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Hagbom, M. & Svensson, L. (2024). Rotavirus (9ed.). In: James Cherry, Sheldon L. Kaplan, Gail J. Demmler-Harrison, William Steinbach, Peter J Hotez, John V Williams (Ed.), Feigin and Cherry's Textbook of Pediatric Infectious Diseases, 9th Edition: . Elsevier
Open this publication in new window or tab >>Rotavirus
2024 (English)In: Feigin and Cherry's Textbook of Pediatric Infectious Diseases, 9th Edition / [ed] James Cherry, Sheldon L. Kaplan, Gail J. Demmler-Harrison, William Steinbach, Peter J Hotez, John V Williams, Elsevier, 2024, 9Chapter in book (Other academic)
Place, publisher, year, edition, pages
Elsevier, 2024 Edition: 9
Identifiers
urn:nbn:se:liu:diva-202408 (URN)9780323827638 (ISBN)9780323827652 (ISBN)9780323827645 (ISBN)
Available from: 2024-04-09 Created: 2024-04-09 Last updated: 2024-04-09
Hellysaz, A., Nordgren, J., Neijd, M., Generó, M. M., Svensson, L. & Hagbom, M. (2023). Microbiota do not restrict rotavirus infection of colon. Journal of Virology, 97(11), Article ID e01526-23.
Open this publication in new window or tab >>Microbiota do not restrict rotavirus infection of colon
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2023 (English)In: Journal of Virology, ISSN 0022-538X, E-ISSN 1098-5514, Vol. 97, no 11, article id e01526-23Article in journal (Refereed) Published
Abstract [en]

Rotavirus is associated with extensive infection of the small intestine, whereas colon is considered to be uninfected. Considering that almost all bacteria in the gut colonize the colon, we hypothesized that the microbiota may act as a physical barrier preventing rotavirus infection in the colon in vivo. To address this hypothesis, we used human and mice colonoids, and biopsies of different intestinal segments of untreated and antibiotic-treated adult and infant mice. Rotavirus quantification was performed by qPCR and volumetric 3D imaging of intestinal segments. By 3D imaging, we observed infection in all the small intestinal segments, most extensively in the ileum, with most limited number of infected cells in colon. Broad-spectrum antibiotic treatment yielded no significant change in infection in either ileum or colon of adults and mice pups, although there is a substantial decrease in microbial load. We also show that rotavirus can successfully infect and replicate in colonoids from both mice and humans. Collectively, our data, including novel 3D imaging of the gut, mouse, and human colonoids, conclude that microbiota does not affect rotavirus infection in colon.

IMPORTANCE

Alterations of the gut microbiome can have significant effects on gastrointestinal homeostasis leading to various diseases and symptoms. Increased understanding of rotavirus infection in relation to the microbiota can provide better understanding on how microbiota can be used for clinical prevention as well as treatment strategies. Our volumetric 3D imaging data show that antibiotic treatment and its consequent reduction of the microbial load does not alter the extent of rotavirus infection of enterocytes in the small intestine and that restriction factors other than bacteria limit the infection of colonocytes.

Place, publisher, year, edition, pages
American Society for Microbiology, 2023
Keywords
rotavirus, colon, enterocytes, microbiota
National Category
Microbiology in the medical area
Identifiers
urn:nbn:se:liu:diva-199297 (URN)10.1128/jvi.01526-23 (DOI)001099953200004 ()37905839 (PubMedID)
Funder
Swedish Research Council, 2018-02862Swedish Research Council, 2020-06116
Note

Funding: This work was supported by the Swedish Research Council (Grants 2014-02827, 2017-01479, 2018-02862). [2014-02827, 2017-01479, 2018-02862]; Swedish Research Council

Available from: 2023-11-24 Created: 2023-11-24 Last updated: 2024-05-03
Lennerstrand, J., Svensson, L. & Lundkvist, Å. (2022). Hur har omikron uppstått och varför sprider den sig så snabbt?: Fyra hypoteser om variantens ursprung och tänkbara mekanismer bakom den snabba spridningen presenteras [How did Omicron evolve and why does this SARS-CoV-2 variant spread so fast?]. Läkartidningen, 119, Article ID 21242.
Open this publication in new window or tab >>Hur har omikron uppstått och varför sprider den sig så snabbt?: Fyra hypoteser om variantens ursprung och tänkbara mekanismer bakom den snabba spridningen presenteras [How did Omicron evolve and why does this SARS-CoV-2 variant spread so fast?]
2022 (Swedish)In: Läkartidningen, ISSN 0023-7205, E-ISSN 1652-7518, Vol. 119, article id 21242Article, review/survey (Refereed) Published
Abstract [en]

Omicron has more than twenty new mutations in the S1 domain of the spike gene as compared to the other previously known variants of SARS-CoV-2. Many of these new mutations, especially those located in the receptor binding domain, are likely to improve binding to the ACE2 receptor and to avoid binding to antibodies induced by a previous infection or by vaccination. Today there are several different hypotheses about the origin of Omicron, for example that it would have arisen in an immunosuppressed individual. Alternatively, a SARS-CoV-2 variant could have infected an unknown animal, and re-infection of humans would then have occurred. Furthermore, Omicron may have picked up a piece of a human common cold coronavirus.  The hitherto available data suggest that the rapid spread of Omicron is a combination of properties of the virus replication ability in addition to its ability to avoid pre-existing immune responses.

Abstract [sv]

Omikron har mer än 20 nya mutationer i spikgenens S1-domän. Många av dessa mutationer ökar sannolikt förmågan att binda bättre till ACE-2-receptorn och undvika bindning av antikroppar inducerade av en tidigare infektion eller genom vaccination. 

I dag finns det flera hypoteser om omikrons ursprung, till exempel att den skulle ha uppstått hos en immun­supprimerad individ. Alternativt kan en tidigare sars-cov-2-variant ha infekterat en okänd djurpopulation och återinfektion av människor skulle då ha inträffat.

De data som finns talar för att den snabba spridningen av omikron är en kombination av egenskaper hos virusets replikationsförmåga och dess förmåga att undvika preexisterande immunsvar.

Place, publisher, year, edition, pages
Sveriges Läkarförbund, 2022
National Category
Infectious Medicine
Identifiers
urn:nbn:se:liu:diva-193507 (URN)35041755 (PubMedID)
Available from: 2023-05-02 Created: 2023-05-02 Last updated: 2023-05-10Bibliographically approved
Sharma, S., Hagbom, M., Svensson, L. & Nordgren, J. (2021). Human Norovirus and Sapovirus (2ed.). In: Dennis H. Bamford; Mark Zuckerman (Ed.), Encyclopedia of Virology: Fourth Edition (pp. 483-492). Academic Press
Open this publication in new window or tab >>Human Norovirus and Sapovirus
2021 (English)In: Encyclopedia of Virology: Fourth Edition / [ed] Dennis H. Bamford; Mark Zuckerman, Academic Press, 2021, 2, p. 483-492Chapter in book (Other academic)
Abstract [en]

The Caliciviridae family includes human norovirus and sapovirus. These are a diverse set of viruses causing acute gastroenteritis (AGE) in people of all ages, with norovirus being responsible for approximately 20% of all AGE worldwide and sapovirus 3%–17% of AGE in children, respectively. Susceptibility to norovirus is associated with human genetics, with approximately one-fifth of the population being resistant to the predominant GII.4 genotype. A human enteroid model has recently been successfully established to address questions regarding pathogenesis and virus–host interactions. While no specific antivirals are available, norovirus vaccine candidates are in clinical trials.

Place, publisher, year, edition, pages
Academic Press, 2021 Edition: 2
National Category
Infectious Medicine Microbiology in the medical area
Identifiers
urn:nbn:se:liu:diva-202392 (URN)10.1016/B978-0-12-809633-8.21543-4 (DOI)978-0-12-814516-6 (ISBN)
Available from: 2024-04-08 Created: 2024-04-08 Last updated: 2024-04-08
Nordgren, J., Sharma, S., Kambhampati, A., Lopman, B. & Svensson, L. (2016). Innate Resistance and Susceptibility to Norovirus Infection. PLoS Pathogens, 12(4), e1005385
Open this publication in new window or tab >>Innate Resistance and Susceptibility to Norovirus Infection
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2016 (English)In: PLoS Pathogens, ISSN 1553-7366, E-ISSN 1553-7374, Vol. 12, no 4, p. e1005385-Article in journal (Refereed) Published
Abstract [en]

n/a

Place, publisher, year, edition, pages
PUBLIC LIBRARY SCIENCE, 2016
National Category
Clinical Medicine
Identifiers
urn:nbn:se:liu:diva-130446 (URN)10.1371/journal.ppat.1005385 (DOI)000378156900003 ()27115484 (PubMedID)
Note

Funding Agencies|Swedish Foundation for Strategic Research

Available from: 2016-08-06 Created: 2016-08-05 Last updated: 2021-12-28
Hagbom, M., Nordgren, J., Nybom, R., Hedlund, K.-O., Wigzell, H. & Svensson, L. (2015). Ionizing air affects influenza virus infectivity and prevents airborne-transmission. Scientific Reports, 5(11431)
Open this publication in new window or tab >>Ionizing air affects influenza virus infectivity and prevents airborne-transmission
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2015 (English)In: Scientific Reports, E-ISSN 2045-2322, Vol. 5, no 11431Article in journal (Refereed) Published
Abstract [en]

By the use of a modified ionizer device we describe effective prevention of airborne transmitted influenza A (strain Panama 99) virus infection between animals and inactivation of virus (greater than 97%). Active ionizer prevented 100% (4/4) of guinea pigs from infection. Moreover, the device effectively captured airborne transmitted calicivirus, rotavirus and influenza virus, with recovery rates up to 21% after 40 min in a 19 m(3) room. The ionizer generates negative ions, rendering airborne particles/aerosol droplets negatively charged and electrostatically attracts them to a positively charged collector plate. Trapped viruses are then identified by reverse transcription quantitative real-time PCR. The device enables unique possibilities for rapid and simple removal of virus from air and offers possibilities to simultaneously identify and prevent airborne transmission of viruses.

Place, publisher, year, edition, pages
Nature Publishing Group: Open Access Journals - Option C / Nature Publishing Group, 2015
National Category
Clinical Medicine
Identifiers
urn:nbn:se:liu:diva-120165 (URN)10.1038/srep11431 (DOI)000356662300002 ()26101102 (PubMedID)
Note

Funding Agencies|Swedish Research Council [320301]

Available from: 2015-07-13 Created: 2015-07-13 Last updated: 2024-01-08
Nordgren, J., Sharma, S., Bucardo, F., Nasir, W., Gunaydin, G., Ouermi, D., . . . Svensson, L. (2014). Both Lewis and Secretor Status Mediate Susceptibility to Rotavirus Infections in a Rotavirus Genotype-Dependent Manner. Clinical Infectious Diseases, 59(11), 1567-1573
Open this publication in new window or tab >>Both Lewis and Secretor Status Mediate Susceptibility to Rotavirus Infections in a Rotavirus Genotype-Dependent Manner
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2014 (English)In: Clinical Infectious Diseases, ISSN 1058-4838, E-ISSN 1537-6591, Vol. 59, no 11, p. 1567-1573Article in journal (Refereed) Published
Abstract [en]

Background. The live oral rotavirus (RV) vaccines have shown a reduced efficacy in Africa. Recent in vitro studies have shown binding of the RV surface protein (VP4) to histo-blood group antigens (HBGAs) in an RV genotype-dependent manner, suggesting them to be putative receptors for RV. The diversity of HBGA phenotypes in different ethnic populations, combined with prevalence/absence of specific RV genotypes, led us to hypothesize whether the genetic variations in HBGAs in a population limit susceptibility to certain RV genotypes, plausibly leading to reduced vaccine efficacy. Methods. Association between HBGAs status and susceptibility to RV P genotypes was investigated in children in Burkina Faso and Nicaragua. In total, 242 children with diarrhea in Burkina Faso and Nicaragua were investigated, 93 of whom were RV positive. Results. In Burkina Faso, the P[8] RV strains (n = 27) infected only Lewis-and secretor-positive children (27/27; P less than .0001), but no Lewis-negative children. In contrast, the P[6] strains (n = 27) infected predominantly Lewis-negative children (n = 18; P less than.0001) but also Lewis-positive children, irrespective of their secretor status. The results from Nicaragua confirmed that all P[8]-infected children (n = 22) were secretor Lewis positive. Conclusions. As VP4 of genotype P[8] is a component of current RV vaccines, our finding that Lewis-negative children are resistant to P[8] strains provides a plausible explanation for the reduced vaccine efficacy in populations with a high percentage of Lewis-negative individuals, such as in Africa. Furthermore, our findings provide a plausible explanation as to why P[6] RV strains are more common in Africa.

Place, publisher, year, edition, pages
Oxford University Press (OUP): Policy A1 - Oxford Open Option C, 2014
Keywords
rotavirus; histo-blood group antigen; Lewis; susceptibility; vaccine
National Category
Clinical Medicine
Identifiers
urn:nbn:se:liu:diva-113179 (URN)10.1093/cid/ciu633 (DOI)000345841900011 ()25097083 (PubMedID)
Note

Funding Agencies|Swedish Research Council [8266, 3485, dnr-348-2011-7420]

Available from: 2015-01-13 Created: 2015-01-12 Last updated: 2021-12-28
Becker-Dreps, S., Bucardo, F., Vilchez, S., Enrique Zambrana, L., Liu, L., Weber, D. J., . . . Paniagua, M. (2014). Etiology of Childhood Diarrhea After Rotavirus Vaccine Introduction A Prospective, Population-based Study in Nicaragua. The Pediatric Infectious Disease Journal, 33(11), 1156-1163
Open this publication in new window or tab >>Etiology of Childhood Diarrhea After Rotavirus Vaccine Introduction A Prospective, Population-based Study in Nicaragua
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2014 (English)In: The Pediatric Infectious Disease Journal, ISSN 0891-3668, E-ISSN 1532-0987, Vol. 33, no 11, p. 1156-1163Article in journal (Refereed) Published
Abstract [en]

Background: Nicaragua was the first developing nation to implement routine immunization with the pentavalent rotavirus vaccine (RV5). In this RV5-immunized population, understanding infectious etiologies of childhood diarrhea is necessary to direct diarrhea treatment and prevention efforts. Methods: We followed a population-based sample of children less than5 years in Leon, Nicaragua for diarrhea episodes through household visits. Information was obtained on RV5 history and sociodemographics. Stool samples collected during diarrhea episodes and among healthy children underwent laboratory analysis for viral, bacterial and parasitic enteropathogens. Detection frequency and incidence of each enteropathogen was calculated. Results: The 826 children in the cohort experienced 677 diarrhea episodes during 607.5 child-years of exposure time (1.1 episodes per child-year). At least 1 enteropathogen was detected among 61.1% of the 337 diarrheal stools collected. The most common enteropathogens among diarrheal stools were: norovirus (20.4%), sapovirus (16.6%), enteropathogenic Escherichia coli (11.3%), Entamoeba histolytica/dispar (8.3%), Giardia lamblia (8.0%) and enterotoxigenic E. coli (7.7%), with rotavirus detected among 5.3% of diarrheal stools. Enteropathogenic Escherichia coli and enterotoxigenic E. coli were frequently detected among stools from healthy children. Among children with diarrhea, norovirus was more commonly detected among younger children (less than2 years) and G. lamblia was more commonly detected among older children (2-4 years). The mean age of rotavirus detection was 34.6 months. Conclusions: In this Central American community after RV5 introduction, rotavirus was not commonly detected among children with diarrhea. Prevention and appropriate management of norovirus and sapovirus should be considered to further reduce the burden of diarrheal disease.

Place, publisher, year, edition, pages
Lippincott, Williams andamp; Wilkins, 2014
Keywords
childhood; community; diarrhea; Nicaragua; Rotavirus vaccine
National Category
Clinical Medicine
Identifiers
urn:nbn:se:liu:diva-112630 (URN)10.1097/INF.0000000000000427 (DOI)000344354400017 ()24879131 (PubMedID)
Note

Funding Agencies|Merck Investigator-Initiated Studies Program; Thrasher Research Fund; Fogarty International Center at the National Institutes of Health [5K01TW008401-04]; NETROPICA [05-N-2010]

Available from: 2014-12-08 Created: 2014-12-05 Last updated: 2021-12-28
Gunaydin, G., Nordgren, J., Svensson, L. & Hammarstrom, L. (2014). Mutations in Toll-Like Receptor 3 Are Associated with Elevated Levels of Rotavirus-Specific IgG Antibodies in IgA-Deficient but Not IgA-Sufficient Individuals. Clinical and Vaccine Immunology, 21(3), 298-301
Open this publication in new window or tab >>Mutations in Toll-Like Receptor 3 Are Associated with Elevated Levels of Rotavirus-Specific IgG Antibodies in IgA-Deficient but Not IgA-Sufficient Individuals
2014 (English)In: Clinical and Vaccine Immunology, ISSN 1556-6811, E-ISSN 1556-679X, Vol. 21, no 3, p. 298-301Article in journal (Refereed) Published
Abstract [en]

Double-stranded RNA (dsRNA) triggers immune-mediated responses through toll-like receptor 3 (TLR3), which is involved in innate antiviral defense. Low expression of TLR3 was recently suggested to contribute to susceptibility to rotavirus infection. Thus, we investigated the role of two TLR3 polymorphisms (rs3775291 and rs5743305), both of which resulted in reduced protein function or expression, in healthy blood donors and IgA-deficient (IgAD) individuals. These polymorphisms were associated with elevated rotavirus-specific IgG titers in IgAD individuals but not in healthy individuals. Thus, we propose that TLR3 signaling does not contribute to the rotavirus-specific antibody response in IgA-sufficient individuals, whereas it is associated with elevated antibody titers in IgAD individuals.

Place, publisher, year, edition, pages
American Society for Microbiology, 2014
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-105572 (URN)10.1128/CVI.00666-13 (DOI)000332036900005 ()
Available from: 2014-03-31 Created: 2014-03-27 Last updated: 2021-12-28
Nenonen, N. P., Hannoun, C., Svensson, L., Toren, K., Andersson, L.-M., Westin, J. & Bergstrom, T. (2014). Norovirus GII.4 Detection in Environmental Samples from Patient Rooms during Nosocomial Outbreaks. Journal of Clinical Microbiology, 52(7), 2352-2358
Open this publication in new window or tab >>Norovirus GII.4 Detection in Environmental Samples from Patient Rooms during Nosocomial Outbreaks
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2014 (English)In: Journal of Clinical Microbiology, ISSN 0095-1137, E-ISSN 1098-660X, Vol. 52, no 7, p. 2352-2358Article in journal (Refereed) Published
Abstract [en]

Norovirus (NoV) is an important cause of nosocomial gastroenteric outbreaks. This 5-month study was designed to characterize NoV contamination and airborne dispersal in patient rooms during hospital outbreaks. Air vents, overbed tables, washbasins, dust, and virus traps designed to collect charged particles from the air were swabbed to investigate the possibility of NoV contamination in patient rooms during outbreaks in seven wards and in an outbreak-free ward. Symptomatic inpatients were also sampled. Nucleic acid extracts of the samples were examined for NoV RNA using genogroup I (GI) and GII real-time reverse transcription-PCR (RT-PCR). The NoV strains were characterized by RT-PCR, sequencing, and phylogenetic analysis of the RNA-dependent RNA-polymerase-N/S capsid-coding region (1,040 nucleotides [nt]). Patient strains from two outbreaks in one ward were sequenced across the RNA-dependent-RNA-polymerase major capsid-coding region (2.5 kb), including the hypervariable P2 domain. In the outbreak wards, NoV GII was detected in 48 of 101 (47%) environmental swabs and 63 of 108 patients (58%); NoV genotype II.4 was sequenced from 18 environmental samples, dust (n = 8), virus traps (n = 4), surfaces (n = 6), and 56 patients. In contrast, NoV GII was detected in 2 (GII. 4) of 28 (7%) environmental samples and in 2 (GII. 6 and GII. 4) of 17 patients in the outbreak-free ward. Sequence analyses revealed a high degree of similarity (greater than99.5%, 1,040 nt) between NoV GII.4 environmental and patient strains from a given ward at a given time. The strains clustered on 11 subbranches of the phylogenetic tree, with strong correlations to time and place. The high nucleotide similarity between the NoV GII.4 strains from patients and their hospital room environment provided molecular evidence of GII.4 dispersal in the air and dust; therefore, interventional cleaning studies are justified.

Place, publisher, year, edition, pages
American Society for Microbiology, 2014
National Category
Clinical Medicine
Identifiers
urn:nbn:se:liu:diva-109598 (URN)10.1128/JCM.00266-14 (DOI)000339279700011 ()24759712 (PubMedID)
Available from: 2014-08-21 Created: 2014-08-21 Last updated: 2017-12-05
Organisations
Identifiers
ORCID iD: ORCID iD iconorcid.org/0000-0001-9306-8458

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