|| R. L. Ward, D. I. Bernstein, E. C. Young, J. R. Sherwood, D. R. Knowlton, G. M. Schiff, Human rotavirus studies in volunteers: Determination of infectious dose and serological response to infection. J. Infect. Dis. 154, 871–880 (1986). doi: 10.1093/infdis/154.5.871  M. Katz, S. A. Plotkin, Minimal infective dose of attenuated poliovirus for man. Am. J. Public Health Nations Health 57, 1837–1840 (1967). doi: 10.2105/AJPH.57.10.1837  P. F. Teunis, C. L. Moe, P. Liu, S. E. Miller, L. Lindesmith, R. S. Baric, J. Le Pendu, R. L. Calderon, Norwalk virus: How infectious is it? J. Med. Virol. 80, 1468–1476 (2008). doi: 10.1002/jmv.21237PubMed ID3021869, 4293371, 18551613
||P.aad5872-1 right column 2nd paragraph: "For successful propagation and transmission, enteric viruses must navigate several unique niches within the gastrointestinal tract. Fewer than 100 viral particles are frequently sufficient for infection with human enteric viruses such as norovirus, rotavirus, and poliovirus (primary sources). Enteric viruses encounter low pH, proteolytic enzymes, microbiota, and intestinal mucus before replication in the intestine. Therefore, initiation of viral replication from the intestinal lumen is likely to be far more difficult than subsequent cycles of viral replication initiated by spread from previously infected intestinal cells or between cells in tissue culture. Different enteric viruses replicate in different cell types, ranging from enterocytes to lymphocytes to myeloid cells. After viral replication, progeny viruses are shed into the lumen, leading to transmission to new hosts."