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Based on present data, the M-P virus appears antigenically and morphologically to be a strain of the lymphocytic choriomeningitis virus, with some different biological properties.

SYNOPSIS. Octogenic reproductive cysts are transformed into resting cysts when returned to optimal temperature following prior exposure to cold (5°C) for at least 36 hours. In the cold, the reproductive process ceases and macronuclei revert to the interphase condition. Transformation to resting cysts is synchronous. Induced encystment is accompanied by excessive macronuclear extrusion and is associated with a loss in division potential, resulting in no division, or 1 or 2 divisions in the induced resting cyst. These observations support the hypothesis that exposure to cold during a critical period of the predivisional stage may alter reproductive protein synthesis and favor cyst protein synthesis. The extensive macronuclear extrusions associated with this transition suggest their biochemical involvement in the encystment process.

Pichinde virus (PV), a member of the Arenaviridae family, protects mice from a lethal inoculation with the sarcoma 180 (S180) tumor cell line. Virus replication, which is required for protection, occurs primarily in the spleen and tumor. During the first 4 days, elevated natural killer (NK) cell activity parallels an increase in serum interferon in PV-infected mice. On day 7 after infection virus-specific cytotoxic T cells (CTLs) are found in the mouse. This strong response peaks on day 13 and gradually declines over the next 17 days. The tumor-specific CTL response appears more slowly and is less intense than the virus-specific response, especially in the uninfected mouse. However, CTLs from either type of mouse recognize PV-infected tissue culture S180 target cells better than uninfected ones. Even though the primary tumor-specific immune response appears weak, mice that have cleared both virus and tumor are refractory to a subsequent challenge with S180 cells and rapidly produce tumor-specific CTLs. Thus, our data indicate a number of ways in which virus infection could lead to immune elimination of tumors: (1) Virus-induced interferon stimulates NK-cell activity, which in turn could control tumor load until a specific response is mounted against the S180 cells; (2) early onset of the tumor-specific T-cell response could be brought about by viral-enhanced tumor antigen presentation to the immune system; and (3) the tumor-specific T-cell response could be augmented through a "bystander' phenomenon involving factors associated with T cells responding specifically and vigorously to the virus itself.