ArticleJournal of virology2008
Characterization of the New World monkey homologues of human poliovirus receptor CD155.
Article in Journal of virology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed, 8 citations in OpenAlex.
- Recombinant Poliovirus for Cancer Immunotherapy.Annual review of medicine · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
In contrast to Old World monkeys, most New World monkeys (NWMs) are not susceptible to poliovirus (PV), regardless of the route of infection. We have investigated the molecular basis of restricted PV pathogenesis of NWMs with two kidney cell lines of NWMs, TMX (tamarin) and NZP-60 (marmoset), and characterized their PV receptor homologues. TMX cells were susceptible to infection by PV1 (Mahoney) and PV3 (Leon) but not by PV2 (Lansing). Binding studies to TMX cells indicated that the formation of PV/receptor complexes increased when measured first at 4 degrees C and then at 25 degrees C, whereas PV2 did not significantly bind to TMX cells at either temperature. On the other hand, NZP-60 cells were not susceptible to infection by any of the PV serotypes. However, a low amount of PV1 bound to NZP-60 cells at 4 degrees C, but there was no increase of binding at 25 degrees C. In contrast, both NWM cell lines supported genome replication and virion formation when transfected with viral RNAs of either serotype, an observation indicating that infection was blocked in receptor-virus interaction. To overcome the receptor block, we substituted 3 amino acids in the marmoset receptor (nCD155), H80Q, N85S, and P87S, found in the human PV receptor, hCD155. Cells expressing the mutant receptor (L-nCD155mt) were now susceptible to infection with PV1, which correlated with an increase in PV1-bound receptor complexes from 4 degrees C to 25 degrees C. L-nCD155mt cells were, however, still resistant to PV2 and PV3. These data show that an increase in the formation of PV/receptor complexes, when measured at 4 degrees C and at 25 degrees C, correlates with and is an indicator of successful infection at 37 degrees C, suggesting that the complex formed at 25 degrees C may be an intermediate in PV uptake.
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Registered trials
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