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.

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.

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.

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.

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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.

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.

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.

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.