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Abstract
This paper re-engages with the science versus religion debate in the light of the last three decades of scholarly progress in the study of religion coming from the cognitive and evolutionary sciences of religion. I begin by asking (1) 'if it is indeed possible to account for the origins of religious belief, its cultural transmission and evolution, and its maintenance—without any appeal to the real existence of any supernatural deity—then are we in a position to say we have explained it all away?' If we are, how does this affect central themes in the philosophy of religion about God's existence? In (2) I provide an outline of the cognitive and evolutionary approach to explaining religion. In section (3) I discuss abductive reasoning (3.1), problems with the accusation of having committed the genetic fallacy when answering (1) in favour of positive atheism (3.2), the need for first-order justifications of religious belief (3.3), and in (3.4) a peculiar divine attribute (i.e. omnipotent potential in a causal chain of events) that appears to immunise religious belief in a particular kind of supernatural deity from having been explained away.

The primary analysis of time‐to‐event data typically makes the censoring at random assumption, that is, that—conditional on covariates in the model—the distribution of event times is the same, whether they are observed or unobserved. In such cases, we need to explore the robustness of inference to more pragmatic assumptions about patients post‐censoring insensitivity analyses. Reference‐based multiple imputation, which avoids analysts explicitly specifying the parameters of the unobserved data distribution, has proved attractive to researchers. Building on results for longitudinal continuous data, we show that inference using a Tobit regression imputation model for reference‐based sensitivity analysis with right censored log normal data isinformation anchored, meaning the proportion of information lost due to missing data under the primary analysis is held constant across the sensitivity analyses. We illustrate our theoretical results using simulation and a clinical trial case study.

AbstractIntroduction: Chronic immune activation due to ongoing HIV replication may lead to impaired immune responses against opportunistic infections such as tuberculosis (TB). We studied the role of HIV replication as a risk factor for incident TB after starting antiretroviral therapy (ART).Methods: We included all HIV‐positive adult patients (≥16 years) in care between 2000 and 2014 at three ART programmes in South Africa. Patients with previous TB were excluded. Missing CD4 cell counts and HIV‐RNA viral loads at ART start (baseline) and during follow‐up were imputed. We used parametric survival models to assess TB incidence (pulmonary and extrapulmonary) by CD4 cell and HIV‐RNA levels, and estimated the rate ratios for TB by including age, sex, baseline viral loads, CD4 cell counts, and WHO clinical stage in the model. We also used Poisson general additive regression models with time‐updated CD4 and HIV‐RNA values, adjusting for age and sex.Results: We included 44,260 patients with a median follow‐up time of 2.7 years (interquartile range [IQR] 1.0–5.0); 3,819 incident TB cases were recorded (8.6%). At baseline, the median age was 34 years (IQR 28–41); 30,675 patients (69.3%) were female. The median CD4 cell count was 156 cells/µL (IQR 79–229) and the median HIV‐RNA viral load 58,000 copies/mL (IQR 6,000–240,000). Overall TB incidence was 26.2/1,000 person‐years (95% confidence interval [CI] 25.3–27.0). Compared to the lowest viral load category (0–999 copies/mL), the adjusted rate ratio for TB was 1.41 (95% CI 1.15–1.75, p < 0.001) in the highest group (>10,000 copies/mL). Time‐updated analyses for CD4/HIV‐RNA confirmed the association of viral load with the risk for TB.Conclusions: Our results indicate that ongoing HIV replication is an important risk factor for TB, regardless of CD4 cell counts, and underline the importance of early ART start and retention on ART.

AbstractIntroductionSince the beginning of the HIV epidemic in resource‐rich countries, Pneumocystis jirovecii pneumonia (PjP) is one of the most frequent opportunistic AIDS‐defining infections. The Collaboration of Observational HIV Epidemiological Research Europe (COHERE) has shown that primary Pneumocystis jirovecii Pneumonia (PjP) prophylaxis can be safely withdrawn in patients with CD4 counts of 100 to 200 cells/µL if plasma HIV‐RNA is suppressed on combination antiretroviral therapy. Whether this holds true for secondary prophylaxis is not known, and this has proved difficult to determine due to the much lower population at risk.MethodsWe estimated the incidence of secondary PjP by including patient data collected from 1998 to 2015 from the COHERE cohort collaboration according to time‐updated CD4 counts, HIV‐RNA and use of PjP prophylaxis in persons >16 years of age. We fitted a Poisson generalized additive model in which the smoothed effect of CD4 was modelled by a restricted cubic spline, and HIV‐RNA was stratified as low (<400), medium (400 to 10,000) or high (>10,000copies/mL).ResultsThere were 373 recurrences of PjP during 74,295 person‐years (py) in 10,476 patients. The PjP incidence in the different plasma HIV‐RNA strata differed significantly and was lowest in the low stratum. For patients off prophylaxis with CD4 counts between 100 and 200 cells/µL and HIV‐RNA below 400 copies/mL, the incidence of recurrent PjP was 3.9 (95% CI: 2.0 to 5.8) per 1000 py, not significantly different from patients on prophylaxis in the same stratum (1.9, 95% CI: 0.1 to 3.7).ConclusionsHIV viraemia importantly affects the risk of recurrent PjP. In virologically suppressed patients on ART with CD4 counts of 100 to 200/µL, the incidence of PjP off prophylaxis is below 10/1000 py. Secondary PjP prophylaxis may be safely withheld in such patients. While European guidelines recommend discontinuing secondary PjP prophylaxis only if CD4 counts rise above 200 cells/mL, the latest US Guidelines consider secondary prophylaxis discontinuation even in patients with a CD4 count above 100 cells/µL and suppressed viral load. Our results strengthen and support this US recommendation.