␣/␤ from triggering a host antiviral response. This prediction is based on sequence similarity to B18R, the viral IFN-␣/␤-R from vaccinia virus (VV), which has been demonstrated to bind and inhibit type I interferons. However, M135R is only half the size of VV B18R. All other poxvirus-encoded IFN-␣/␤-R homologs align only to the amino-terminal half of M135R. Peptide antibodies raised against M135R were used for immunoblotting and immunofluorescence and indicate that M135R is expressed as an early gene and that the product is a cell surface N-linked glycoprotein that is not secreted. In contrast to the predicted properties of M135R as an inhibitor of type I interferon, all binding and inhibition assays designed to demonstrate whether M135R can interact with IFN-␣/␤ have been negative. However, pathogenesis studies with a targeted M135-knockout MV construct (vMyx135KO) indicate that the deletion of M135R severely attenuates MV pathogenesis in the European rabbit. We propose that M135R is an important immunomodulatory virulence factor for myxomatosis but that the target immune ligand is not from the predicted type I interferon family and remains to be identified.

show abstract

“…In addition to the soluble B18R, antiserum raised against VACV proteins recognized a protein on the surface of virus-infected cells at early time points p.i. (694,696). This protein is a membrane-bound B18R (695) that might be anchored in the plasma membrane through its N-terminus hydrophobic sequence (443).…”

Section: Vacv-induced Immunomodulationmentioning

confidence: 99%

The role of CCR5 in vaccinia virus pathogenesis

Rahbar

Fish

2009

Cytokine

View full text Add to dashboard Cite

Viral appropriation of chemokine receptors is an effective way to prevent a host immune response against the invading virus. Many viruses, including poxviruses, subvert the host immune response by encoding several chemokine receptor homologues, capable of binding to and thereby precluding chemokines from activating their cognate cell surface receptors. All poxviruses employ strategies to modulate chemokine activity, including virus-encoded chemokine-binding proteins, receptor homologues and ligand mimics. The potential for the involvement of certain chemokine receptors in poxviral infection was suggested in studies utilizing the rabbit poxvirus, myxoma. Specifically, CCR5 was implicated in mediating cell target susceptibility to infection. Our data suggest virus-CCR5 interactions may lead to the selective activation of distinct signaling pathways that are advantageous for the virus.VACV, a member of the poxvirus family, produces two structurally distinct forms of virions, the intracellular mature virus (IMV) and the extracellular enveloped virus (EEV), for which the immediate events following cell entry are illiii defined. Using confocal microscopy, we provided evidence that IMV and EEV enter both permissive and non-permissive cells, and that introduction of CCR5 into non-permissive cells -mouse fibroblasts and human PM1 T cells -renders them permissive for VACV replication. We showed that virus activation of CCR5 leads to the selective activation of distinct signaling pathways that are advantageous for the virus. We demonstrated that VACV infection in permissive cells is inhibited by siRNA knockdown of cell surface

show abstract

Studies on the early antigens induced by vaccinia virus

Cited by 30 publications

References 11 publications

Target cell‐dependent T cell‐mediated lysis of vaccinia virus‐infected cells

Target cell‐dependent T cell‐mediated lysis of vaccinia virus‐infected cells

M135R Is a Novel Cell Surface Virulence Factor of Myxoma Virus

The role of CCR5 in vaccinia virus pathogenesis

Contact Info

Product

Resources

About