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While cervix screening using cytology is recommended at 2- to 3-year intervals, given the increased sensitivity of human papillomavirus (HPV)-based screening to detect precancer, HPV-based screening is recommended every 4- to 5-years. As organized cervix screening programs transition from cytology to HPV-based screening with extended intervals, there is some concern that cancers will be missed between screens. Participants in HPV FOr CervicAL Cancer (HPV FOCAL) trial received cytology (Cytology Arm) at 24-month intervals or HPV-based screening (HPV Arm) at 48-month intervals; both arms received co-testing (cytology and HPV testing) at exit. We investigated the results of the co-test to identify participants with cervical intraepithelial neoplasia grade 2 or higher (CIN2+) who would not have had their precancer detected if they had only their arm's respective primary screen. In the Cytology Arm, 25/62 (40.3%) identified CIN2+s were missed by primary screen (ie, normal cytology/positive HPV test) and all 25 had normal cytology at the prior 24-month screen. In the HPV arm, three CIN2+s (3/49, 6.1%) were missed by primary screen (ie, negative HPV test/abnormal cytology). One of these three misses had low-grade cytology findings and would also not have been referred to colposcopy outside of the trial. Multiple rounds of cytology did not detect some precancerous lesions detected with one round of HPV-based screening. In our population, cytology missed more CIN2+, even at shorter screening intervals, than HPV-based screening. This assuages concerns about missed detection postimplementation of an extended interval HPV-based screening program. We recommend that policymakers consider a shift from cytology to HPV-based cervix screening.

Background: Our objective was to describe the characteristics of acute and established HIV infections diagnosedin the Canadian province of British Columbia. Province-wide HIV testing and surveillance data were analyzed toinform recommendations for targeted use of screening algorithms to detect acute HIV infections.Methods: Acute HIV infection was defined as a confirmed reactive HIV p24 antigen test (or HIV nucleic acid test), anon-reactive or reactive HIV EIA screening test and a non-reactive or indeterminate Western Blot. Characteristics ofunique individuals were identified from the British Columbia HIV/AIDS Surveillance System. Primary drug resistanceand HIV subtypes were identified by analyzing HIV pol sequences from residual sera from newly infectedindividuals.Results: From February 2006 to October 2008, 61 individuals met the acute HIV infection case definition,representing 6.2% of the 987 newly diagnosed HIV infections during the analysis period. Acute HIV infection caseswere more likely to be men who have sex with men (crude OR 1.71; 95% CI 1.01-2.89], to have had a documentedprevious negative HIV test result (crude OR 2.89; 95% CI 1.52-5.51), and to have reported a reason for testing dueto suspected seroconversion symptoms (crude OR 5.16; 95% CI 2.88-9.23). HIV subtypes and rates of transmitteddrug resistance across all classes of drugs were similar in persons with both acute and established HIV infections.Conclusions: Targeted screening to detect acute HIV infection is a logical public health response to the HIVepidemic. Our findings suggest that acute HIV infection screening strategies, in our setting, are helpful for earlydiagnosis in men who have sex with men, in persons with seroconversion symptoms and in previously negativerepeat testers.

COUNTRIES WITH A LOW RISK OF HEPATITIS B (HB) lack data on the effectiveness of universal HB vaccination programs for children. British Columbia began a program in 1992, offering HB vaccination to 11 year olds. We conducted an anonymous, unlinked serologic survey 7 years later, analyzing a random sample of specimens (n = 1215) from women aged 15–44 years who had undergone antenatal rubella testing. Among those aged 15–19 years inclusive there was no evidence of chronic HB (HB surface antigen), the proportion with evidence of acute HB (anti-HB core antibody) was only 0.6% (compared with 6.5% for the entire sample), and evidence of protective immunity was strong: the prevalence of anti-HB surface antibody (anti-HBs) was 79.1% (compared with 41.4% for the entire sample) and the geometric mean titre was 34.9 IU/mL (compared with 0.6–0.8 IU/mL for the older groups [p < 0.001]).

Background: We characterized the twin epidemics of new and prevalent hepatitis C virus (HCV) infections in British Columbia, Canada to inform prevention, care and treatment programs. Methods: The BC Hepatitis Testers Cohort (BC-HTC) includes individuals tested for HCV, HIV or reported as a case of HBV, HCV, HIV or active TB between 1990–2013 linked with data on their medical visits, hospitalizations, cancers, prescription drugs and mortality. Prevalent infection was defined as being anti-HCV positive at first test. Those with a negative test followed by a positive test were considered seroconverters or new infections. Results: Of 1,132,855 individuals tested for HCV, 64,634 (5.8 %) were positive and an additional 3092 cases tested positive elsewhere for a total of 67,726. Of 55,781 HCV positive individuals alive at the end of 2013, 7064 were seroconverters while 48,717 had prevalent infection at diagnosis. The HCV positivity rate (11.2 %) was highest in birth cohort 1945–1964 which declined over time. New infections were more likely to be male, 15–34 years of age (born 1965-1984), HIV- or HBV-coinfected, socioeconomically disadvantaged, have problematic drug and alcohol use and a mental health illness. The profile was similar for individuals with prevalent infection, except for lower odds of HBV-coinfection, major mental health diagnoses and birth cohort >1975. Conclusions: The HCV positivity rate is highest in birth cohort 1945–1964 which represents most prevalent infections. New infections occur in younger birth cohorts who are commonly coinfected with HIV and/or HBV, socioeconomically marginalized, and living with mental illness and addictions.

Definitions for comorbid conditions. Table S2. Distribution HCV seroconverters by seroconversion interval in BC HTC, Canada 1990-2013. Table S3. Characteristics of currently alive recently diagnosed (2010-2013) HCV positive and negative individuals, BC-HTC, 2010 - 2013. Table S4. Percentage positive for hepatitis C by diagnosis year and birth cohort in British Columbia, 1992-2013. Figure S1. Hepatitis C percentage positive by year of diagnosis and birth cohort, BC-HTC, British Columbia, Canada, 2000-2013. Table S5. Multivariable multinomial logistic regression model for factors associated with seroconversion and chronic HCV infection including age as covariate in BC HTC, Canada 1990-2012 a,b. Table S6. Multivariable multinomial logistic regression model for factors associated with seroconversion and chronic HCV infection including indicators for recent risk activities in BC HTC, Canada 1990-2012 a,b. (DOCX 68 kb)

Definitions for comorbid conditions. Table S2. Distribution HCV seroconverters by seroconversion interval in BC HTC, Canada 1990-2013. Table S3. Characteristics of currently alive recently diagnosed (2010-2013) HCV positive and negative individuals, BC-HTC, 2010 - 2013. Table S4. Percentage positive for hepatitis C by diagnosis year and birth cohort in British Columbia, 1992-2013. Figure S1. Hepatitis C percentage positive by year of diagnosis and birth cohort, BC-HTC, British Columbia, Canada, 2000-2013. Table S5. Multivariable multinomial logistic regression model for factors associated with seroconversion and chronic HCV infection including age as covariate in BC HTC, Canada 1990-2012 a,b. Table S6. Multivariable multinomial logistic regression model for factors associated with seroconversion and chronic HCV infection including indicators for recent risk activities in BC HTC, Canada 1990-2012 a,b. (DOCX 68 kb)

Supplemental material, sj-pdf-1-tam-10.1177_1758835921992987 for Elevated risk of colorectal, liver, and pancreatic cancers among HCV, HBV and/or HIV (co)infected individuals in a population based cohort in Canada by Maryam Darvishian, Zahid A. Butt, Stanley Wong, Eric M. Yoshida, Jaskaran Khinda, Michael Otterstatter, Amanda Yu, Mawuena Binka, Carmine Rossi, Geoff McKee, Margo Pearce, Maria Alvarez, Jason Wong, Darrel Cook, Troy Grennan, Jane Buxton, Mark Tyndall, Ryan Woods, Mel Krajden, Parveen Bhatti and Naveed Z. Janjua in Therapeutic Advances in Medical Oncology

Background: In the HPV FOCAL trial, we will establish the efficacy of hr-HPV DNA testing as a stand-alone screening test followed by liquid based cytology (LBC) triage of hr-HPV-positive women compared to LBC followed by hr-HPV triage with ≥ CIN3 as the outcome. Methods/Design: HPV-FOCAL is a randomized, controlled, three-armed study over a four year period conducted in British Columbia. It will recruit 33,000 women aged 25-65 through the province's population based cervical cancer screening program. Control arm: LBC at entry and two years, and combined LBC and hr-HPV at four years among those with initial negative results and hr-HPV triage of ASCUS cases; Two Year Safety Check arm: hr-HPV at entry and LBC at two years in those with initial negative results with LBC triage of hr-HPV positives; Four Year Intervention Arm: hr-HPV at entry and combined hr-HPV and LBC at four years among those with initial negative results with LBC triage of hr-HPV positive cases Discussion: To date, 6150 participants have a completed sample and epidemiologic questionnaire. Of the 2019 women enrolled in the control arm, 1908 (94.5%) were cytology negative. Women aged 25-29 had the highest rates of HSIL (1.4%). In the safety arm 92.2% of women were hr-HPV negative, with the highest rate of hr-HPV positivity found in 25-29 year old women (23.5%). Similar results were obtained in the intervention arm HPV FOCAL is the first randomized trial in North America to examine hr-HPV testing as the primary screen for cervical cancer within a population-based cervical cancer screening program. Trial Registration: International Standard Randomised Controlled Trial Number Register, ISRCTN79347302

Table S1. Baseline Digene HC2/Roche COBAS Results Stratified by LA and Cytology. Table S2. Baseline Digene HC2 and Roche COBAS Abnormal Cytology Rates Stratified by Linear Array Genotyping. (DOCX 16 kb)

Table S1. Baseline Digene HC2/Roche COBAS Results Stratified by LA and Cytology. Table S2. Baseline Digene HC2 and Roche COBAS Abnormal Cytology Rates Stratified by Linear Array Genotyping. (DOCX 16 kb)

Supplemental material, sj-pdf-1-tam-10.1177_1758835921992987 for Elevated risk of colorectal, liver, and pancreatic cancers among HCV, HBV and/or HIV (co)infected individuals in a population based cohort in Canada by Maryam Darvishian, Zahid A. Butt, Stanley Wong, Eric M. Yoshida, Jaskaran Khinda, Michael Otterstatter, Amanda Yu, Mawuena Binka, Carmine Rossi, Geoff McKee, Margo Pearce, Maria Alvarez, Jason Wong, Darrel Cook, Troy Grennan, Jane Buxton, Mark Tyndall, Ryan Woods, Mel Krajden, Parveen Bhatti and Naveed Z. Janjua in Therapeutic Advances in Medical Oncology