Norwalk virus: How infectious is it
Noroviruses are major agents of viral gastroenteritis worldwide. The infectivity of Norwalk virus, the prototype norovirus, has been studied in susceptible human volunteers. A new variant of the hit theory model of microbial infection was developed to estimate the variation in Norwalk virus infectiv...
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| Published in | Journal of medical virology Vol. 80; no. 8; pp. 1468 - 1476 |
|---|---|
| Main Authors | , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Hoboken
Wiley Subscription Services, Inc., A Wiley Company
01.08.2008
Wiley-Liss |
| Subjects | |
| Online Access | Get full text |
| ISSN | 0146-6615 1096-9071 1096-9071 |
| DOI | 10.1002/jmv.21237 |
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| Abstract | Noroviruses are major agents of viral gastroenteritis worldwide. The infectivity of Norwalk virus, the prototype norovirus, has been studied in susceptible human volunteers. A new variant of the hit theory model of microbial infection was developed to estimate the variation in Norwalk virus infectivity, as well as the degree of virus aggregation, consistent with independent (electron microscopic) observations. Explicit modeling of viral aggregation allows us to express virus infectivity per single infectious unit (particle). Comparison of a primary and a secondary inoculum showed that passage through a human host does not change Norwalk virus infectivity. We estimate the average probability of infection for a single Norwalk virus particle to be close to 0.5, exceeding that reported for any other virus studied to date. Infected subjects had a dose-dependent probability of becoming ill, ranging from 0.1 (at a dose of 10³ NV genomes) to 0.7 (at 10⁸ virus genomes). A norovirus dose response model is important for understanding its transmission and essential for development of a quantitative risk model. Norwalk virus is a valuable model system to study virulence because genetic factors are known for both complete and partial protection; the latter can be quantitatively described as heterogeneity in dose response models. J. Med. Virol. 80:1468-1476, 2008. |
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| AbstractList | Noroviruses are major agents of viral gastroenteritis worldwide. The infectivity of Norwalk virus, the prototype norovirus, has been studied in susceptible human volunteers. A new variant of the hit theory model of microbial infection was developed to estimate the variation in Norwalk virus infectivity, as well as the degree of virus aggregation, consistent with independent (electron microscopic) observations. Explicit modeling of viral aggregation allows us to express virus infectivity per single infectious unit (particle). Comparison of a primary and a secondary inoculum showed that passage through a human host does not change Norwalk virus infectivity. We estimate the average probability of infection for a single Norwalk virus particle to be close to 0.5, exceeding that reported for any other virus studied to date. Infected subjects had a dose-dependent probability of becoming ill, ranging from 0.1 (at a dose of 10³ NV genomes) to 0.7 (at 10⁸ virus genomes). A norovirus dose response model is important for understanding its transmission and essential for development of a quantitative risk model. Norwalk virus is a valuable model system to study virulence because genetic factors are known for both complete and partial protection; the latter can be quantitatively described as heterogeneity in dose response models. J. Med. Virol. 80:1468-1476, 2008. Noroviruses are major agents of viral gastroenteritis worldwide. The infectivity of Norwalk virus, the prototype norovirus, has been studied in susceptible human volunteers. A new variant of the hit theory model of microbial infection was developed to estimate the variation in Norwalk virus infectivity, as well as the degree of virus aggregation, consistent with independent (electron microscopic) observations. Explicit modeling of viral aggregation allows us to express virus infectivity per single infectious unit (particle). Comparison of a primary and a secondary inoculum showed that passage through a human host does not change Norwalk virus infectivity. We estimate the average probability of infection for a single Norwalk virus particle to be close to 0.5, exceeding that reported for any other virus studied to date. Infected subjects had a dose-dependent probability of becoming ill, ranging from 0.1 (at a dose of 10³ NV genomes) to 0.7 (at 10¸ virus genomes). A norovirus dose response model is important for understanding its transmission and essential for development of a quantitative risk model. Norwalk virus is a valuable model system to study virulence because genetic factors are known for both complete and partial protection; the latter can be quantitatively described as heterogeneity in dose response models. J. Med. Virol. 80:1468-1476, 2008. Noroviruses are major agents of viral gastroenteritis worldwide. The infectivity of Norwalk virus, the prototype norovirus, has been studied in susceptible human volunteers. A new variant of the hit theory model of microbial infection was developed to estimate the variation in Norwalk virus infectivity, as well as the degree of virus aggregation, consistent with independent (electron microscopic) observations. Explicit modeling of viral aggregation allows us to express virus infectivity per single infectious unit (particle). Comparison of a primary and a secondary inoculum showed that passage through a human host does not change Norwalk virus infectivity. We estimate the average probability of infection for a single Norwalk virus particle to be close to 0.5, exceeding that reported for any other virus studied to date. Infected subjects had a dose-dependent probability of becoming ill, ranging from 0.1 (at a dose of 10(3) NV genomes) to 0.7 (at 10(8) virus genomes). A norovirus dose response model is important for understanding its transmission and essential for development of a quantitative risk model. Norwalk virus is a valuable model system to study virulence because genetic factors are known for both complete and partial protection; the latter can be quantitatively described as heterogeneity in dose response models. Noroviruses are major agents of viral gastroenteritis worldwide. The infectivity of Norwalk virus, the prototype norovirus, has been studied in susceptible human volunteers. A new variant of the hit theory model of microbial infection was developed to estimate the variation in Norwalk virus infectivity, as well as the degree of virus aggregation, consistent with independent (electron microscopic) observations. Explicit modeling of viral aggregation allows us to express virus infectivity per single infectious unit (particle). Comparison of a primary and a secondary inoculum showed that passage through a human host does not change Norwalk virus infectivity. We estimate the average probability of infection for a single Norwalk virus particle to be close to 0.5, exceeding that reported for any other virus studied to date. Infected subjects had a dose‐dependent probability of becoming ill, ranging from 0.1 (at a dose of 10 3 NV genomes) to 0.7 (at 10 8 virus genomes). A norovirus dose response model is important for understanding its transmission and essential for development of a quantitative risk model. Norwalk virus is a valuable model system to study virulence because genetic factors are known for both complete and partial protection; the latter can be quantitatively described as heterogeneity in dose response models. J. Med. Virol. 80:1468–1476, 2008. © 2008 Wiley‐Liss, Inc. Noroviruses are major agents of viral gastroenteritis worldwide. The infectivity of Norwalk virus, the prototype norovirus, has been studied in susceptible human volunteers. A new variant of the hit theory model of microbial infection was developed to estimate the variation in Norwalk virus infectivity, as well as the degree of virus aggregation, consistent with independent (electron microscopic) observations. Explicit modeling of viral aggregation allows us to express virus infectivity per single infectious unit (particle). Comparison of a primary and a secondary inoculum showed that passage through a human host does not change Norwalk virus infectivity. We estimate the average probability of infection for a single Norwalk virus particle to be close to 0.5, exceeding that reported for any other virus studied to date. Infected subjects had a dose‐dependent probability of becoming ill, ranging from 0.1 (at a dose of 103 NV genomes) to 0.7 (at 108 virus genomes). A norovirus dose response model is important for understanding its transmission and essential for development of a quantitative risk model. Norwalk virus is a valuable model system to study virulence because genetic factors are known for both complete and partial protection; the latter can be quantitatively described as heterogeneity in dose response models. J. Med. Virol. 80:1468–1476, 2008. © 2008 Wiley‐Liss, Inc. Noroviruses are major agents of viral gastroenteritis worldwide. The infectivity of Norwalk virus, the prototype norovirus, has been studied in susceptible human volunteers. A new variant of the hit theory model of microbial infection was developed to estimate the variation in Norwalk virus infectivity, as well as the degree of virus aggregation, consistent with independent (electron microscopic) observations. Explicit modeling of viral aggregation allows us to express virus infectivity per single infectious unit (particle). Comparison of a primary and a secondary inoculum showed that passage through a human host does not change Norwalk virus infectivity. We estimate the average probability of infection for a single Norwalk virus particle to be close to 0.5, exceeding that reported for any other virus studied to date. Infected subjects had a dose-dependent probability of becoming ill, ranging from 0.1 (at a dose of 10(3) NV genomes) to 0.7 (at 10(8) virus genomes). A norovirus dose response model is important for understanding its transmission and essential for development of a quantitative risk model. Norwalk virus is a valuable model system to study virulence because genetic factors are known for both complete and partial protection; the latter can be quantitatively described as heterogeneity in dose response models.Noroviruses are major agents of viral gastroenteritis worldwide. The infectivity of Norwalk virus, the prototype norovirus, has been studied in susceptible human volunteers. A new variant of the hit theory model of microbial infection was developed to estimate the variation in Norwalk virus infectivity, as well as the degree of virus aggregation, consistent with independent (electron microscopic) observations. Explicit modeling of viral aggregation allows us to express virus infectivity per single infectious unit (particle). Comparison of a primary and a secondary inoculum showed that passage through a human host does not change Norwalk virus infectivity. We estimate the average probability of infection for a single Norwalk virus particle to be close to 0.5, exceeding that reported for any other virus studied to date. Infected subjects had a dose-dependent probability of becoming ill, ranging from 0.1 (at a dose of 10(3) NV genomes) to 0.7 (at 10(8) virus genomes). A norovirus dose response model is important for understanding its transmission and essential for development of a quantitative risk model. Norwalk virus is a valuable model system to study virulence because genetic factors are known for both complete and partial protection; the latter can be quantitatively described as heterogeneity in dose response models. Noroviruses are major agents of viral gastroenteritis worldwide. The infectivity of Norwalk virus, the prototype norovirus, has been studied in susceptible human volunteers. A new variant of the hit theory model of microbial infection was developed to estimate the variation in Norwalk virus infectivity, as well as the degree of virus aggregation, consistent with independent (electron microscopic) observations. Explicit modeling of viral aggregation allows us to express virus infectivity per single infectious unit (particle). Comparison of a primary and a secondary inoculum showed that passage through a human host does not change Norwalk virus infectivity. We estimate the average probability of infection for a single Norwalk virus particle to be close to 0.5, exceeding that reported for any other virus studied to date. Infected subjects had a dose-dependent probability of becoming ill, ranging from 0.1 (at a dose of 103 NV genomes) to 0.7 (at 108 virus genomes). A norovirus dose response model is important for understanding its transmission and essential for development of a quantitative risk model. Norwalk virus is a valuable model system to study virulence because genetic factors are known for both complete and partial protection; the latter can be quantitatively described as heterogeneity in dose response models. J. Med. Virol. 80:1468-1476, 2008. |
| Author | E. Miller, Sara Le Pendu, Jacques Teunis, Peter F.M. Moe, Christine L. Baric, Ralph S. Liu, Pengbo Calderon, Rebecca L. Lindesmith, Lisa |
| Author_xml | – sequence: 1 fullname: Teunis, Peter F.M – sequence: 2 fullname: Moe, Christine L – sequence: 3 fullname: Liu, Pengbo – sequence: 4 fullname: Miller, Sara E – sequence: 5 fullname: Lindesmith, Lisa – sequence: 6 fullname: Baric, Ralph S – sequence: 7 fullname: Le Pendu, Jacques – sequence: 8 fullname: Calderon, Rebecca L |
| BackLink | http://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=20466302$$DView record in Pascal Francis https://www.ncbi.nlm.nih.gov/pubmed/18551613$$D View this record in MEDLINE/PubMed |
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| References | Dolin R, Blacklow NR, DuPont HL, Formal S, Buscho RF, Kasel JA, Chames RP, Hornick R, Chanock RM. 1971. Transmission of acute infectious nonbacterial gastroenteritis to volunteers by oral administration of stool filtrates. J Infect Dis 123: 307-312. Haas CN, Rose JB, Gerba C, Regli S. 1993. Risk assessment of virus in drinking water. Risk Analysis 13: 545-552. Cheetham S, Souza M, McGregor R, Meulia T, Wang Q, Saif LJ. 2007. Binding patterns of human norovirus-like particles to buccal and intestinal tissues of gnotobiotic pigs in relation to A/H histo-blood group antigen expression. J Virol 81: 3535-3544. Dolin R, Blacklow NR, DuPont H, Buscho RF, Wyatt RG, Kasel JA, Hornick R, Chanock RM. 1972. Biological properties of Norwalk agent of acute infectious nonbacterial gastroenteritis (36508). Proc Soc Exp Biol Med 140: 578-583. Goodgame R. 2007. Norovirus gastroenteritis. Curr Infect Dis Rep 9: 102-109. Lindesmith L, Moe C, Marionneau S, Ruvoen N, Jiang X, Lindbland L, Stewart P, le Pendu J, Baric R. 2003. Human susceptibility and resistance to Norwalk virus infection. Nat Med 9: 548-553. Hutson AM, Atmar RL, Graham DY, Estes MK. 2002. Norwalk virus infection and disease is associated with ABO histo-blood group type. J Infect Dis 185: 1335-1337. Okhuysen PC, Jiang X, Ye L, Johnson PC, Estes MK. 1995. Viral shedding and fecal IgA response after Norwalk virus infection. J Infect Dis 171: 566-569. Tillett HE, Lightfoot NF. 1995. Quality control in environmental microbiology compared with chemistry: What is homogeneous and what is random? Water Sci Technol 31: 471-477. Furumoto WA, Mickey R. 1967. A mathematical model for the infectivity-dilution curve of tobacco mosaic virus: Theoretical considerations. Virology 32: 216-223. Lindesmith L, Moe C, Le Pendu J, Frelinger JA, Treanor J, Baric RS. 2005. Cellular and humoral immunity following Snow Mountain virus challenge. J Virol 79: 2900-2909. Rohayem J, Munch J, Rethwilm A. 2005. Evidence of recombination in the norovirus capsid gene. J Virol 79: 4977-4990. Ward RL, Bernstein DI, Young EC, Sherwood JR, Knowlton DR, Schiff GM. 1986. Human Rotavirus studies in volunteers: Determination of infectious dose and serological response to infection. J Infect Dis 154: 871-880. Graham DY, Jiang X, Tanaka T, Opekun AR, Madore HP, Estes MK. 1994. Norwalk virus infection of volunteers: New insights based on improved assays. J Infect Dis 170: 34-43. Kroneman A, Vennema H, Harris J, Reuter G, von Bonsdorff C, Hedlund K, Vainio K, Jackson V, Pothier P, Koch J, Schreier E, Böttiger B, Koopmans M. 2006. Increase in norovirus activity reported in Europe. Euro Surveill 11: E061214.1. Ciarlet M, Estes MK. 2001. Rotavirus and calicivirus infections of the gastrointestinal tract. Curr Opin Gastroenterol 17: 10-16. Teunis PFM, Nagelkerke NJD, Haas CN. 1999. Dose response models for infectious gastroenteritis. Risk Anal 19: 1251-1260. Smith DR, Aguilar PV, Coffey LL, Gromowski GD, Wang E, Weaver SC. 2006. Venezuelan equine encephalitis virus transmission and effect on pathogenesis. Emerg Infect Dis 12: 1190-1196. Yang S, Benson SK, Du C, Healey MC. 2000. Infection of immunosuppressed C57BL/6N adult mice with a single oocyst of Cryptosporidium parvum. J Parasitol 86: 884-887. Johnson PC, Mathewson JJ, DuPont HL, Greenberg HB. 1990. Multiple challenge study of host susceptibility to Norwalk gastroenteritis in US adults. J Infect Dis 161: 18-21. Adler JL, Zickl R. 1969. Winter vomiting disease. J Infect Dis 119: 668-673. Haas CN. 1983. Estimation of risk due to low doses of microorganisms: A comparison of alternative methodologies. Am J Epidemiol 118: 573-582. Marionneau S, Airaud F, Bovin NV, Le Pendu J, Ruvoen-Clouet N. 2005. Influence of the combined ABO, FUT2, and FUT3 polymorphism on susceptibility to Norwalk virus attachment. J Infect Dis 192: 1071-1077. Bull RA, Hansman GS, Clancy LE, Tanaka MM, Rawlinson WD, White PA. 2005. Norovirus recombination in ORF1/ORF2 overlap. Emerg Infect Dis 11: 1079-1085. Gilks WR, Richardson S, Spiegelhalter DJ, editors. 1996. Markov Chain Monte Carlo in practice. London: Chapman and Hall. Mead PS, Slutsker L, Dietz V, McCaig LF, Bresee JS, Shapiro C, Griffin PM, Tauxe RV. 1999. Food-related illness and death in the United States. Emerg Infect Dis 5: 607-625. Straub TM, Höner zu Bentrup K, Orosz-Coghlan P, Dohnalkova A, Mayer BK, Bartholomew RA, Valdez CO, Bruckner-Lea CJ, Gerba CP, Abbaszadegan M, Nickerson CA. 2007. In vitro cell culture infectivity assay for human noroviruses. Emerg Infect Dis 13: 396-403. Estes MK, Prasad BV, Atmar RL. 2006. Noroviruses everywhere: Has something changed? Curr Opin Infect Dis 19: 467-474. Hutson AM, Airaud F, LePendu J, Estes MK, Atmar RL. 2005. Norwalk virus infection associates with secretor status genotyped from sera. J Med Virol 77: 116-120. Teunis PFM, Havelaar AH. 2000. The Beta Poisson model is not a single hit model. Risk Anal 20: 511-518. Teunis PFM, Chappell CL, Okhuysen PC. 2002. Cryptosporidium dose response studies: Variation between isolates Risk Analysis 22: 175-183. Glass RI, Noel J, Ando T, Fankhauser R, Belliot G, Mounts A, Parashar UD, Bresee JS, Monroe SS. 2000. The epidemiology of enteric caliciviruses from humans: A reassessment using new diagnostics. J Infect Dis 18: S254-S261. 1995; 31 2005; 192 1994; 170 2006; 12 1986; 154 2006; 11 2000; 20 2000; 86 1996 2006; 19 1971; 123 1999; 5 1995; 171 2007; 13 1990; 161 1983; 118 1993; 13 2000; 18 1967; 32 1999; 19 2002; 185 2003; 9 2002; 22 2007; 9 2007; 81 1969; 119 2001; 17 1972; 140 2005; 11 2005; 77 2005; 79 e_1_2_1_20_1 e_1_2_1_23_1 e_1_2_1_24_1 e_1_2_1_21_1 e_1_2_1_22_1 e_1_2_1_27_1 e_1_2_1_28_1 e_1_2_1_25_1 e_1_2_1_26_1 Teunis PFM (e_1_2_1_31_1) 2002; 22 e_1_2_1_29_1 Kroneman A (e_1_2_1_19_1) 2006; 11 e_1_2_1_7_1 e_1_2_1_8_1 e_1_2_1_30_1 e_1_2_1_5_1 e_1_2_1_6_1 e_1_2_1_3_1 e_1_2_1_12_1 e_1_2_1_35_1 e_1_2_1_4_1 e_1_2_1_13_1 e_1_2_1_34_1 e_1_2_1_10_1 e_1_2_1_33_1 e_1_2_1_2_1 e_1_2_1_11_1 e_1_2_1_32_1 e_1_2_1_16_1 e_1_2_1_17_1 e_1_2_1_14_1 e_1_2_1_15_1 e_1_2_1_9_1 e_1_2_1_18_1 |
| References_xml | – reference: Cheetham S, Souza M, McGregor R, Meulia T, Wang Q, Saif LJ. 2007. Binding patterns of human norovirus-like particles to buccal and intestinal tissues of gnotobiotic pigs in relation to A/H histo-blood group antigen expression. J Virol 81: 3535-3544. – reference: Rohayem J, Munch J, Rethwilm A. 2005. Evidence of recombination in the norovirus capsid gene. J Virol 79: 4977-4990. – reference: Teunis PFM, Havelaar AH. 2000. The Beta Poisson model is not a single hit model. Risk Anal 20: 511-518. – reference: Kroneman A, Vennema H, Harris J, Reuter G, von Bonsdorff C, Hedlund K, Vainio K, Jackson V, Pothier P, Koch J, Schreier E, Böttiger B, Koopmans M. 2006. Increase in norovirus activity reported in Europe. Euro Surveill 11: E061214.1. – reference: Goodgame R. 2007. Norovirus gastroenteritis. Curr Infect Dis Rep 9: 102-109. – reference: Okhuysen PC, Jiang X, Ye L, Johnson PC, Estes MK. 1995. Viral shedding and fecal IgA response after Norwalk virus infection. J Infect Dis 171: 566-569. – reference: Ciarlet M, Estes MK. 2001. Rotavirus and calicivirus infections of the gastrointestinal tract. Curr Opin Gastroenterol 17: 10-16. – reference: Haas CN, Rose JB, Gerba C, Regli S. 1993. Risk assessment of virus in drinking water. Risk Analysis 13: 545-552. – reference: Ward RL, Bernstein DI, Young EC, Sherwood JR, Knowlton DR, Schiff GM. 1986. Human Rotavirus studies in volunteers: Determination of infectious dose and serological response to infection. J Infect Dis 154: 871-880. – reference: Hutson AM, Airaud F, LePendu J, Estes MK, Atmar RL. 2005. Norwalk virus infection associates with secretor status genotyped from sera. J Med Virol 77: 116-120. – reference: Adler JL, Zickl R. 1969. Winter vomiting disease. J Infect Dis 119: 668-673. – reference: Marionneau S, Airaud F, Bovin NV, Le Pendu J, Ruvoen-Clouet N. 2005. Influence of the combined ABO, FUT2, and FUT3 polymorphism on susceptibility to Norwalk virus attachment. J Infect Dis 192: 1071-1077. – reference: Yang S, Benson SK, Du C, Healey MC. 2000. Infection of immunosuppressed C57BL/6N adult mice with a single oocyst of Cryptosporidium parvum. J Parasitol 86: 884-887. – reference: Hutson AM, Atmar RL, Graham DY, Estes MK. 2002. Norwalk virus infection and disease is associated with ABO histo-blood group type. J Infect Dis 185: 1335-1337. – reference: Gilks WR, Richardson S, Spiegelhalter DJ, editors. 1996. Markov Chain Monte Carlo in practice. London: Chapman and Hall. – reference: Glass RI, Noel J, Ando T, Fankhauser R, Belliot G, Mounts A, Parashar UD, Bresee JS, Monroe SS. 2000. The epidemiology of enteric caliciviruses from humans: A reassessment using new diagnostics. J Infect Dis 18: S254-S261. – reference: Tillett HE, Lightfoot NF. 1995. Quality control in environmental microbiology compared with chemistry: What is homogeneous and what is random? Water Sci Technol 31: 471-477. – reference: Lindesmith L, Moe C, Marionneau S, Ruvoen N, Jiang X, Lindbland L, Stewart P, le Pendu J, Baric R. 2003. Human susceptibility and resistance to Norwalk virus infection. Nat Med 9: 548-553. – reference: Teunis PFM, Chappell CL, Okhuysen PC. 2002. Cryptosporidium dose response studies: Variation between isolates Risk Analysis 22: 175-183. – reference: Haas CN. 1983. Estimation of risk due to low doses of microorganisms: A comparison of alternative methodologies. Am J Epidemiol 118: 573-582. – reference: Johnson PC, Mathewson JJ, DuPont HL, Greenberg HB. 1990. Multiple challenge study of host susceptibility to Norwalk gastroenteritis in US adults. J Infect Dis 161: 18-21. – reference: Smith DR, Aguilar PV, Coffey LL, Gromowski GD, Wang E, Weaver SC. 2006. Venezuelan equine encephalitis virus transmission and effect on pathogenesis. Emerg Infect Dis 12: 1190-1196. – reference: Estes MK, Prasad BV, Atmar RL. 2006. Noroviruses everywhere: Has something changed? Curr Opin Infect Dis 19: 467-474. – reference: Bull RA, Hansman GS, Clancy LE, Tanaka MM, Rawlinson WD, White PA. 2005. Norovirus recombination in ORF1/ORF2 overlap. Emerg Infect Dis 11: 1079-1085. – reference: Mead PS, Slutsker L, Dietz V, McCaig LF, Bresee JS, Shapiro C, Griffin PM, Tauxe RV. 1999. Food-related illness and death in the United States. Emerg Infect Dis 5: 607-625. – reference: Lindesmith L, Moe C, Le Pendu J, Frelinger JA, Treanor J, Baric RS. 2005. Cellular and humoral immunity following Snow Mountain virus challenge. J Virol 79: 2900-2909. – reference: Dolin R, Blacklow NR, DuPont HL, Formal S, Buscho RF, Kasel JA, Chames RP, Hornick R, Chanock RM. 1971. Transmission of acute infectious nonbacterial gastroenteritis to volunteers by oral administration of stool filtrates. J Infect Dis 123: 307-312. – reference: Teunis PFM, Nagelkerke NJD, Haas CN. 1999. Dose response models for infectious gastroenteritis. Risk Anal 19: 1251-1260. – reference: Straub TM, Höner zu Bentrup K, Orosz-Coghlan P, Dohnalkova A, Mayer BK, Bartholomew RA, Valdez CO, Bruckner-Lea CJ, Gerba CP, Abbaszadegan M, Nickerson CA. 2007. In vitro cell culture infectivity assay for human noroviruses. Emerg Infect Dis 13: 396-403. – reference: Graham DY, Jiang X, Tanaka T, Opekun AR, Madore HP, Estes MK. 1994. Norwalk virus infection of volunteers: New insights based on improved assays. J Infect Dis 170: 34-43. – reference: Furumoto WA, Mickey R. 1967. A mathematical model for the infectivity-dilution curve of tobacco mosaic virus: Theoretical considerations. Virology 32: 216-223. – reference: Dolin R, Blacklow NR, DuPont H, Buscho RF, Wyatt RG, Kasel JA, Hornick R, Chanock RM. 1972. Biological properties of Norwalk agent of acute infectious nonbacterial gastroenteritis (36508). Proc Soc Exp Biol Med 140: 578-583. – volume: 79 start-page: 4977 year: 2005 end-page: 4990 article-title: Evidence of recombination in the norovirus capsid gene publication-title: J Virol – volume: 185 start-page: 1335 year: 2002 end-page: 1337 article-title: Norwalk virus infection and disease is associated with ABO histo‐blood group type publication-title: J Infect Dis – volume: 81 start-page: 3535 year: 2007 end-page: 3544 article-title: Binding patterns of human norovirus‐like particles to buccal and intestinal tissues of gnotobiotic pigs in relation to A/H histo‐blood group antigen expression publication-title: J Virol – year: 1996 – volume: 13 start-page: 545 year: 1993 end-page: 552 article-title: Risk assessment of virus in drinking water publication-title: Risk Analysis – volume: 119 start-page: 668 year: 1969 end-page: 673 article-title: Winter vomiting disease publication-title: J Infect Dis – volume: 170 start-page: 34 year: 1994 end-page: 43 article-title: Norwalk virus infection of volunteers: New insights based on improved assays publication-title: J Infect Dis – volume: 19 start-page: 467 year: 2006 end-page: 474 article-title: Noroviruses everywhere: Has something changed? publication-title: Curr Opin Infect Dis – volume: 140 start-page: 578 year: 1972 end-page: 583 article-title: Biological properties of Norwalk agent of acute infectious nonbacterial gastroenteritis (36508) publication-title: Proc Soc Exp Biol Med – volume: 22 start-page: 175 year: 2002 end-page: 183 publication-title: Cryptosporidium dose response studies: Variation between isolates Risk Analysis – volume: 5 start-page: 607 year: 1999 end-page: 625 article-title: Food‐related illness and death in the United States publication-title: Emerg Infect Dis – volume: 11 start-page: 1079 year: 2005 end-page: 1085 article-title: Norovirus recombination in ORF1/ORF2 overlap publication-title: Emerg Infect Dis – volume: 18 start-page: S254 year: 2000 end-page: S261 article-title: The epidemiology of enteric caliciviruses from humans: A reassessment using new diagnostics publication-title: J Infect Dis – volume: 123 start-page: 307 year: 1971 end-page: 312 article-title: Transmission of acute infectious nonbacterial gastroenteritis to volunteers by oral administration of stool filtrates publication-title: J Infect Dis – volume: 12 start-page: 1190 year: 2006 end-page: 1196 article-title: Venezuelan equine encephalitis virus transmission and effect on pathogenesis publication-title: Emerg Infect Dis – volume: 17 start-page: 10 year: 2001 end-page: 16 article-title: Rotavirus and calicivirus infections of the gastrointestinal tract publication-title: Curr Opin Gastroenterol – volume: 9 start-page: 102 year: 2007 end-page: 109 article-title: Norovirus gastroenteritis publication-title: Curr Infect Dis Rep – volume: 118 start-page: 573 year: 1983 end-page: 582 article-title: Estimation of risk due to low doses of microorganisms: A comparison of alternative methodologies publication-title: Am J Epidemiol – volume: 20 start-page: 511 year: 2000 end-page: 518 article-title: The Beta Poisson model is not a single hit model publication-title: Risk Anal – volume: 19 start-page: 1251 year: 1999 end-page: 1260 article-title: Dose response models for infectious gastroenteritis publication-title: Risk Anal – volume: 86 start-page: 884 year: 2000 end-page: 887 article-title: Infection of immunosuppressed C57BL/6N adult mice with a single oocyst of publication-title: J Parasitol – volume: 77 start-page: 116 year: 2005 end-page: 120 article-title: Norwalk virus infection associates with secretor status genotyped from sera publication-title: J Med Virol – volume: 79 start-page: 2900 year: 2005 end-page: 2909 article-title: Cellular and humoral immunity following Snow Mountain virus challenge publication-title: J Virol – volume: 161 start-page: 18 year: 1990 end-page: 21 article-title: Multiple challenge study of host susceptibility to Norwalk gastroenteritis in US adults publication-title: J Infect Dis – volume: 171 start-page: 566 year: 1995 end-page: 569 article-title: Viral shedding and fecal IgA response after Norwalk virus infection publication-title: J Infect Dis – volume: 31 start-page: 471 year: 1995 end-page: 477 article-title: Quality control in environmental microbiology compared with chemistry: What is homogeneous and what is random? publication-title: Water Sci Technol – volume: 11 start-page: E061214.1 year: 2006 article-title: Increase in norovirus activity reported in Europe publication-title: Euro Surveill – volume: 32 start-page: 216 year: 1967 end-page: 223 article-title: A mathematical model for the infectivity‐dilution curve of tobacco mosaic virus: Theoretical considerations publication-title: Virology – volume: 9 start-page: 548 year: 2003 end-page: 553 article-title: Human susceptibility and resistance to Norwalk virus infection publication-title: Nat Med – volume: 192 start-page: 1071 year: 2005 end-page: 1077 article-title: Influence of the combined ABO, FUT2, and FUT3 polymorphism on susceptibility to Norwalk virus attachment publication-title: J Infect Dis – volume: 13 start-page: 396 year: 2007 end-page: 403 article-title: In vitro cell culture infectivity assay for human noroviruses publication-title: Emerg Infect Dis – volume: 154 start-page: 871 year: 1986 end-page: 880 article-title: Human Rotavirus studies in volunteers: Determination of infectious dose and serological response to infection publication-title: J Infect Dis – volume: 11 start-page: E061214.1 year: 2006 ident: e_1_2_1_19_1 article-title: Increase in norovirus activity reported in Europe publication-title: Euro Surveill – ident: e_1_2_1_5_1 doi: 10.1097/00001574-200101000-00003 – ident: e_1_2_1_33_1 doi: 10.1093/infdis/154.5.871 – ident: e_1_2_1_10_1 doi: 10.1007/978-1-4899-4485-6 – ident: e_1_2_1_30_1 doi: 10.1111/j.1539-6924.1999.tb01143.x – ident: e_1_2_1_2_1 doi: 10.1093/infdis/119.6.668 – ident: e_1_2_1_6_1 doi: 10.1093/infdis/123.3.307 – ident: e_1_2_1_22_1 doi: 10.1086/432546 – ident: e_1_2_1_11_1 doi: 10.1086/315588 – ident: e_1_2_1_18_1 doi: 10.1093/infdis/161.1.18 – ident: e_1_2_1_27_1 doi: 10.3201/eid1303.060549 – ident: e_1_2_1_29_1 – ident: e_1_2_1_34_1 – ident: e_1_2_1_4_1 doi: 10.1128/JVI.01306-06 – ident: e_1_2_1_23_1 doi: 10.3201/eid0505.990502 – ident: e_1_2_1_15_1 doi: 10.1111/j.1539-6924.1993.tb00013.x – ident: e_1_2_1_24_1 doi: 10.1093/infdis/171.3.566 – volume: 22 start-page: 175 year: 2002 ident: e_1_2_1_31_1 publication-title: Cryptosporidium dose response studies: Variation between isolates Risk Analysis – ident: e_1_2_1_17_1 doi: 10.1002/jmv.20423 – ident: e_1_2_1_14_1 doi: 10.1093/oxfordjournals.aje.a113662 – ident: e_1_2_1_20_1 doi: 10.1038/nm860 – ident: e_1_2_1_35_1 doi: 10.1645/0022-3395(2000)086[0884:IOICAM]2.0.CO;2 – ident: e_1_2_1_28_1 doi: 10.1111/0272-4332.204048 – ident: e_1_2_1_3_1 doi: 10.3201/eid1107.041273 – ident: e_1_2_1_16_1 doi: 10.1086/339883 – ident: e_1_2_1_25_1 doi: 10.1128/JVI.79.8.4977-4990.2005 – ident: e_1_2_1_7_1 doi: 10.3181/00379727-140-36508 – ident: e_1_2_1_9_1 doi: 10.1016/0042-6822(67)90271-1 – ident: e_1_2_1_8_1 doi: 10.1097/01.qco.0000244053.69253.3d – ident: e_1_2_1_26_1 doi: 10.3201/eid1708.050841 – ident: e_1_2_1_12_1 doi: 10.1007/s11908-007-0004-5 – ident: e_1_2_1_13_1 doi: 10.1093/infdis/170.1.34 – ident: e_1_2_1_32_1 doi: 10.1016/0273-1223(95)00314-D – ident: e_1_2_1_21_1 doi: 10.1128/JVI.79.5.2900-2909.2005 |
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| SubjectTerms | Biological and medical sciences Caliciviridae Infections - genetics Caliciviridae Infections - physiopathology Caliciviridae Infections - transmission Caliciviridae Infections - virology dose response Fundamental and applied biological sciences. Psychology Gastroenteritis - genetics Gastroenteritis - physiopathology Gastroenteritis - virology Human viral diseases Humans Infectious diseases Medical sciences Microbiology Microscopy, Electron Miscellaneous Models, Biological Monte Carlo Method Norovirus Norwalk virus Norwalk virus - genetics Norwalk virus - isolation & purification Norwalk virus - pathogenicity Norwalk virus - ultrastructure primary inoculum Reverse Transcriptase Polymerase Chain Reaction Risk Assessment RNA, Viral - analysis secondary inoculum Viral diseases viral gastroenteritis Virology virus aggregation |
| Title | Norwalk virus: How infectious is it |
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