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12 result(s) for "Greening, Gail"
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Recurring Norovirus Transmission on an Airplane
Background. Previously reported outbreaks of norovirus gastroenteritis associated with aircraft have been limited to transmission during a single flight sector. During October 2009, an outbreak of diarrhea and vomiting occurred among different groups of flight attendants who had worked on separate flight sectors on the same airplane. We investigated the cause of the outbreak and whether the illnesses were attributable to work on the airplane. Methods. Information was obtained from flight attendants on demographic characteristics, symptoms, and possible transmission risk factors. Case patients were defined as flight attendants with diarrhea or vomiting <51 hours after the end of their first flight sector on the airplane during 13—18 October 2009. Stool samples were tested for norovirus RNA. Results. A passenger had vomited on the Boeing 777-200 airplane on the 13 October flight sector. Sixty-three (82%) of 77 flight attendants who worked on the airplane during 13—18 October provided information, and 27 (43%) met the case definition. The attack rate among flight attendants decreased significantly over successive flight sectors from 13 October onward (P <.001). Working as a supervisor was independently associated with development of illness (adjusted odds ratio, 5.8; 95% confidence interval, 1.3—25.6). Norovirus genotype GI.6 was detected in stool samples from 2 case patients who worked on different flight sectors. Conclusions. Sustained transmission of norovirus is likely to have occurred because of exposures on this airplane during successive flight sectors. Airlines should make provision for adequate disinfection of airplanes with use of products effective against norovirus and other common infectious agents after vomiting has occurred.
Norovirus Illness Is a Global Problem: Emergence and Spread of Norovirus GII.4 Variants, 2001–2007
BackgroundNoroviruses (NoVs) are the most common cause of viral gastroenteritis. Their high incidence and importance in health care facilities result in a great impact on public health. Studies from around the world describing increasing prevalence have been difficult to compare because of differing nomenclatures for variants of the dominant genotype, GII.4. We studied the global patterns of GII.4 epidemiology in relation to its genetic diversity MethodsData from NoV outbreaks with dates of onset from January 2001 through March 2007 were collected from 15 institutions on 5 continents. Partial genome sequences (n=775) were collected, allowing phylogenetic comparison of data from different countries ResultsThe 15 institutions reported 3098 GII.4 outbreaks, 62% of all reported NoV outbreaks. Eight GII.4 variants were identified. Four had a global distribution—the 1996, 2002, 2004, and 2006b variants. The 2003Asia and 2006a variants caused epidemics, but they were geographically limited. Finally, the 2001Japan and 2001Henry variants were found across the world but at low frequencies ConclusionsNoV epidemics resulted from the global spread of GII.4 strains that evolved under the influence of population immunity. Lineages show notable (and currently unexplained) differences in geographic prevalence. Establishing a global NoV network by which data on strains with the potential to cause pandemics can be rapidly exchanged may lead to improved prevention and intervention strategies
Epidemics of Gastroenteritis during 2006 Were Associated with the Spread of Norovirus GII.4 Variants 2006a and 2006b
Background.Acute gastroenteritis is commonly associated with norovirus genogroup II (GII) infection. Norovirus GII has 17 classified genotypes (GII.1–GII.17), but only 1 norovirus genotype (GII.4) is associated with global epidemics of gastroenteritis. In 2006, an increase in global norovirus activity was observed. Methods.During the period from December 2005 through August 2006, a total of 231 fecal samples were obtained from patients with acute gastroenteritis from Australia and New Zealand. Norovirus RNA was amplified and sequenced to determine norovirus genotype and relatedness to known epidemic norovirus GII.4 variants. Results.Two GII.4 variants, designated 2006a and 2006b, were identified in 61.8% and 11.3%, respectively, of the 186 cases investigated. Norovirus 2006a and 2006b have also been implicated as the predominant causes of norovirus-associated gastroenteritis across Europe in 2006. Conclusions.The global increase in norovirus-associated gastroenteritis in 2006 was linked to the emergence of 2 novel GII.4 variants, 2006a and 2006b.
Challenges of Culturing Human Norovirus in Three-Dimensional Organoid Intestinal Cell Culture Models
Human noroviruses are the most common cause of acute gastroenteritis worldwide. Recently, cell culture systems have been described using either human embryonic intestinal epithelial cells (Int-407) or human epithelial colorectal adenocarcinoma cells (Caco-2) growing on collagen-I porous micro carrier beads in a rotating bioreactor under conditions of physiological fluid shear. Here, we describe the efforts from two independent laboratories to implement this three dimensional (3D) cell culture system for the replication of norovirus. Int-407 and Caco-2 were grown in a rotating bioreactor for up to 28 days. Prior to infection, cells were screened for the presence of microvilli by electron microscopy and stained for junction proteins (zonula occludens-1, claudin-1, and β-catenin). Differentiated 3D cells were transferred to 24-well plates and infected with bacteria-free filtrates of various norovirus genotypes (GI.1, GI.3, GI.8, GII.2, GII.4, GII.7, and GII.8). At 12 h, 24 h, and 48 h post inoculation, viral RNA from both cells and supernatants were collected and analyzed for norovirus RNA by real-time reverse transcription PCR. Despite observations of high expression of junction proteins and microvilli development in stained thin sections, our data suggest no significant increase in viral titer based on norovirus RNA copy number during the first 48 h after inoculation for the different samples and virus culture conditions tested. Our combined efforts demonstrate that 3D cell culture models using Int-407 or Caco-2 cells do not support norovirus replication and highlight the complexity and difficulty of developing a reproducible in vitro cell culture system for human norovirus.
Foodborne viruses: a focus on challenges associated with detection methods
Human enteric viruses are now recognised as one of the commonest causes of foodborne disease with norovirus and hepatitis A virus (HAV) the main viruses implicated in foodborne outbreaks. Norovirus is the main cause of acute nonbacterial gastroenteritis worldwide. Foods at risk of virus contamination are bivalve shellfish, fresh produce, manually prepared ready to eat (RTE) foods and bakery products. Analysis of foods for virus presence is challenging for many reasons. Complex food matrices present processing problems for efficient recovery and detection of viruses, current molecular methods do not allow for determination of virus infectivity and low virus copy number in foods means that exquisitely sensitive methods and multiple controls are required for virus detection. There are still no international standard methods for viral analysis of foods. However significant progress towards a standard method for detection of norovirus and HAV in foodstuffs has been made by a European Committee for Standardisation (CEN) technical working group. This method is due for publication in 2013 as a two-part joint ISO/CEN Technical Specification. In later years it will be replaced by a fully validated standard.
A New Zealand outbreak of norovirus gastroenteritis linked to the consumption of imported raw Korean oysters
Reports on the investigation of an outbreak of gastroenteritis that occurred following an international rugby test at Eden Park (Auckland, New Zealand) on 17 June 2006. Source: National Library of New Zealand Te Puna Matauranga o Aotearoa, licensed by the Department of Internal Affairs for re-use under the Creative Commons Attribution 3.0 New Zealand Licence.
Persistence of oral polio vaccine virus after its removal from the immunisation schedule in New Zealand
On Feb 1, 2002, inactivated poliomyelitis vaccines replaced live-attenuated oral poliovirus vaccine (OPV) in New Zealand's immunisation schedule, allowing systematic monitoring of OPV virus circulation. Findings of paediatric-inpatient surveillance indicate that 7% of children excreted polioviruses before this switch, but none did so 1 month afterwards. Acute flaccid paralysis surveillance detected no poliovirus during and after the switch, whereas enterovirus surveillance detected poliovirus only once during the switch. Environmental surveillance identified polioviruses in sewage samples until May, 2002, after which they were detected infrequently. Intratypic differentiation and sequencing showed that all polioviruses were Sabin-like. Multiple surveillance methods hence showed that OPV strains did not persist for extended periods after a vaccine switch in a developed country with a temperate climate. Sequence homology with Sabin vaccine parent strains indicated that polioviruses detected more than 4 months after the switch were of recent origin, consistent with importation from OPV-using countries.
Challenges of Culturing Human Norovirus in Three-Dimensional Organoid Intestinal Cell Culture Models. e63485
Human noroviruses are the most common cause of acute gastroenteritis worldwide. Recently, cell culture systems have been described using either human embryonic intestinal epithelial cells (Int-407) or human epithelial colorectal adenocarcinoma cells (Caco-2) growing on collagen-I porous micro carrier beads in a rotating bioreactor under conditions of physiological fluid shear. Here, we describe the efforts from two independent laboratories to implement this three dimensional (3D) cell culture system for the replication of norovirus. Int-407 and Caco-2 were grown in a rotating bioreactor for up to 28 days. Prior to infection, cells were screened for the presence of microvilli by electron microscopy and stained for junction proteins (zonula occludens-1, claudin-1, and beta -catenin). Differentiated 3D cells were transferred to 24-well plates and infected with bacteria-free filtrates of various norovirus genotypes (GI.1, GI.3, GI.8, GII.2, GII.4, GII.7, and GII.8). At 12 h, 24 h, and 48 h post inoculation, viral RNA from both cells and supernatants were collected and analyzed for norovirus RNA by real-time reverse transcription PCR. Despite observations of high expression of junction proteins and microvilli development in stained thin sections, our data suggest no significant increase in viral titer based on norovirus RNA copy number during the first 48 h after inoculation for the different samples and virus culture conditions tested. Our combined efforts demonstrate that 3D cell culture models using Int-407 or Caco-2 cells do not support norovirus replication and highlight the complexity and difficulty of developing a reproducible in vitro cell culture system for human norovirus.
Epidemics of Gastroenteritis during 2006 Were Associated with the Spread of Norovirus GII. 4 Variants 2006a and 2006b
Background. Acute gastroenteritis is commonly associated with norovirus genogroup II (Gil) infection. Norovirus Gil has 17 classified genotypes (GII.l-GII. 17), but only 1 norovirus genotype (GII. 4) is associated with global epidemics of gastroenteritis. In 2006, an increase in global norovirus activity was observed. Methods. During the period from December 2005 through August 2006, a total of 231 fecal samples were obtained from patients with acute gastroenteritis from Australia and New Zealand. Norovirus RNA was amplified and sequenced to determine norovirus genotype and relatedness to known epidemic norovirus GII. 4 variants. Results. Two GII. 4 variants, designated 2006a and 2006b, were identified in 61.8% and 11.3%, respectively, of the 186 cases investigated. Norovirus 2006a and 2006b have also been implicated as the predominant causes of norovirus-associated gastroenteritis across Europe in 2006. Conclusions. The global increase in norovirus-associated gastroenteritis in 2006 was linked to the emergence of 2 novel GII. 4 variants, 2006a and 2006b.