Viral infections of the gastrointestinal tract

Current Opinion in Gastroenterology

Volumn 16, Issue 1, 2000, Pages 12-17

  Shaw, Robert D ^a,b  

^a VETERANS AFFAIRS MEDICAL CENTER   (United States)

^b STONY BROOK UNIVERSITY   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

ROTAVIRUS VACCINE;

ARTICLE; DRUG APPROVAL; DRUG WITHDRAWAL; GASTROENTERITIS; GASTROINTESTINAL INFECTION; HUMAN; IMMUNE RESPONSE; IMMUNITY; INTUSSUSCEPTION; ROTAVIRUS; VIROLOGY; VIRUS INFECTION; VIRUS PATHOGENESIS;

EID: 0034095646     PISSN: 02671379     EISSN: None     Source Type: Journal    
DOI: 10.1097/00001574-200001000-00003     Document Type: Article

References (44)

1. 1 Fankhauser RL, Noel JS, Monroe SS, Ando T, Glass RI: Molecular epidemiology of "Norwalk-like viruses" in outbreaks of gastroenteritis in the United States. J Infect Dis 1998, 178:1571-1578. Outbreaks of nonbacterial gastroenteritis reported to 33 state health departments were examined to determine the importance of Norwalk-like viruses in these outbreaks. Nursing homes and hospitals were the most common sites of outbreaks (43%), followed by restaurants and events with catered meals (26%). Consumption of contaminated food was the most common mode of transmission (37%). The use of improved molecular techniques to detect Norwalk-like viruses shows that most nonbacterial gastroenteritis outbreaks in the United States seem to be associated with these viruses.
2. 2 Dedman D, Laurichesse H, Caul EO, Wall PG: Surveillance of small round structured virus (SRSV) infection in England and Wales, 1990-1995. Epidemiol Infect 1998, 121:139-149. Small round-structured virus infections in England and Wales were noted in 7492 laboratory reports between 1990 and 1995. Rates of reported illness were highest in young children and the elderly. Outbreaks in hospital wards and residential facilities for the elderly accounted for 76% of the total number of cases.
3. 3 Norwalk-like viral gastroenteritis in U.S. Army trainees-Texas, 1998. MMWR Morb Mortal Wkly Rep 1999, 48:225-227.
4. 4 Brugha R, Vipond IB, Evans MR, Sandifer QD, Roberts RJ, Salmon RL, et al.: A community outbreak of food-borne small round-structured virus gastroenteritis caused by a contaminated water supply. Epidemiol Infect 1999, 122(1):145-154. An outbreak of gastroenteritis affected 30 of 135 employees of a bakery plant (23%) and more than 100 people from South Wales and Bristol in the United Kingdom. Studies of employees and community clusters found illness to be associated with drinking cold water at the bakery and eating custard slices produced at the bakery. Small round-structured viruses were identified in stool specimens from four employees and seven community cases. Analysis of the polymerase and capsid regions of the small round-structured virus genome by reverse transcriptase polymerase chain reaction showed heterogeneous viruses, indicating that the custard mix may have been reconstituted with contaminated water. The usefulness of molecular techniques in supporting classic epidemiclogic methods in outbreak investigations is shown.
5. 5 Pang XL, Joensuu J, Vesikari T: Human calicivirus-associated sporadic gastroenteritis in Finnish children less than two years of age followed prospectively during a rotavirus vaccine trial. Pediatr Infect Dis J 1999, 18:420-426. Human caliciviruses cause gastroenteritis outbreaks, but their role in sporadic diarrhea in young children is not well established. This study evaluated 2398 children 2 months to 2 years of age who were participating in a rotavirus vaccine trial. Stool specimens from 1477 episodes of acute gastroenteritis (788 in a placebo group; 689 in a vaccine group) were tested for human calicivirus by reverse transcriptase polymerase chain reaction, and positive results were confirmed by southern hybridization. Human calicivirus was detected in 20% and 22% of gastroenteritis cases in the placebo and vaccine groups, respectively. The peak season of human caliciviral gastroenteritis was from November to February. Of the 148 patients with pure human caliciviral infection in the placebo group, 89% had vomiting, 79% had watery diarrhea, 21% had fever, 28% needed oral rehydration, and 1.4% were hospitalized. The diarrhea in human caliciviral gastroenteritis was much less severe than that in rotaviral gastroenteritis, but vomiting was equally severe in the two conditions. The RRV-TV (tetravalent rhesus rotavirus) vaccine had no effect on the frequency or clinical severity of human caliciviral gastroenteritis. The authors concluded that in Finland, human caliciviruses are second in frequency to rotaviruses as causes of acute gastroenteritis in young children in the community.
6. 6 Levy DA, Bens MS, Craun GF, Calderon RL, Herwaldt BL: Surveillance for waterborne-disease outbreaks-United States, 1995-1996. MMWR CDC Surveill Summ 1998, 47:1-34.
7. 7 Mitchell DK, Matson DO, Jiang X, Berke T, Monroe SS, Carter MJ, et al.: Molecular epidemiology of childhood astrovirus infection in child care centers. J Infect Dis 1999, 180:514-517. The role of human astrovirus in outbreaks and sporadic cases of diarrhea was assessed in children attending day care centers. Eight astrovirus outbreaks occurred in six centers. Of 179 children with diarrhea, 36 (20%) had astrovirus-associated diarrhea. Diarrheal stools obtained during diarrheal outbreaks were more likely to contain astrovirus than were samples not associated with a diarrheal outbreak (40 compared with 14 of 452; P < 0.001). It was concluded that astrovirus was a significant cause of diarrheal outbreaks in this setting.
8. 8 Pang XL, Vesikari T: Human astrovirus-associated gastroenteritis in children under 2 years of age followed prospectively during a rotavirus vaccine trial. Acta Paediatr 1999, 88:532-536.
9. 9 Guerrero ML, Noel JS, Mitchell DK, Calva JJ, Morrow AL, Martinez J, et al.: A prospective study of astrovirus diarrhea of infancy in Mexico City. Pediatr Infect Dis J 1998, 17:723-727. In this study, 214 children were monitored from birth to 18 months of age. Astrovirus was detected in 5% of 510 diarrheal episodes. Astrovirus-associated diarrhea was characterized by a median of four stools (range, two to 10 stools) during the first 24 hours, a median duration of 3 days (range, 1 to 21 days), vomiting (20%), and fever (7%). No dehydration or repeated symptomatic infection was seen. Astrovirus-associated diarrhea was was less severe than diarrhea caused by rotavirus, as is typical in other studies.
10. 10 Maldonado Y, Cantwell M, Old M, Hill D, Sanchez ML, Logan L, et al.: Population-based prevalence of symptomatic and asymptomatic astrovirus infection in rural Mayan infants. J Infect Dis 1998, 178:334-339. Symptomatic and asymptomatic astroviral infection was prospectively studied in a 3-year birth cohort of Mayan infants. Stool samples from 271 infants and 268 older siblings were tested for astrovirus, adenovirus types 40 and 41, rotavirus, salmonella, shigella, and campylobacter. Astrovirus was found in 164 infants (61%) and 20 siblings (7%). Rotavirus (4%) and adenovirus 40 and 41 (13%) were isolated less often. Of all diarrheal episodes reported at a visit, 26% (78 of 305) were associated with astrovirus; 17% (78 of 452) of astroviral infections were associated with diarrhea, and 9% were associated with other symptoms. Of infants with astrovirus, 70% shed at multiple visits over a period of 2 to 17 weeks (median, 5 weeks). Astrovirus was identified throughout the year; its incidence peaked in March and May and decreased in September. In this population, astrovirus was the most common enteric pathogen isolated and often caused relatively mild symptoms in infants.
11. 11 Cubitt WD, Mitchell DK, Carter MJ, Willcocks MM, Holzel H: Application of electronmicroscopy, enzyme immunoassay, and RT-PCR to monitor an outbreak of astrovirus type 1 in a paediatric bone marrow transplant unit. J Med Virol 1999, 57:313-321.
12. 12 Shastri S, Doane AM, Gonzales J, Upadhyayula U, Bass DM: Prevalence of astroviruses in a children's hospital. J Clin Microbiol 1998, 36(9):2571-5274.
13. 13 Caeiro JP, Mathewson JJ, Smith MA, Jiang ZD, Kaplan MA, Dupont HL: Etiology of outpatient pediatric nondysenteric diarrhea: a multicenter study in the United States. Pediatr Infect Dis J 1999, 18:94-97. Acute diarrhea in 147 children 2 and 11 years of age presenting to outpatient clinics in various regions of the United States was evaluated by conventional laboratory methods. A recognized etiologic agent was detected in stools from 60.5% of children, and multiple agents were detected in 10%. Rotavirus was found in 29.3% of the children, with peaks in occurrence in spring and winter. Giardia lamblia was identified in 15% of patients and had a spring peak, and HEp-2 cell-adherent E. coli was found in 10%. Other agents found included enteric adenovirus (4.8%), salmonella (3.4%), enterohemorrhagic E. coli (3.4%), and enteropathogenic or toxigenic E. coli (1.4% each). Single cases of Entamoeba histolytica and Campylobacter jejuni infection were reported.
14. 14 Souza DF, Kisielius JJ, Ueda M, Gabbay YB, Carmona RC, St Timenetsky MdC, et al.: An outbreak of group C rotavirus gastroenteritis among adults living in Valentim Gentil, Sao Paulo State, Brazil. J Diarrhoeal Dis Res 1998, 16:59-65.
15. 15 Santos N, Lima RC, Nozawa CM, Linhares RE, Gouvea V: Detection of porcine rotavirus type G9 and of a mixture of types G1 and G5 associated with wa-like VP4 specificity: evidence for natural human-porcine genetic reassortment. J Clin Microbiol 1999, 37:2734-2736. Rotavirus type G5 is a primarily porcine pathogen that has caused frequent and widespread diarrhea in children in Brazil and in piglets elsewhere. G5 refers to the viral protein vp7. A secondary typing, designated P, is a function of another viral protein, vp4. This paper shows that many of the porcine strains in Brazil have a human P type, P8. This is additional evidence that rotaviruses of human and porcine origins may reassort to produce novel strains.
16. 16 Unicomb LE, Podder G, Gentsch JR, Woods PA, Hasan KZ, Faruque AS, et al.: Evidence of high-frequency genomic reassortment of group A rotavirus strains in Bangladesh: emergence of type G9 in 1995. J Clin Microbiol 1999, 37:1885-1891. This study characterized a large number of rotavirus strains obtained in Bangladesh over several years. The authors report that in addition to the four main human rotavirus serotypes (G1-G4), there was emergence of another type, G9, that in later years made up 16% of isolates. In addition, antigenic changes were also identified among other types. These data are important for vaccine strategies.
17. 17 Giordano MO, Martinez LC, Rinaldi D, Guinard S, Naretto E, Casero R, et al.: Detection of picobirnavirus in HIV-infected patients with diarrhea in Argentina. J Acquir Immune Defic Syndr Hum Retrovirol 1998, 18:380-383.
18. 18 Hale GA, Heslop HE, Krance RA, Brenner MA, Jayawardene D, Srivastava DK, Patrick CC: Adenovirus infection after pediatric bone marrow transplantation. Bone Marrow Transplant 1999, 23:277-282.
19. 19 Jamieson FB, Wang EE, Bain C, Good J, Duckmanton L, Petric M: Human torovirus: a new nosocomial gastrointestinal pathogen. J Infect Dis 1998, 178:1263-1269. Torovirus was identified in 35.0% of 206 patients with gastroenteritis and 14.5% of 206 controls (P < 0.001). Clinical features of toroviral gastroenteritis were compared with those of rotaviral or astroviral gastroenteritis. Persons infected with torovirus were more often immunocompromised (43.0% compared with 15.7%) and nosocomially infected (57.6% compared with 31.3%), experienced less vomiting (46.4% compared with 66.7%), and had more bloody diarrhea (11.2% compared with 1.8%). Thus, torovirus was associated with gastroenteritis in a pediatric population, especially in immunocompromised hospitalized patients.
20. 20 Denisova E, Dowling W, LaMonica R, Shaw R, Scarlata S, Ruggeri F, Mackow ER: Rotavirus capsid protein VP5* permeabilizes membranes. J Virol 1999, 73:3147-1353. The outer capsid proteins of rotavirus interact with the cell membrane to permit infection in a manner not yet understood. These authors report that a fragment of one outer capsid protein (VP5*) caused release of a label from within artificial membrane spheres. This permeability was completely inhibited by neutralizing monoclonal antibodies. Thus, VP5* is a specific membrane-permeabilizing capsid protein that is likely to play a role in the cellular entry of rotaviruses. Definition of the requirements of cell entry and infection may eventually lead to superior treatment of rotaviral diarrhea by preventing or aborting infection.
21. 21 Jourdan N, Brunet JP, Sapin C, Blais A, Cotte-Laffitte J, Forestier F, et al.: Rotavirus infection reduces sucrase-isomaltase expression in human intestinal epithelial cells by perturbing protein targeting and organization of microvillar cytoskeleton. J Virol 1998, 72:7228-7236. It was previously hypothesized that reduced disaccharidase activity during rotaviral infection resulted from the destruction of rotavirus-infected enterocytes at the villus tips. However, this pathophysiologic model cannot explain situations in which low disaccharidase activity is seen and rotavirus-infected intestine shows few, if any, histopathologic changes. RRV-infected Caco-2 cells showed selectively decreased sucrase-isomaltase activity and apical expression without apparent cell destruction. RRV infection induced 1) blockade of sucrase-isomaltase transport to the brush border and 2) important alterations of the cytoskeleton that correlate with decreased sucrase-isomaltase apical surface expression.
22. 22 Dwinell MB, Eckmann L, Leopard JD, Varki NM, Kagnoff MF: Chemokine receptor expression by human intestinal epithelial cells. Gastroenterology 1999, 117:359-367. Although not specifically about intestinal viruses, this paper has important implications for intestinal viral infection. Inflammatory mediators, including the group of small proteins known as chemokines, are elaborated from intestinal epithelial cells during viral infection. Various immune and pathophysiologic functions for these substances have been considered, but realistic appraisal of a potential role for chemokines during intestinal infections has been limited by uncertainties about the range of target cells. This report shows that human intestinal epithelial cell lines have the potential to serve as targets for chemokine signaling, perhaps in an autocrine or paracrine fashion. This suggests that these substances may be important in the earliest phases of the host response to intestinal viruses.
23. 23 Perez JF, Chemello ME, Liprandi F, Ruiz MC, Michelangeli F: Oncosis in MA104 cells is induced by rotavirus infection through an increase in intracellular Ca2+ concentration. Virology 1998, 252:17-27.
24. 24 Perez JF, Ruiz MC, Chemello ME, Michelangeli F: Characterization of a membrane calcium pathway induced by rotavirus infection in cultured cells. J Virol 1999, 73:2481-2490. In these two reports, the authors build on work showing that rotavirus increases cell permeability to sodium, potassium, and calcium during replication in cultured cells. They characterize a divalent cation entry pathway by measuring intracellular calcium in epithelial cells in suspension. Evidence is presented to show specific regulation of this pathway and suggests that rotaviral infection of cultured cells activates a specific cation channel rather than nonspecific permeation through the plasma membrane. The increase in intracellular calcium induced by activation of this channel may be related to the increase in cytoplasmic and endoplasmic reticulum calcium pools required for virus maturation and may contribute eventually to cell death, at least in vitro.
25. 25 Piron M, Vende P, Cohen J, Poncet D: Rotavirus RNA-binding protein NSP3 interacts with elF4GI and evicts the poly(A) binding protein from elF4F. Embo J 1998, 17:5811-5821.
26. 26 Piron M, Delaunay T, Grosclaude J, Poncet D: Identification of the RNA-binding, dimerization, and elF4GI-binding domains of rotavirus nonstructural protein NSP3. J Virol 1999, 73:5411-5421. These two papers reveal interactions between an nonstructural rotaviral protein produced during viral replication (NSP3) and cell regulators of transcription. These findings are important to an understanding of the mechanism of viral replication and, perhaps, the effects of the virus on host cell transcriptional processes during infection.
27. 27 Nabuurs MJ: Weaning piglets as a model for studying pathophysiology of diarrhea. Vet Q 1998, 20(suppl 3):S42-S45. Weaning piglets have diarrhea from changes in the flora, morphology, and function of the intestine. Function of the large intestine also influences the severity of diarrhea in just-weaned piglets. Nutritional and dietary variables are important in maintaining villus height. Weaning-piglet models of diarrhea must be interpreted with caution.
28. 28 Zijlstra RT, McCracken BA, Odle J, Donovan SM, Gelberg HB, Petschow BW, et al.: Malnutrition modifies pig small intestinal inflammatory responses to rotavirus. J Nutr 1999, 129:838-843.
29. 29 Mrukowicz JZ, Thompson J, Reed GW, Tollefson SJ, Kobayashi M, Araki K, Wright PF: Epidemiology of rotavirus in infants and protection against symptomatic illness afforded by primary infection and vaccination. Vaccine 1999, 17:745-753. This study 1) assessed the frequency of symptomatic and asymptomatic primary and secondary rotaviral infections in children younger than 24 months of age and 2) determined protection against symptomatic illness afforded by rhesus and human-rhesus rotavirus reassortant vaccines. It followed 236 children through five winter rotavirus seasons. Almost all children were infected by 2 years of age. The relative risk for rotavirus-associated gastroenteritis was 2.4 (1.1, 5.3) in naive children compared with naturally immune children and 4.1 (1.6, 10.7) in naive children compared with vaccinated children. This protection is similar to that provided by the tetravalent rotavirus vaccine, at least for infection with the G1 serotype.
30. 30 Moulton LH, Staat MA, Santosham M, Ward RL: The protective effectiveness of natural rotavirus infection in an American Indian population. J Infect Dis 1998, 178:1562-1566.
31. 31 Gorrell RJ, Bishop RF: Homotypic and heterotypic serum neutralizing antibody response to rotavirus proteins following natural primary infection and reinfection in children. J Med Virol 1999, 57:204-211. Heterotypic neutralizing antibody produced after primary infection seems to be primarily against VP4. However, on reinfection, VP7 becomes increasingly immunodominant in terms of both cross-reactive neutralizing antibody production and increases in neutralizing antibody titer.
32. 32 Angel J, Franco MA, Greenberg HB, Bass D: Lack of a role for type I and type II interferons in the resolution of rotavirus-induced diarrhea and infection in mice. J Interferon Cytokine Res 1999, 19:655-659. Immunocompetent suckling mice were treated with type I and II murine interferons before and after challenge with virulent murine rotavirus. Treated animals developed diarrhea indistinguishable from that seen in untreated controls. In other experiments, type I interferon receptor -/-suckling mice and interferon-γ -/-suckling mice compared with immunocompetent mice developed diarrhea with similar characteristics and duration and had comparable quantities of viral antigen in their intestines. Furthermore, type I interferon receptor -/-adult mice infected with rotavirus and control mice shed equivalent quantities of viral antigen and had similar kinetics. Thus, interferons do not seem to be major inhibitors of rotaviral diarrhea or replication in mice.
33. 33 Williams MB, Rose JR, Rott LS, Franco MA, Greenberg HB, Butcher EC: The memory B cell subset responsible for the secretory IgA response and protective humoral immunity to rotavirus expresses the intestinal homing receptor, alpha4beta7. J Immunol 1998, 161:4227-4235.
34. 34 Dennehy PH, Hartin M, Nelson SM, Reising SF: Evaluation of the ImmunoCardSTAT! rotavirus assay for detection of group A rotavirus in fecal specimens. J Clin Microbiol 1999, 37:1977-1979. This rapid, office-based, immunogold-based, horizontal-flow membrane technology is marketed by Meridian Diagnostics, Cincinnati, Ohio. The sensitivity, specificity, positive predictive value, and negative predictive value were 94.0%, 100%, 100%, and 93.4%, respectively, for ICS-RV; 95.5%, 100%, 100%, and 95.0%, respectively, for Rotaclone; and 97.0%, 96.5%, 97.0%, and 96.5% for TestPack. The ImmunoCardSTAT! rotavirus assay was sensitive, specific, and relatively simple to perform and interpret.
35. 35 McCaughey C, O'Neill HJ, Wyatt DE, Christie SN, Jackson PT, Coyle PV: Effect of faecal consistency on virological diagnosis. J Infect 1998, 36:145-148. Solid fecal specimens at the end of an episode of diarrhea have a higher diagnostic yield than liquid specimens at the peak of symptoms.
36. 36 Konno T, Suzuki H, KutsuzawaT, Imai A, Katsushima N, Sakamoto M, et al.: Human rotavirus infection in infants and young children with intussusception. J Med Virol 1978, 2:265-269.
37. 37 Nicolas JC, Ingrand D, Fortier B, Bricout F: A one-year virological survey of acute intussusception in childhood. J Med Virol 1982, 9:267-271.
38. 38 Mulcahy DL, Kamath KR, de Silva LM, Hodges S, Carter IW, Cloonan MJ: A two-part study of the aetiological role of rotavirus in intussusception. J Med Virol 1982, 9:51-55.
39. 39 Rennels MB, Parashar UD, Holman RC, Le CT, Chang HG, Glass RI: Lack of an apparent association between intussusception and wild or vaccine rotavirus infection. Pediatr Infect Dis J 1998, 17:924-925.
40. 40 Intussusception among recipients of rotavirus vaccine - United States, 1998-1999. MMWR Morb Mortal Wkly Rep 1999, 48:577-581. Recent data on the rate of intussusception in children vaccinated with the RotaShield vaccine is reviewed. The rationale for halting vaccination pending further data collection is discussed.
41. 41 Herrmann JE, Chen SC, Jones DH, Tinsley-Bown A, Fynan EF, Greenberg HB, Farrar GH: Immune responses and protection obtained by oral immunization with rotavirus VP4 and VP7 DNA vaccines encapsulated in microparticies. Virology 1999, 259:148-153. Protective immune responses in mice were obtained after oral immunization with rotavirus DNA vaccines encapsulated in microparticles. The DNA vaccines used encoded outer capsid proteins VP4 and VP7, proteins that are the basis for rotavirus serotyping and the generation of virus-neutralizing antibodies. Intestinal IgA antibodies were detectable by 6 weeks after immunization. Protective immunity from infection was seen at 12 weeks after immunization, and fecal rotavirus antigen was reduced significantly in immunized mice compared with controls.
42. 42 Choi AH, Basu M, Rae MM, McNeal MM, Ward RL: Particle-bombardment-mediated DNA vaccination with rotavirus VP4 or VP7 induces high levels of serum rotavirus IgG but fails to protect mice against challenge. Virology 1998, 250:230-240.
43. 43 McNeal MM, Rae MN, Conner ME, Ward RL: Stimulation of local immunity and protection in mice by intramuscular immunization with triple-or double-layered rotavirus particles and QS-21. Virology 1998, 243:158-166.
44. 44 Clements-Mann ML, Makhene MK, Mrukowicz J, Wright PF, Hoshino Y, Midthun K, et al.: Safety and immunogenicity of live attenuated human-bovine (UK) reassortant rotavirus vaccines with VP7-specificity for serotypes 1, 2, 3 or 4 in adults, children and infants. Vaccine 1999, 17:2715-2725.