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ABSTRACT The COVID-19 pandemic highlighted the critical need for rapid and accurate molecular diagnostic testing. The Cue COVID-19 Point-of-Care Test (Cue POCT) is a nucleic acid amplification test (NAAT), authorized by Health Canada and FDA as a POCT for SARS-CoV-2 detection. Cue POCT was deployed at a network of clinics in Ontario, Canada with n = 13,848 patrons tested between 17 July 2021 and 31 January 2022. The clinical performance and operational experience with Cue POCT were examined for this testing population composed mostly of asymptomatic individuals (93.7%). A head-to-head prospective clinical verification was performed between 17 July and 4 October for all POCT service clients (n = 3,037) with paired COVID-19 testing by Cue and RT-PCR. Prospective verification demonstrated a clinical sensitivity of 100% and clinical specificity of 99.4% for Cue COVID-19 POCT. The lack of false negatives and low false positive rate (0.64%), underscores the high accuracy (99.4%) of Cue POCT to provide rapid PCR quality results. Low error rates (cancellation rate of 0% and invalid rate of 0.63%) with the current software version were additionally noted. Taken together, these findings highlight the value of accurate molecular COVID-19 POCT in a distributed service delivery model to rapidly detect cases in the community with the potential to curb transmission in high-exposure settings (i.e., in-flight, congregate workplace, and social events). The insights gleaned from this operational implementation are readily transferable to future POCT diagnostic services. IMPORTANCE This manuscript reports on the findings of a large asymptomatic population who underwent surveillance COVID testing on the Cue COVID-19 Point-of-Care Test (POCT). Review of test performance of this rapid molecular POCT, as compared to gold standard RT-PCR, is valuable to many audiences, including public health, emergency testing services, employers, and the general population of consumers who are seeking a user-friendly, accurate, cost-effective, and sustainable testing model for COVID screening. The findings from this operational experience also inform future models of POCT services beyond COVID.

We analyzed population-based surveillance data from the Toronto Invasive Bacterial Diseases Network to describe carbapenemase-producing Enterobacteriaceae (CPE) infections during 2007–2015 in south-central Ontario, Canada. We reviewed patients’ medical records and travel histories, analyzed microbiologic and clinical characteristics of CPE infections, and calculated incidence. Among 291 cases identified, New Delhi metallo-β-lactamase was the predominant carbapenemase (51%). The proportion of CPE-positive patients with prior admission to a hospital in Canada who had not received healthcare abroad or traveled to high-risk areas was 13% for patients with oxacillinase-48, 24% for patients with New Delhi metallo-β-lactamase, 55% for patients with Klebsiella pneumoniae carbapenemase, and 67% for patients with Verona integron-encoded metallo-β-lactamase. Incidence of CPE infection increased, reaching 0.33 cases/100,000 population in 2015. For a substantial proportion of patients, no healthcare abroad or high-risk travel could be established, suggesting CPE acquisition in Canada. Policy and practice changes are needed to mitigate nosocomial CPE transmission in hospitals in Canada.

BackgroundWe designed a seroprevalence study using multiple testing assays and population sources to estimate the community seroprevalence of pH1N1/09 and risk factors for infection before the outbreak was recognized and throughout the pandemic to the end of 2009/10 influenza season.MethodsResidual serum specimens from five time points (between 01/2009 and 05/2010) and samples from two time points from a prospectively recruited cohort were included. The distribution of risk factors was explored in multivariate adjusted analyses using logistic regression among the cohort. Antibody levels were measured by hemagglutination inhibition (HAI) and microneutralization (MN) assays.ResultsResidual sera from 3375 patients and 1024 prospectively recruited cohort participants were analyzed. Pre-pandemic seroprevalence ranged from 2%-12% across age groups. Overall seropositivity ranged from 10%-19% post-first wave and 32%-41% by the end of the 2009/10 influenza season. Seroprevalence and risk factors differed between MN and HAI assays, particularly in older age groups and between waves. Following the H1N1 vaccination program, higher GMT were noted among vaccinated individuals. Overall, 20-30% of the population was estimated to be infected.ConclusionsCombining population sources of sera across five time points with prospectively collected epidemiological information yielded a complete description of the evolution of pH1N1 infection.

We evaluated a cohort of Canadian donors for T cell and antibody responses against influenza A/California/7/2009 (pH1N1) at 8-10 months after the 2nd pandemic wave by flow cytometry and microneutralization assays. Memory CD8 T cell responses to pH1N1 were detectable in 58% (61/105) of donors. These responses were largely due to cross-reactive CD8 T cell epitopes as, for those donors tested, similar recall responses were obtained to A/California 2009 and A/PR8 1934 H1N1 Hviruses. Longitudinal analysis of a single infected individual showed only a small and transient increase in neutralizing antibody levels, but a robust CD8 T cell response that rose rapidly post symptom onset, peaking at 3 weeks, followed by a gradual decline to the baseline levels seen in a seroprevalence cohort post-pandemic. The magnitude of the influenza-specific CD8 T cell memory response at one year post-pandemic was similar in cases and controls as well as in vaccinated and unvaccinated donors, suggesting that any T cell boosting from infection was transient. Pandemic H1-specific antibodies were only detectable in approximately half of vaccinated donors. However, those who were vaccinated within a few months following infection had the highest persisting antibody titers, suggesting that vaccination shortly after influenza infection can boost or sustain antibody levels. For the most part the circulating influenza-specific T cell and serum antibody levels in the population at one year post-pandemic were not different between cases and controls, suggesting that natural infection does not lead to higher long term T cell and antibody responses in donors with pre-existing immunity to influenza. However, based on the responses of one longitudinal donor, it is possible for a small population of pre-existing cross-reactive memory CD8 T cells to expand rapidly following infection and this response may aid in viral clearance and contribute to a lessening of disease severity.

AbstractWe conducted a comprehensive cross-sectional analysis of total and HIV-specific cervical antibody levels in HIV-1-resistant, uninfected, and infected women in order to examine the role of HIV-specific antibody responses in the female genital tract and examine the effect on antibody levels of various epidemiologic factors in this population. Cervical lavages were collected from 272 subjects of the Pumwani commercial sex worker cohort. Total and HIV-specific genital tract IgA and IgG levels were measured using an ELISA and correlated with behavioral and demographic factors. No significant difference was seen between cervical HIV-specific IgA levels in infected, uninfected, and resistant individuals, nor were any correlations between cervical HIV-specific IgA and neutralization capacity or viral shedding seen. We did, however, note increased HIV-specific IgA in HIV-negative women with four or more clients per day, and decreased HIV-specific IgA in both long-term nonprogressors and long-term survivors. These results show that there is not a strong cohort-wide correlation between HIV-specific cervical IgA levels and resistance to infection by HIV-1 as previously believed, but there is a correlation between exposure to HIV and HIV-specific cervical IgA. Our findings do not preclude the possibility that functional differences in the cervical IgA of HEPS women may play a role in resistance, but argue that HIV-specific responses may not be a universal protective factor. They also indicate that resistance to HIV is a complex condition related to more factors than exposure. Further studies of correlates of immune protection in these individuals would be beneficial to the field. [ABSTRACT FROM AUTHOR]