The Experts below are selected from a list of 300 Experts worldwide ranked by ideXlab platform
Gagandeep Kang - One of the best experts on this subject based on the ideXlab platform.
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Rotavirus Infection
Nature Reviews Disease Primers, 2017Co-Authors: Sue E. Crawford, H B Greenberg, Marie Hagbom, Lennart Svensson, Sasirekha Ramani, Jacqueline E. Tate, Umesh D. Parashar, Manuel A. Franco, Miguel O'ryan, Gagandeep KangAbstract:Rotavirus Infections are a leading cause of severe, dehydrating gastroenteritis in children 200,000 deaths annually, mostly in low-income countries. Rotavirus primarily infects enterocytes and induces diarrhoea through the destruction of absorptive enterocytes (leading to malabsorption), intestinal secretion stimulated by Rotavirus non-structural protein 4 and activation of the enteric nervous system. In addition, Rotavirus Infections can lead to antigenaemia (which is associated with more severe manifestations of acute gastroenteritis) and viraemia, and Rotavirus can replicate in systemic sites, although this is limited. ReInfections with Rotavirus are common throughout life, although the disease severity is reduced with repeat Infections. The immune correlates of protection against Rotavirus reInfection and recovery from Infection are poorly understood, although Rotavirus-specific immunoglobulin A has a role in both aspects. The management of Rotavirus Infection focuses on the prevention and treatment of dehydration, although the use of antiviral and anti-emetic drugs can be indicated in some cases. Rotaviruses are double-stranded RNA viruses that are a leading cause of severe, dehydrating gastroenteritis in children
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Rotavirus Infection.
Nature Reviews Disease Primers, 2017Co-Authors: Sue E. Crawford, H B Greenberg, Marie Hagbom, Lennart Svensson, Sasirekha Ramani, Jacqueline E. Tate, Umesh D. Parashar, Manuel A. Franco, Miguel O'ryan, Gagandeep KangAbstract:Rotavirus Infections are a leading cause of severe, dehydrating gastroenteritis in children 200,000 deaths annually, mostly in low-income countries. Rotavirus primarily infects enterocytes and induces diarrhoea through the destruction of absorptive enterocytes (leading to malabsorption), intestinal secretion stimulated by Rotavirus non-structural protein 4 and activation of the enteric nervous system. In addition, Rotavirus Infections can lead to antigenaemia (which is associated with more severe manifestations of acute gastroenteritis) and viraemia, and Rotavirus can replicate in systemic sites, although this is limited. ReInfections with Rotavirus are common throughout life, although the disease severity is reduced with repeat Infections. The immune correlates of protection against Rotavirus reInfection and recovery from Infection are poorly understood, although Rotavirus-specific immunoglobulin A has a role in both aspects. The management of Rotavirus Infection focuses on the prevention and treatment of dehydration, although the use of antiviral and anti-emetic drugs can be indicated in some cases.
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Association of serum antibodies with protection against Rotavirus Infection and disease in South Indian children.
Vaccine, 2014Co-Authors: Prasanna S. Premkumar, Sasirekha Ramani, Umesh D. Parashar, Ben Lopman, Anu Paul, Beryl Primrose Gladstone, Jayaprakash Muliyil, Indrani Mukhopadhya, Gagandeep KangAbstract:Serum antibodies play an important role in natural protection from Rotavirus Infection and disease, but conflicting estimates of association have emerged from epidemiological studies in different geographical settings. In this study, we aim to assess the relationship between pre-existing serum immunoglobulin (Ig)G and IgA titers with protection against Rotavirus Infection and disease in a birth cohort of Indian children. Children were recruited at birth and followed up for 36 months. Stool samples were collected every 2 weeks and during episodes of diarrhea and serum samples were obtained at least every 6 months. The incidence rate of Rotavirus Infection and diarrhea was 0.9 (95% CI: 0.88, 0.99) and 0.2 (95% CI: 0.19, 0.25) episodes per child year, respectively. The risk of Rotavirus Infection and diarrhea decreased with age, while antibody titers (IgG and IgA) increased with age. After adjusting for age and number of previous Infections, higher levels of IgG and IgA were independently associated with reduced risk of Rotavirus Infection. However, we did not find a clear association of IgG or IgA with Rotavirus diarrhea risk or a threshold level of protection. The study supports a correlation of serum antibodies in reducing the risk of Rotavirus Infections, however the potential of serum antibody titer as a correlate of protection is not clear for children in lower income settings.
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Rotavirus Infection Enhances Lipopolysaccharide-Induced Intussusception in a Mouse Model
Journal of virology, 2006Co-Authors: Kelly L. Warfield, Sue E. Crawford, Gagandeep Kang, Sarah E. Blutt, Margaret E. ConnerAbstract:Unexpected reports of intussusception after vaccination with the live tetravalent Rotavirus vaccine RotaShield resulted in voluntary withdrawal of the vaccine. Intussusception, a condition in which the intestine acutely invaginates upon itself, is the most common cause of intestinal obstruction in children. We report here the development of a mouse model to study Rotavirus-induced intussusception. In this model, both homologous murine and heterologous simian Rotavirus strains significantly enhanced the rate of lipopolysaccharide (LPS)-induced intussusception, and this enhancement was replication dependent, requiring Rotavirus doses of greater than one 50% infectious dose. Rotavirus-induced intussusceptions did not have observable lymphoid lead points, despite the induction of intestinal lymphoid hyperplasia after Rotavirus Infection. Intussusceptions are also postulated to result from altered intestinal motility, but Rotavirus Infection had no effect on gastrointestinal transit. LPS-induced intussusception is associated with the induction of inflammatory mediators, and intussusception rates can be modified by inflammatory antagonists. We show that Rotavirus Infection significantly enhanced serum tumor necrosis factor alpha and gamma interferon cytokine levels after LPS treatment compared to uninfected mice. Together, these data suggest that Rotavirus Infection sensitized mice to the inflammatory effects of subsequent LPS treatment to enhance intussusception rates.
H B Greenberg - One of the best experts on this subject based on the ideXlab platform.
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Rotavirus Infection
Nature Reviews Disease Primers, 2017Co-Authors: Sue E. Crawford, H B Greenberg, Marie Hagbom, Lennart Svensson, Sasirekha Ramani, Jacqueline E. Tate, Umesh D. Parashar, Manuel A. Franco, Miguel O'ryan, Gagandeep KangAbstract:Rotavirus Infections are a leading cause of severe, dehydrating gastroenteritis in children 200,000 deaths annually, mostly in low-income countries. Rotavirus primarily infects enterocytes and induces diarrhoea through the destruction of absorptive enterocytes (leading to malabsorption), intestinal secretion stimulated by Rotavirus non-structural protein 4 and activation of the enteric nervous system. In addition, Rotavirus Infections can lead to antigenaemia (which is associated with more severe manifestations of acute gastroenteritis) and viraemia, and Rotavirus can replicate in systemic sites, although this is limited. ReInfections with Rotavirus are common throughout life, although the disease severity is reduced with repeat Infections. The immune correlates of protection against Rotavirus reInfection and recovery from Infection are poorly understood, although Rotavirus-specific immunoglobulin A has a role in both aspects. The management of Rotavirus Infection focuses on the prevention and treatment of dehydration, although the use of antiviral and anti-emetic drugs can be indicated in some cases. Rotaviruses are double-stranded RNA viruses that are a leading cause of severe, dehydrating gastroenteritis in children
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Rotavirus Infection.
Nature Reviews Disease Primers, 2017Co-Authors: Sue E. Crawford, H B Greenberg, Marie Hagbom, Lennart Svensson, Sasirekha Ramani, Jacqueline E. Tate, Umesh D. Parashar, Manuel A. Franco, Miguel O'ryan, Gagandeep KangAbstract:Rotavirus Infections are a leading cause of severe, dehydrating gastroenteritis in children 200,000 deaths annually, mostly in low-income countries. Rotavirus primarily infects enterocytes and induces diarrhoea through the destruction of absorptive enterocytes (leading to malabsorption), intestinal secretion stimulated by Rotavirus non-structural protein 4 and activation of the enteric nervous system. In addition, Rotavirus Infections can lead to antigenaemia (which is associated with more severe manifestations of acute gastroenteritis) and viraemia, and Rotavirus can replicate in systemic sites, although this is limited. ReInfections with Rotavirus are common throughout life, although the disease severity is reduced with repeat Infections. The immune correlates of protection against Rotavirus reInfection and recovery from Infection are poorly understood, although Rotavirus-specific immunoglobulin A has a role in both aspects. The management of Rotavirus Infection focuses on the prevention and treatment of dehydration, although the use of antiviral and anti-emetic drugs can be indicated in some cases.
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gene expression pattern in caco 2 cells following Rotavirus Infection
T200204845.pdf, 2002Co-Authors: Mariela A Cuadras, Dino A Feigelstock, H B GreenbergAbstract:Rotaviruses are recognized as the leading cause of severe dehydrating diarrhea in infants and young children worldwide. Preventive and therapeutic strategies are urgently needed to fight this pathogen. In tissue culture and in vivo, Rotavirus induces structural and functional alterations in the host cell. In order to better understand the molecular mechanisms involved in the events after Rotavirus Infection, we identified host cellular genes whose mRNA levels changed after Infection. For this analysis, we used microarrays containing more than 38,000 human cDNAs to study the transcriptional response of the human intestinal cell line Caco-2 to Rotavirus Infection. We found that 508 genes were differentially regulated >2-fold at 16 h after Rotavirus Infection, and only one gene was similarly regulated at 1 h postInfection. Of these transcriptional changes, 73% corresponded to the upregulation of genes, with the majority of them occurring late, at 12 or more hours postInfection. Some of the regulated genes were classified according to known biological function and included genes encoding integral membrane proteins, interferon-regulated genes, transcriptional and translational regulators, and calcium metabolism-related genes. A new picture of global transcriptional regulation in the infected cell is presented and families of genes which may be involved in viral pathogenesis are discussed.
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The epithelial cell response to Rotavirus Infection
J Immunol, 1999Co-Authors: E E Rollo, N C Reich, John Angel, Rubik Sheth, H B Greenberg, B. Oh, K. P. Kumar, J Cohen, J. Anderson, S J HempsonAbstract:Rotavirus is the most important worldwide cause of severe gastroenteritis in infants and young children. Intestinal epithelial cells are the principal targets of Rotavirus Infection, but the response of enterocytes to Rotavirus Infection is largely unknown. We determined that Rotavirus Infection of HT-29 intestinal epithelial cells results in prompt activation of NF-kappaB (
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Immunity to Rotavirus Infection in mice.
The Journal of infectious diseases, 1999Co-Authors: Manuel A. Franco, H B GreenbergAbstract:Recent findings from our laboratory regarding the immune response of mice to Rotavirus (a mucosal pathogen) show that although in most situations an acquired (T or B cell or both) response is necessary for elimination of primary Rotavirus Infection, unidentified innate mechanisms can also play a role in some mouse strains. Similar to what is seen with many other viruses, CD8+ T cells appear to provide the first but not the exclusive mechanism that mediates clearance of a primary Rotavirus Infection. Antibodies are the critical mediators of prevention against Rotavirus reInfection. Nonneutralizing IgA monoclonal antibodies directed against VP6 (an internal structural Rotavirus protein) can mediate immunity against Rotaviruses in vivo. Rotavirus-specific CD8+ T cells can mediate their antiviral effect in the absence of perforin, fas, or interferon-gamma and are preferentially represented in the subset that expresses high levels of the enteric mucosal homing receptor alpha4beta7.
Manuel A. Franco - One of the best experts on this subject based on the ideXlab platform.
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Rotavirus Infection
Nature Reviews Disease Primers, 2017Co-Authors: Sue E. Crawford, H B Greenberg, Marie Hagbom, Lennart Svensson, Sasirekha Ramani, Jacqueline E. Tate, Umesh D. Parashar, Manuel A. Franco, Miguel O'ryan, Gagandeep KangAbstract:Rotavirus Infections are a leading cause of severe, dehydrating gastroenteritis in children 200,000 deaths annually, mostly in low-income countries. Rotavirus primarily infects enterocytes and induces diarrhoea through the destruction of absorptive enterocytes (leading to malabsorption), intestinal secretion stimulated by Rotavirus non-structural protein 4 and activation of the enteric nervous system. In addition, Rotavirus Infections can lead to antigenaemia (which is associated with more severe manifestations of acute gastroenteritis) and viraemia, and Rotavirus can replicate in systemic sites, although this is limited. ReInfections with Rotavirus are common throughout life, although the disease severity is reduced with repeat Infections. The immune correlates of protection against Rotavirus reInfection and recovery from Infection are poorly understood, although Rotavirus-specific immunoglobulin A has a role in both aspects. The management of Rotavirus Infection focuses on the prevention and treatment of dehydration, although the use of antiviral and anti-emetic drugs can be indicated in some cases. Rotaviruses are double-stranded RNA viruses that are a leading cause of severe, dehydrating gastroenteritis in children
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Rotavirus Infection.
Nature Reviews Disease Primers, 2017Co-Authors: Sue E. Crawford, H B Greenberg, Marie Hagbom, Lennart Svensson, Sasirekha Ramani, Jacqueline E. Tate, Umesh D. Parashar, Manuel A. Franco, Miguel O'ryan, Gagandeep KangAbstract:Rotavirus Infections are a leading cause of severe, dehydrating gastroenteritis in children 200,000 deaths annually, mostly in low-income countries. Rotavirus primarily infects enterocytes and induces diarrhoea through the destruction of absorptive enterocytes (leading to malabsorption), intestinal secretion stimulated by Rotavirus non-structural protein 4 and activation of the enteric nervous system. In addition, Rotavirus Infections can lead to antigenaemia (which is associated with more severe manifestations of acute gastroenteritis) and viraemia, and Rotavirus can replicate in systemic sites, although this is limited. ReInfections with Rotavirus are common throughout life, although the disease severity is reduced with repeat Infections. The immune correlates of protection against Rotavirus reInfection and recovery from Infection are poorly understood, although Rotavirus-specific immunoglobulin A has a role in both aspects. The management of Rotavirus Infection focuses on the prevention and treatment of dehydration, although the use of antiviral and anti-emetic drugs can be indicated in some cases.
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Immunity to Rotavirus Infection in mice.
The Journal of infectious diseases, 1999Co-Authors: Manuel A. Franco, H B GreenbergAbstract:Recent findings from our laboratory regarding the immune response of mice to Rotavirus (a mucosal pathogen) show that although in most situations an acquired (T or B cell or both) response is necessary for elimination of primary Rotavirus Infection, unidentified innate mechanisms can also play a role in some mouse strains. Similar to what is seen with many other viruses, CD8+ T cells appear to provide the first but not the exclusive mechanism that mediates clearance of a primary Rotavirus Infection. Antibodies are the critical mediators of prevention against Rotavirus reInfection. Nonneutralizing IgA monoclonal antibodies directed against VP6 (an internal structural Rotavirus protein) can mediate immunity against Rotaviruses in vivo. Rotavirus-specific CD8+ T cells can mediate their antiviral effect in the absence of perforin, fas, or interferon-gamma and are preferentially represented in the subset that expresses high levels of the enteric mucosal homing receptor alpha4beta7.
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The immunology of Rotavirus Infection in the mouse.
Advances in Virus Research, 1998Co-Authors: Jason R. Rosé, Manuel A. Franco, H B GreenbergAbstract:Publisher Summary The Rotaviruses represent a major health concern, and a detailed understanding of viral immunity is desirable for the development of a vaccine. The most extensively studied model of Rotavirus immunity is that provided by Infection of mice with murine Rotaviruses. This chapter addresses the initial discovery of the murine Rotavirus and the development of the murine model of Rotavirus Infection, the state of the current understanding about Rotavirus immunology in the mouse, and issues related to treatment of and protection from Rotavirus Infection that have been raised as a result of studying the murine model. The study of Rotavirus immunity is subdivided by first addressing the development and characteristics of the humoral and cellular responses, followed by description of the effector mechanisms of Rotavirus immunity, and studies of passive and active protection of mice from Rotavirus Infection.
Lennart Svensson - One of the best experts on this subject based on the ideXlab platform.
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Rotavirus Infection
Nature Reviews Disease Primers, 2017Co-Authors: Sue E. Crawford, H B Greenberg, Marie Hagbom, Lennart Svensson, Sasirekha Ramani, Jacqueline E. Tate, Umesh D. Parashar, Manuel A. Franco, Miguel O'ryan, Gagandeep KangAbstract:Rotavirus Infections are a leading cause of severe, dehydrating gastroenteritis in children 200,000 deaths annually, mostly in low-income countries. Rotavirus primarily infects enterocytes and induces diarrhoea through the destruction of absorptive enterocytes (leading to malabsorption), intestinal secretion stimulated by Rotavirus non-structural protein 4 and activation of the enteric nervous system. In addition, Rotavirus Infections can lead to antigenaemia (which is associated with more severe manifestations of acute gastroenteritis) and viraemia, and Rotavirus can replicate in systemic sites, although this is limited. ReInfections with Rotavirus are common throughout life, although the disease severity is reduced with repeat Infections. The immune correlates of protection against Rotavirus reInfection and recovery from Infection are poorly understood, although Rotavirus-specific immunoglobulin A has a role in both aspects. The management of Rotavirus Infection focuses on the prevention and treatment of dehydration, although the use of antiviral and anti-emetic drugs can be indicated in some cases. Rotaviruses are double-stranded RNA viruses that are a leading cause of severe, dehydrating gastroenteritis in children
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Rotavirus Infection.
Nature Reviews Disease Primers, 2017Co-Authors: Sue E. Crawford, H B Greenberg, Marie Hagbom, Lennart Svensson, Sasirekha Ramani, Jacqueline E. Tate, Umesh D. Parashar, Manuel A. Franco, Miguel O'ryan, Gagandeep KangAbstract:Rotavirus Infections are a leading cause of severe, dehydrating gastroenteritis in children 200,000 deaths annually, mostly in low-income countries. Rotavirus primarily infects enterocytes and induces diarrhoea through the destruction of absorptive enterocytes (leading to malabsorption), intestinal secretion stimulated by Rotavirus non-structural protein 4 and activation of the enteric nervous system. In addition, Rotavirus Infections can lead to antigenaemia (which is associated with more severe manifestations of acute gastroenteritis) and viraemia, and Rotavirus can replicate in systemic sites, although this is limited. ReInfections with Rotavirus are common throughout life, although the disease severity is reduced with repeat Infections. The immune correlates of protection against Rotavirus reInfection and recovery from Infection are poorly understood, although Rotavirus-specific immunoglobulin A has a role in both aspects. The management of Rotavirus Infection focuses on the prevention and treatment of dehydration, although the use of antiviral and anti-emetic drugs can be indicated in some cases.
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The Cholinergic Anti-Inflammatory Pathway Contributes to the Limited Inflammatory Response following Rotavirus Infection
2015Co-Authors: Marie Hagbom, Johan Nordgren, Samuel Lundin, Hans Wigzell, John A. Taylor, Ulf Andersson, Lennart SvenssonAbstract:Rotavirus Infections cause diarrhea and vomiting that can lead to severe dehydration. Despite extensive tissue damage and cell death, the inflammatory response is very limited. The focus of this thesis was to study pathophysiological mechanisms behind diarrhea and vomiting during Rotavirus Infection and also to investigate the mechanism behind the limited inflammatory response.An important discovery in this thesis was that Rotavirus Infection and the Rotavirus toxin NSP4 stimulate release of the neurotransmitter serotonin from intestinal sensory enterochromaffin cells, in vitro and ex vivo. Interestingly, serotonin is known to be a mediator of both diarrhea and vomiting. Moreover, mice pups infected with Rotavirus responded with central nervous system (CNS) activation in brain structures associated with vomiting, thus indicating a cross-talk between the gut and brain in Rotavirus disease.Our finding that Rotavirus Infection activates the CNS led us to address the hypothesis that Rotavirus Infection not only activates the vagus nerve to stimulate vomiting, but also suppresses the inflammatory response via the cholinergic anti-inflammatory pathway, both of which are mediated by activated vagal afferent nerve signals into the brain stem. We found that mice lacking an intact vagus nerve, and mice lacking the α7 nicotine acetylcholine receptor (nAChR), being involved in cytokine suppression from macrophages, responded with a higher inflammatory response.Moreover, stimulated cytokine release from macrophages, by the Rotavirus toxin NSP4, could be attenuated by nicotine, an agonist of the α7 nAChR. Thus, it seems most reasonable that the cholinergic anti-inflammatory pathway contributes to the limited inflammatory response during Rotavirus Infection. Moreover, Rotavirus-infected mice displayed increased intestinal motility at the onset of diarrhea, which was not associated with increased intestinal permeability. The increased motility and diarrhea in infant mice could be attenuated by drugs acting on the enteric nervous system, indicating the importance and contribution of nerves in the Rotavirus mediated disease.In conclusion, this thesis provides further insight into the pathophysiology of diarrhea and describe for the first time how Rotavirus and host cross-talk to induce the vomiting reflex and limit inflammation. Results from these studies strongly support our hypothesis that serotonin and activation of the enteric nervous system and CNS contributes to diarrhea, vomiting and suppression of the inflammatory response in Rotavirus disease.
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Role of nitric oxide during Rotavirus Infection.
Journal of medical virology, 2006Co-Authors: Jesús Rodríguez-díaz, Mahanez Banasaz, Claudia Istrate, Javier Buesa, Ove Lundgren, Felix Espinoza, Tommy Sundqvist, Martin E. Rottenberg, Lennart SvenssonAbstract:The pathophysiological mechanisms behind Rotavirus-induced diarrhoea still remain incomplete. Current views suggest that the non-structural protein 4 (NSP4) of Rotavirus and the enteric nervous system (ENS) participate in water secretion and diarrhoea. In the present work the role of nitric oxide (NO) in Rotavirus Infection and disease has been studied in vitro, mice and humans. Incubation of human intestinal epithelial cells (HT-29) with purified NSP4 but not with infectious virus produced NO2/NO3 accumulation in the incubation media. The NSP4-induced release of NO metabolites occurred within the first minutes after the addition of the toxin. Mice infected with murine Rotavirus (strain EDIM) accumulated NO2/NO3 in the urine at the onset for diarrhoea. Following Rotavirus Infection, inducible nitric oxide synthetase (iNOS) mRNA was upregulated in ileum, but not in duodenum or jejunum of newborn pups within 5 days post-Infection. A prospective clinical study including 46 children with acute Rotavirus Infection and age-matched controls concluded that Rotavirus Infection stimulates NO production during the course of the disease (P < 0.001). These observations identify NO as an important mediator of host responses during Rotavirus Infection.
Thea Kolsen Fischer - One of the best experts on this subject based on the ideXlab platform.
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hospital surveillance of Rotavirus Infection and nosocomial transmission of Rotavirus disease among children in guinea bissau
Pediatric Infectious Disease Journal, 2007Co-Authors: Amabelia Rodrigues, Peter Aaby, Kare Molbak, Melo De Carvalho, Serifo Monteiro, Carsten Sauer Mikkelsen, Thea Kolsen FischerAbstract:Vaccination against Rotavirus is protective against severe disease. Surveillance of Rotavirus Infection in developing countries might direct vaccination policy more efficiently. We implemented WHOs generic protocols for hospital- and community-based surveillance of Rotavirus gastroenteritis. From April 2001 to May 2002 and from January 2003 to June 2003 we conducted hospital surveillance for Rotavirus Infection at the only pediatric ward in the capital of Guinea-Bissau. Children less than 5 years of age admitted with diarrhea or developing diarrhea during hospitalization were enrolled in the study. Rotavirus Infection was detected in the feces samples using an ELISA assay. Rectal swabs were also obtained and its use was validated against stool specimen. During the surveillance period 161 cases of Rotavirus Infection were registered. During the season Rotavirus accounted for 35% of all hospitalized diarrhea cases. The rate of nosocomial disease was 1.6 per 1000 child-days (95% confidence interval [CI] = 1.02-2.51) with high rates for children aged 12 to 23 months of age (rate: 3.09; 95% CI = 1.47-6.48). Most of the Rotavirus cases (93%) were in children less than 2 years of age and only 10 children aged less than 3 months were infected. Fever (risk ratio (RR) 1.56; 95% CI = 1.16-2.10) and vomiting (RR 1.38; 95% CI = 1.11-1.73) were more common in patients with Rotavirus than in patients with nonRotavirus diarrhea. The case-fatality was 8%. Results from stool samples and rectal swabs were concordant in 96% of the pairs. Rectal swabs increased the detection of Rotavirus cases by 6% and deaths by 33% over stool sample results. Rotavirus Infections were confined to a 4-month period each year. It is an important cause of childhood diarrhea with high case-fatality ratio in Guinea-Bissau. The use of rectal swab appeared to increase the detection rate of Rotavirus Infection and the case-fatality rate. The high rate of nosocomial Infections in hospitalized children emphasizes the need for prevention of disease. (authors)
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protective immunity after natural Rotavirus Infection a community cohort study of newborn children in guinea bissau west africa
The Journal of Infectious Diseases, 2002Co-Authors: Thea Kolsen Fischer, Palle Valentinerbranth, Hans Steinsland, Michael Perch, Gina Santos, Peter Aaby, Kare Molbak, Halvor SommerfeltAbstract:To study the natural history of Rotavirus Infection and to determine the protection it confers against reInfection and diarrhea, 200 newborns in Guinea-Bissau were prospectively followed for up to 2 years. Rotavirus was detected in stool specimens collected weekly. By age 2 years, the incidence of primary Rotavirus Infection was 74%. In the first 3 months of life, 17% of the Infections were diarrhea associated, compared with 60% at 9-11 months; after age 18 months, all Infections were asymptomatic. A primary Infection conferred 52% (95% confidence interval [CI], 16% to 73%) and 70% (95% CI, 29% to 87%) protection against subsequent Rotavirus Infection and Rotavirus diarrhea, respectively. The protection was 66% (95% CI, 24% to 85%) against reInfection within the same epidemic, compared with 34% (95% CI, -29% to 67%) against reInfection in any subsequent epidemic. The high level of protection against symptomatic Rotavirus Infection provides an important incentive for development of a Rotavirus vaccine.
