Murid herpesvirus 4 strain 68 M2 protein is a B-cell-associated antigen important for latency but not lymphocytosis

Alastair I. Macrae, Edward J. Usherwood, S. Mazher Husain, Emilio Flaño, In Jeong Kim, David L. Woodland, Anthony A. Nash, Marcia A. Blackman, Jeffery T. Sample, James P. Stewart

Research output: Contribution to journalArticle

34 Citations (Scopus)

Abstract

This work describes analyses of the function of the murid herpesvirus 4 strain 68 (MHV-68) M2 gene. A frameshift mutation was made in the M2 open reading frame that caused premature termination of translation of M2 after amino acid residue 90. The M2 mutant showed no defect in productive replication in vitro or in lungs after infection of mice. Likewise, the characteristic transient increase in spleen cell number, Vβ4 T-cell-receptor-positive CD8+ T-cell mononucleosis, and establishment of latency were unaffected. However, the M2 mutant virus was defective in its ability to cause the transient sharp rise in latently infected cells normally seen in the spleen after infection of mice. We also demonstrate that expression of M2 is restricted to B cells in the spleen and that M2 encodes a 30-kDa protein localizing predominantly in the cytoplasm and plasma membrane of B cells.

Original languageEnglish (US)
Pages (from-to)9700-9709
Number of pages10
JournalJournal of virology
Volume77
Issue number17
DOIs
StatePublished - Sep 1 2003

Fingerprint

Murid herpesvirus 4
Rhadinovirus
Lymphocytosis
B-lymphocytes
spleen
B-Lymphocytes
Spleen
T-lymphocytes
antigens
frameshift mutation
Antigens
mutants
mice
splenocytes
infection
translation (genetics)
Defective Viruses
open reading frames
Frameshift Mutation
Proteins

All Science Journal Classification (ASJC) codes

  • Microbiology
  • Immunology
  • Insect Science
  • Virology

Cite this

Macrae, A. I., Usherwood, E. J., Husain, S. M., Flaño, E., Kim, I. J., Woodland, D. L., ... Stewart, J. P. (2003). Murid herpesvirus 4 strain 68 M2 protein is a B-cell-associated antigen important for latency but not lymphocytosis. Journal of virology, 77(17), 9700-9709. https://doi.org/10.1128/JVI.77.17.9700-9709.2003
Macrae, Alastair I. ; Usherwood, Edward J. ; Husain, S. Mazher ; Flaño, Emilio ; Kim, In Jeong ; Woodland, David L. ; Nash, Anthony A. ; Blackman, Marcia A. ; Sample, Jeffery T. ; Stewart, James P. / Murid herpesvirus 4 strain 68 M2 protein is a B-cell-associated antigen important for latency but not lymphocytosis. In: Journal of virology. 2003 ; Vol. 77, No. 17. pp. 9700-9709.
@article{be0a9f159aa5416796c61d4738287e96,
title = "Murid herpesvirus 4 strain 68 M2 protein is a B-cell-associated antigen important for latency but not lymphocytosis",
abstract = "This work describes analyses of the function of the murid herpesvirus 4 strain 68 (MHV-68) M2 gene. A frameshift mutation was made in the M2 open reading frame that caused premature termination of translation of M2 after amino acid residue 90. The M2 mutant showed no defect in productive replication in vitro or in lungs after infection of mice. Likewise, the characteristic transient increase in spleen cell number, Vβ4 T-cell-receptor-positive CD8+ T-cell mononucleosis, and establishment of latency were unaffected. However, the M2 mutant virus was defective in its ability to cause the transient sharp rise in latently infected cells normally seen in the spleen after infection of mice. We also demonstrate that expression of M2 is restricted to B cells in the spleen and that M2 encodes a 30-kDa protein localizing predominantly in the cytoplasm and plasma membrane of B cells.",
author = "Macrae, {Alastair I.} and Usherwood, {Edward J.} and Husain, {S. Mazher} and Emilio Fla{\~n}o and Kim, {In Jeong} and Woodland, {David L.} and Nash, {Anthony A.} and Blackman, {Marcia A.} and Sample, {Jeffery T.} and Stewart, {James P.}",
year = "2003",
month = "9",
day = "1",
doi = "10.1128/JVI.77.17.9700-9709.2003",
language = "English (US)",
volume = "77",
pages = "9700--9709",
journal = "Journal of Virology",
issn = "0022-538X",
publisher = "American Society for Microbiology",
number = "17",

}

Macrae, AI, Usherwood, EJ, Husain, SM, Flaño, E, Kim, IJ, Woodland, DL, Nash, AA, Blackman, MA, Sample, JT & Stewart, JP 2003, 'Murid herpesvirus 4 strain 68 M2 protein is a B-cell-associated antigen important for latency but not lymphocytosis', Journal of virology, vol. 77, no. 17, pp. 9700-9709. https://doi.org/10.1128/JVI.77.17.9700-9709.2003

Murid herpesvirus 4 strain 68 M2 protein is a B-cell-associated antigen important for latency but not lymphocytosis. / Macrae, Alastair I.; Usherwood, Edward J.; Husain, S. Mazher; Flaño, Emilio; Kim, In Jeong; Woodland, David L.; Nash, Anthony A.; Blackman, Marcia A.; Sample, Jeffery T.; Stewart, James P.

In: Journal of virology, Vol. 77, No. 17, 01.09.2003, p. 9700-9709.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Murid herpesvirus 4 strain 68 M2 protein is a B-cell-associated antigen important for latency but not lymphocytosis

AU - Macrae, Alastair I.

AU - Usherwood, Edward J.

AU - Husain, S. Mazher

AU - Flaño, Emilio

AU - Kim, In Jeong

AU - Woodland, David L.

AU - Nash, Anthony A.

AU - Blackman, Marcia A.

AU - Sample, Jeffery T.

AU - Stewart, James P.

PY - 2003/9/1

Y1 - 2003/9/1

N2 - This work describes analyses of the function of the murid herpesvirus 4 strain 68 (MHV-68) M2 gene. A frameshift mutation was made in the M2 open reading frame that caused premature termination of translation of M2 after amino acid residue 90. The M2 mutant showed no defect in productive replication in vitro or in lungs after infection of mice. Likewise, the characteristic transient increase in spleen cell number, Vβ4 T-cell-receptor-positive CD8+ T-cell mononucleosis, and establishment of latency were unaffected. However, the M2 mutant virus was defective in its ability to cause the transient sharp rise in latently infected cells normally seen in the spleen after infection of mice. We also demonstrate that expression of M2 is restricted to B cells in the spleen and that M2 encodes a 30-kDa protein localizing predominantly in the cytoplasm and plasma membrane of B cells.

AB - This work describes analyses of the function of the murid herpesvirus 4 strain 68 (MHV-68) M2 gene. A frameshift mutation was made in the M2 open reading frame that caused premature termination of translation of M2 after amino acid residue 90. The M2 mutant showed no defect in productive replication in vitro or in lungs after infection of mice. Likewise, the characteristic transient increase in spleen cell number, Vβ4 T-cell-receptor-positive CD8+ T-cell mononucleosis, and establishment of latency were unaffected. However, the M2 mutant virus was defective in its ability to cause the transient sharp rise in latently infected cells normally seen in the spleen after infection of mice. We also demonstrate that expression of M2 is restricted to B cells in the spleen and that M2 encodes a 30-kDa protein localizing predominantly in the cytoplasm and plasma membrane of B cells.

UR - http://www.scopus.com/inward/record.url?scp=0042890323&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0042890323&partnerID=8YFLogxK

U2 - 10.1128/JVI.77.17.9700-9709.2003

DO - 10.1128/JVI.77.17.9700-9709.2003

M3 - Article

C2 - 12915582

AN - SCOPUS:0042890323

VL - 77

SP - 9700

EP - 9709

JO - Journal of Virology

JF - Journal of Virology

SN - 0022-538X

IS - 17

ER -