Extract

Lipopolysaccharide (LPS) from several gramnegative bacteria significantly increased the spleen focus-forming efficiency of N-tropic Friend virus complex in mice by different mechanisms. One effect was associated with an increase in the number or availability of potential target cells for spleen focus-forming virus (SFFV) in fully susceptible mouse strains. This enhancing effect was optimal when LPS was injected 5 days before SFFV but was nil when LPS and SFFV were given at the same time. In contrast, in mice genetically resistant to the native helper virus of SFFV, the helper effect of LPS was optimal when it was injected with SFFV and nil when given 5 days before or atter the virus. LPS did not affect helper virus expression in a standard cell culture (XC) assay, but it did increase helper virus replication in mice. Mice lacking T cells or complete endogenous murine leukemia virus genomes were just as sensitive to the helper effects of LPS on SFFV expression as were control animals. Most of the helper activity of LPS is associated with the lipid A component. The mechanism of the helper effect of lipid A is still unknown, but hypotheses must take into account that this effect did not occur in fully susceptible hosts, but only in hosts carrying resistance alleles at either the Fv-1 or the Fv-2 locus.

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