In:
Journal of Virology, American Society for Microbiology, Vol. 79, No. 12 ( 2005-06-15), p. 7838-7844
Abstract:
The P gene of measles virus (MV) encodes the P protein and three accessory proteins (C, V, and R). However, the role of these accessory proteins in the natural course of MV infection remains unclear. For this study, we generated a recombinant wild-type MV lacking the C protein, called wtMV(C−), by using a reverse genetics system (M. Takeda, K. Takeuchi, N. Miyajima, F. Kobune, Y. Ami, N. Nagata, Y. Suzaki, Y. Nagai, and M. Tashiro, J. Virol. 74: 6643-6647). When 293 cells expressing the MV receptor SLAM (293/hSLAM) were infected with wtMV(C−) or parental wild-type MV (wtMV), the growth of wtMV(C−) was restricted, particularly during late stages. Enhanced green fluorescent protein-expressing wtMV(C−) consistently induced late-stage cell rounding and cell death in the presence of a fusion-inhibiting peptide, suggesting that the C protein can prevent cell death and is required for long-term MV infection. Neutralizing antibodies against alpha/beta interferon did not restore the growth restriction of wtMV(C−) in 293/hSLAM cells. When cynomolgus monkeys were infected with wtMV(C−) or wtMV, the number of MV-infected cells in the thymus was 〉 1,000-fold smaller for wtMV(C−) than for wtMV. Immunohistochemical analyses showed strong expression of an MV antigen in the spleen, lymph nodes, tonsils, and larynx of a cynomolgus monkey infected with wtMV but dramatically reduced expression in the same tissues in a cynomolgus monkey infected with wtMV(C−). These data indicate that the MV C protein is necessary for efficient MV replication both in vitro and in cynomolgus monkeys.
Type of Medium:
Online Resource
ISSN:
0022-538X
,
1098-5514
DOI:
10.1128/JVI.79.12.7838-7844.2005
Language:
English
Publisher:
American Society for Microbiology
Publication Date:
2005
detail.hit.zdb_id:
1495529-5
