ObjectivesTo estimate occupational differences in COVID-19 mortality and test whether these are confounded by factors such as regional differences, ethnicity and education or due to non-workplace factors, such as deprivation or prepandemic health.MethodsUsing a cohort study of over 14 million people aged 40–64 years living in England, we analysed occupational differences in death involving COVID-19, assessed between 24 January 2020 and 28 December 2020.We estimated age-standardised mortality rates (ASMRs) per 100 000 person-years at risk stratified by sex and occupation. We estimated the effect of occupation on COVID-19 mortality using Cox proportional hazard models adjusted for confounding factors. We further adjusted for non-workplace factors and interpreted the residual effects of occupation as being due to workplace exposures to SARS-CoV-2.ResultsIn men, the ASMRs were highest among those working as taxi and cab drivers or chauffeurs at 119.7 deaths per 100 000 (95% CI 98.0 to 141.4), followed by other elementary occupations at 106.5 (84.5 to 132.4) and care workers and home carers at 99.2 (74.5 to 129.4). Adjusting for confounding factors strongly attenuated the HRs for many occupations, but many remained at elevated risk. Adjusting for living conditions reduced further the HRs, and many occupations were no longer at excess risk. For most occupations, confounding factors and mediators other than workplace exposure to SARS-CoV-2 explained 70%–80% of the excess age-adjusted occupational differences.ConclusionsWorking conditions play a role in COVID-19 mortality, particularly in occupations involving contact with patients or the public. However, there is also a substantial contribution from non-workplace factors.

Data were collected from 104 infected children who were followed up from birth for a mean of 49 (range, 6-153) months in 22 European centers, to outline the natural history of perinatal hepatitis C virus (HCV) infection. Fifty-four children were persistently HCV RNA positive, 44 were occasionally positive, and 6 never had detectable viremia. At least 90% of the children had evidence of ongoing infection at the latest analysis. Eighteen children became HCV RNA negative at their last assessments, but 40% of these had high alanine aminotransferase (ALT) concentrations. Infection was asymptomatic in all but 2 children, who developed hepatomegaly. Mean ALT concentrations decreased substantially after the first 2 years of life; 14 children had persistently normal ALT values. Signs of minimal to moderate inflammation were noted in all 20 patients who underwent liver biopsy. Perinatal HCV infection is usually asymptomatic in the first years of life, but the virus persists in most children, even in the absence of elevated ALT activity.

Objective: To investigate when hepatitis C virus (HCV) infection from mother to child occurs, and evaluate possible associated factors. Design: Prospective cohort study. Patients: Fifty four HCV infected children tested within three days of birth and their mothers. Main outcome measures: HCV RNA polymerase chain reaction (PCR) results. Results: Seventeen of the children (31%, 95% confidence interval 19% to 46%) were positive in the first 3 days of life and could be assumed to have acquired infection in utero. Testing PCR positive was not associated with sex (53% v 49% boys; p = 0.77) or mode of delivery (29% elective caesarean section in both groups; p = 0.98). Children with evidence of intrauterine infection were significantly more likely to be of lower birth weight and infected with genotype 1 (58% v 12%, p = 0.01). Although a higher proportion of infants born to HCV/HIV co-infected women were PCR positive in the first 3 days of life, this difference did not reach statistical significance; excluding infants born to co-infected women did not affect the results. Thirty seven of the children (68%) were negative in the first 3 days of life, 27 of whom were positive when tested again at 3 months, and nine were first PCR positive after 3 months (one child had no further tests). Conclusions: These results suggest that at least one third and up to a half of infected children acquired infection in utero. Although postpartum transmission cannot be excluded, these data suggest that it is rare. The role of HCV genotypes in the timing and mechanism of infection should be explored further.

ObjectiveTo estimate the seroprevalence of cytomegalovirus (CMV), Epstein Barr virus (EBV) and varicella zoster virus (VZV) among pregnant women in Bradford by ethnic group and country of birth.MethodsA stratified random sample of 949 pregnant women enrolled in the Born in Bradford birth cohort was selected to ensure sufficient numbers of White UK born women, Asian UK born women and Asian women born in Asia. Serum samples taken at 24-28 weeks’ gestation were tested for CMV IgG, EBV IgG and VZV IgG. Each woman completed a questionnaire which included socio-demographic information.ResultsCMV seroprevalence was 49% among the White British women, 89% among South Asian UK born women and 98% among South Asian women born in South Asia. These differences remained after adjusting for socio-demographic factors. In contrast, VZV seroprevalence was 95% among women born in the UK but significantly lower at 90% among South Asian women born in Asia. EBV seroprevalence was 94% overall and did not vary by ethnic group/country of birth. ConclusionsAlthough about half of White British women are at risk of primary CMV infection in pregnancy and the associated increased risk of congenital infection, most congenital CMV infections are likely to be in children born to South Asian women with non-primary infection during pregnancy. South Asian women born in South Asia are at risk of VZV infection during pregnancy which could produce congenital varicella syndrome or perinatal chickenpox. Differences in CMV and VZV seroprevalence by ethnic group and country of birth must be taken into account when universal immunisation against these viruses is contemplated.

These reference ranges represent a unique investigation of ALT levels in a healthy child population. We show lower and more detailed age-related cutoffs of normality than available. Additionally, we demonstrate a significant effect of sex on ALT reference ranges, which has not previously been described in children younger than 5 years of age.