National Influenza Annual Report, Canada, 2022-2023: Canada's first fall epidemic since the 2019-2020 season.

Coinciding with the beginning of the coronavirus disease 2019 (COVID-19) pandemic in March 2020, Canadian seasonal influenza circulation was suppressed, which was a trend reported globally. Canada saw a brief and delayed return of community influenza circulation during the spring of the 2021-2022 influenza season. Surveillance for Canada's 2022-2023 seasonal influenza epidemic began in epidemiological week 35 (week starting August 28, 2022) and ended in epidemiological week 34 (week ending August 26, 2023). The 2022-2023 season marked the return to pre-pandemic-like influenza circulation. The epidemic began in epidemiological week 43 (week ending October 29, 2022) and lasted 10 weeks. Driven by influenza A(H3N2), the epidemic was relatively early, extraordinary in intensity, and short in length. This season, a total of 74,344 laboratory-confirmed influenza detections were reported out of 1,188,962 total laboratory tests. A total of 93% of detections were influenza A (n=68,923). Influenza A(H3N2) accounted for 89% of the subtyped specimens (n=17,638/19,876). Late-season, Canada saw community circulation of influenza B for the first time since the 2019-2020 season. The 2022-2023 influenza season in Canada had an extraordinary impact on children and youth; nearly half (n=6,194/13,729, 45%) of reported influenza A(H3N2) detections were in the paediatric (younger than 19 years) population. Weekly paediatric influenza-associated hospital admissions were persistently above historical peak levels for several weeks. The total number of influenza-associated paediatric hospitalizations (n=1,792) far exceeded historical averages (n=1,091). With the return of seasonal influenza circulation and endemic co-circulation of multiple high burden respiratory viruses, sustained vigilance is warranted. Annual seasonal influenza vaccination is a key public health intervention available to protect Canadians.

Development of reverse-transcriptase, real-time PCR assays to distinguish the Southern African Territories (SAT) serotypes 1 and 3 and topotype VII of SAT2 of Foot-and-Mouth Disease Virus.

Foot-and-Mouth Disease Virus (FMDV), the causative agent of Foot-and-Mouth Disease, is a highly feared, economically devastating transboundary pathogen. This is due to the virus' extremely contagious nature and its ability to utilize multiple transmission routes. As such, rapid and accurate diagnostic testing is imperative to the control of FMD. Identification of the FMDV serotype is necessary as it provides the foundation for appropriate vaccine selection and aids in outbreak source tracing. With the vast genetic diversity, there is a desperate need to be able to characterize FMDV without relying on prior knowledge of viral serotypes. In this study, the Neptune bioinformatics tool was used to identify genetic signatures specific to each Southern African Territories (SAT) 1, 2 and 3 genomes but exclusionary to the other circulating FMDV serotypes (A, O, Asia1, and the heterologous SAT1, SAT2 and/or SAT3). Identification of these unique genomic regions allowed the design of TaqMan-based real-time reverse transcriptase PCR (rRT-PCR) primer/probe sets for SAT1, SAT2 and SAT3 viruses. These assays were optimized using prototypic FMDV cell culture isolates using the same reagents and thermocycling conditions as the FMDV pan-serotype 3D rRT-PCR assay. Cross-reactivity was evaluated in tandem with the FMDV pan-serotype 3D rRT-PCR utilizing representative strains from FMDV serotypes A, O, Asia1, SAT1, SAT2 and SAT3. The SAT1, SAT2, and SAT3 primer/probe sets were specific for the homologous serotype and exclusionary to all others. SAT1 and SAT3 primer/probe sets were able to detect several topotypes, whereas the SAT2 assay was revealed to be specific for topotype VII. The SAT2 topotype VII specificity was possibly due to the use of sequence data deposited post-2011to design the rRT-PCR primers and probes. Each assay was tested against a panel of 99 bovine tissue samples from Nigeria, where SAT2 topotype VII viruses were correctly identified and no cross-reactivity was exhibited by the SAT1 and 3 assays. These novel SAT1, SAT3 and SAT2 topotype VII rRT-PCR assays have the potential to detect and differentiate circulating FMD SAT viruses.

Transgenic expression of human equilibrative nucleoside transporter 1 in mouse neurons.

Transgenic mice that express human equilibrative nucleoside transporter subtype 1 (hENT1) under the control of a neuron-specific enolase promoter have been generated. Southern blot and PCR revealed the presence of the transgene in five founder mice. Mice from each founder line were examined by reverse transcriptase (RT)-PCR and found to express hENT1 in RNA isolated from whole brain, cerebral cortex, striatum, hippocampus, and cerebellum but not liver, kidney, heart, lung or skeletal muscle. Cortical synaptosomes prepared from transgenic mice had significantly increased [(3)H]adenosine uptake and [(3)H]nitrobenzylthioinosine binding, relative to samples from wild-type mice. In behavioral tests, transgenic mice had altered responses to caffeine and ethanol, two drugs that inhibit and enhance, respectively, adenosine receptor activity. Caffeine-induced locomotor stimulation was attenuated whereas the hypnotic effect of ethanol was enhanced in transgenic mice. Caffeine was more potent in inhibiting ethanol-induced motor incoordination in wild-type than in transgenic mice. No differences in expression of mouse genes for adenosine receptors, nucleoside transporters, or purine metabolizing enzymes were detected by RT-PCR analyses. These data indicate that expression of hENT1 in neurons does not trigger adaptive changes in expression of adenosine-related genes. Instead, hENT1 expression affects dynamic changes in endogenous adenosine levels, as revealed by altered behavioral responses to drugs that affect adenosine receptor signalling.