Immunocompetent adult mice mount a vigorous cytotoxic T lymphocyte (CTL) response against the Armstrong (ARM) 53b strain of LCMV after primary inoculation. In contrast, the Clone 13 variant of ARM 53b, originally isolated from the spleen of a persistently infected mouse, suppresses LCMV-specific CTL responses (R. Ahmed et al. (1984) J. Exp Med 60, 521). The induction and generation of CTL maps to the short (S) RNA segment and not the long (L) RNA segment of LCMV (Y. Riviere et al. (1986) J. Immunol. 136, 304). The CTL recognition epitope, expressed in virus-infected target cells, also maps to the S segment of the LCMV ARM genome, and is structurally and functionally intact in Clone 13-infected target cells. Here we report the S RNA sequences of both ARM 53b and its variant Clone 13. Comparison reveals a single amino acid difference. However, sequence divergence at this position also occurs among other strains of LCMV (Pasteur, Traub, WE) which do elicit CTL responses. Hence, (1) the amino acid difference is unrelated to the phenotypic divergence of Clone 13, (2) suppression of the CTL response by Clone 13 is not linked to the CTL recognition epitope, and (3) the structure or function responsible for CTL immunosuppression by Clone 13 most likely maps to the L RNA segment. Further, the availability of the complete S RNA sequence for LCMV ARM and ARM Clone 13 variant allows a detailed comparison with WE (V. Romanowski et al. (1985) Virus Res. 3, 110-114), the only other LCMV S RNA so far sequenced.
|Original language||English (US)|
|Number of pages||6|
|State||Published - Jun 1988|
Bibliographical noteFunding Information:
This is Publication Number 5091-IMM from the Department of immunology, Scripps Clinic and Research Foundation, La Jolla, CA 92037. This work was supported in part by USPHS grant and Al-09484 (MS, MBAO), NS-12428 (PS), AG-04342‘(PS), and Al25522-01 (MS). We thank C. D. Pauza for useful comments.