Infection of mammalian skeletal muscle cells by Trichinella spiralis causes host nuclei to become
polyploid (ca. 4N) and abnormally enlarged. It has been postulated that this enlargement reflects an
infection-induced elevation of host transcription.
Anthelmintic treatment of T. spiralis-infected rodents with
mebendazole (MBZ) causes a reduction in the size of infected cell nuclei and a significant reduction in the total
RNA content of individual infected muscle cells. A
monoclonal antibody to the large subunit of
RNA polymerase II (Pol II) was used here to assess the effects of
infection on Pol II levels in isolated infected cell nuclei. Pol II was localized to speckle domains in isolated infected cell nuclei. Similar domains have been previously localized to sites of
RNA synthesis or processing. When compared to the levels in nuclei from other, uninfected host cells, speckle-localized Pol II (SL-Pol II) levels were significantly elevated in infected cell nuclei by a mean of 3.9- to 6.8-fold.
Nuclear antigens (NA) recognized by
antibodies against T. spiralis localized to infected cell nuclei. By use of confocal microscopy, a subpopulation of NA was found colocalized with most speckle domains defined by Pol II. MBZ treatment of chronically infected mice, which depletes NA from infected cell nuclei, caused a significant depletion of SL-Pol II from infected cell nuclei. Control nuclei had a mean of 70% more SL-Pol II than MBZ-treated nuclei. The mean residual level of Pol II in these
polyploid nuclei remained elevated by 120% over the level in 2N control nuclei. These observations may indicate two distinct effects of
infection on Pol II levels in host cells.