Trichomonas vaginalis resistance to Mengo virus infection.
We have investigated the susceptibility of Trichomonas vaginalis to Mengo virus infection by comparing the outcome of Mengo virus or purified Mengo virus RNA infection in T. vaginalis and in CCL-1 mouse fibroblasts. While the adsorption and entry of Mengo virus into T. vaginalis occurred in the same manner as in fibroblasts, the uncoating was much slower. In addition, Mengo virus infection of T. vaginalis displayed no eclipse nor any subsequent production of infectious virus. Purified RNA failed to initiate productive infection in T. vaginalis, whereas it provoked viral replication in the fibroblast controls. It was shown by assessment of protein synthesis in T. vaginalis and mouse fibroblasts cell-free systems that the protozoan ribosomes were able to translate endogenous mRNA and poly-U, but not viral RNA.
D000818:Animals; D002474:Cell-Free System; D004769:Enterovirus Infections / Q000382:microbiology*; D008574:Mengovirus / Q000235:genetics / Q000254:growth & development*; D014176:Protein Biosynthesis; D012367:RNA, Viral / Q000235:genetics; D014246:Trichomonas vaginalis / Q000382:microbiology*; D014764:Viral Proteins / Q000235:genetics; D014779:Virus Replication
D012367:RNA, Viral; D014764:Viral Proteins