David Simons

Dr. David Simons

orcid

Research Focus & Metrics

Academic Career Length

33Years (1994-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

View All Publications
2 March 2022 in New England Journal of Medicine
Verified
Journal Article
Closed access
PDF file
NANick Andrews
Nick Andrews
JSJulia Stowe
Julia Stowe
FKFreja Kirsebom
Freja Kirsebom
STSamuel Toffa
Samuel Toffa
TRTim Rickeard
Tim Rickeard
JBJamie Lopez Bernal
Jamie Lopez Bernal
A rapid increase in coronavirus disease 2019 (Covid-19) cases due to the omicron (B.1.1.529) variant of severe acute respiratory syndrome coronavirus 2 in highly vaccinated populations has aroused concerns about the effectiveness of current vaccines. We used a test-negative case–control design to estimate vaccine effectiveness against symptomatic disease caused by the omicron and delta (B.1.617.2) variants in England. Vaccine effectiveness was calculated after primary immunization with two doses of BNT162b2 (Pfizer–BioNTech), ChAdOx1 nCoV-19 (AstraZeneca), or mRNA-1273 (Moderna) vaccine and after a booster dose of BNT162b2, ChAdOx1 nCoV-19, or mRNA-1273. Between November 27, 2021, and January 12, 2022, a total of 886,774 eligible persons infected with the omicron variant, 204,154 eligible persons infected with the delta variant, and 1,572,621 eligible test-negative controls were identified. At all time points investigated and for all combinations of primary course and booster vaccines, vaccine effectiveness against symptomatic disease was higher for the delta variant than for the omicron variant. No effect against the omicron variant was noted from 20 weeks after two ChAdOx1 nCoV-19 doses, whereas vaccine effectiveness after two BNT162b2 doses was 65.5% (95% confidence interval [CI], 63.9 to 67.0) at 2 to 4 weeks, dropping to 8.8% (95% CI, 7.0 to 10.5) at 25 or more weeks. Among ChAdOx1 nCoV-19 primary course recipients, vaccine effectiveness increased to 62.4% (95% CI, 61.8 to 63.0) at 2 to 4 weeks after a BNT162b2 booster before decreasing to 39.6% (95% CI, 38.0 to 41.1) at 10 or more weeks. Among BNT162b2 primary course recipients, vaccine effectiveness increased to 67.2% (95% CI, 66.5 to 67.8) at 2 to 4 weeks after a BNT162b2 booster before declining to 45.7% (95% CI, 44.7 to 46.7) at 10 or more weeks. Vaccine effectiveness after a ChAdOx1 nCoV-19 primary course increased to 70.1% (95% CI, 69.5 to 70.7) at 2 to 4 weeks after an mRNA-1273 booster and decreased to 60.9% (95% CI, 59.7 to 62.1) at 5 to 9 weeks. After a BNT162b2 primary course, the mRNA-1273 booster increased vaccine effectiveness to 73.9% (95% CI, 73.1 to 74.6) at 2 to 4 weeks; vaccine effectiveness fell to 64.4% (95% CI, 62.6 to 66.1) at 5 to 9 weeks. Primary immunization with two doses of ChAdOx1 nCoV-19 or BNT162b2 vaccine provided limited protection against symptomatic disease caused by the omicron variant. A BNT162b2 or mRNA-1273 booster after either the ChAdOx1 nCoV-19 or BNT162b2 primary course substantially increased protection, but that protection waned over time. (Funded by the U.K. Health Security Agency.)

1 October 2020 in The Lancet Infectious Diseases
Verified
Journal Article
Open access
AKAdam J Kucharski
Adam J Kucharski
PKPetra Klepac
Petra Klepac
ACAndrew J K Conlan
Andrew J K Conlan
SKStephen M Kissler
Stephen M Kissler
MTMaria L Tang
Maria L Tang
DSDavid Simons
David Simons
The isolation of symptomatic cases and tracing of contacts has been used as an early COVID-19 containment measure in many countries, with additional physical distancing measures also introduced as outbreaks have grown. To maintain control of infection while also reducing disruption to populations, there is a need to understand what combination of measures-including novel digital tracing approaches and less intensive physical distancing-might be required to reduce transmission. We aimed to estimate the reduction in transmission under different control measures across settings and how many contacts would be quarantined per day in different strategies for a given level of symptomatic case incidence. For this mathematical modelling study, we used a model of individual-level transmission stratified by setting (household, work, school, or other) based on BBC Pandemic data from 40 162 UK participants. We simulated the effect of a range of different testing, isolation, tracing, and physical distancing scenarios. Under optimistic but plausible assumptions, we estimated reduction in the effective reproduction number and the number of contacts that would be newly quarantined each day under different strategies. We estimated that combined isolation and tracing strategies would reduce transmission more than mass testing or self-isolation alone: mean transmission reduction of 2% for mass random testing of 5% of the population each week, 29% for self-isolation alone of symptomatic cases within the household, 35% for self-isolation alone outside the household, 37% for self-isolation plus household quarantine, 64% for self-isolation and household quarantine with the addition of manual contact tracing of all contacts, 57% with the addition of manual tracing of acquaintances only, and 47% with the addition of app-based tracing only. If limits were placed on gatherings outside of home, school, or work, then manual contact tracing of acquaintances alone could have an effect on transmission reduction similar to that of detailed contact tracing. In a scenario where 1000 new symptomatic cases that met the definition to trigger contact tracing occurred per day, we estimated that, in most contact tracing strategies, 15 000-41 000 contacts would be newly quarantined each day. Consistent with previous modelling studies and country-specific COVID-19 responses to date, our analysis estimated that a high proportion of cases would need to self-isolate and a high proportion of their contacts to be successfully traced to ensure an effective reproduction number lower than 1 in the absence of other measures. If combined with moderate physical distancing measures, self-isolation and contact tracing would be more likely to achieve control of severe acute respiratory syndrome coronavirus 2 transmission. Wellcome Trust, UK Engineering and Physical Sciences Research Council, European Commission, Royal Society, Medical Research Council.

17 November 2020 in Addiction
Verified
Journal Article
Open access
DSDavid Simons
David Simons
Lion ShahabLion Shahab
Lion Shahab
JBJamie Brown
Jamie Brown
OPOlga Perski
Olga Perski
Aims: To estimate the association of smoking status with rates of (i) infection, (ii) hospitalization, (iii) disease severity and (iv) mortality from SARS‐CoV‐2/COVID‐19 disease.Design: Living rapid review of observational and experimental studies with random‐effects hierarchical Bayesian meta‐analyses. Published articles and pre‐prints were identified via MEDLINE and medRxiv.Setting: Community or hospital, no restrictions on location.Participants: Adults who received a SARS‐CoV‐2 test or a COVID‐19 diagnosis.Measurements: Outcomes were SARS‐CoV‐2 infection, hospitalization, disease severity and mortality stratified by smoking status. Study quality was assessed (i.e. ‘good’, ‘fair’ and ‘poor’).Findings: Version 7 (searches up to 25 August 2020) included 233 studies with 32 ‘good’ and ‘fair’ quality studies included in meta‐analyses. Fifty‐seven studies (24.5%) reported current, former and never smoking status. Recorded smoking prevalence among people with COVID‐19 was generally lower than national prevalence. Current compared with never smokers were at reduced risk of SARS‐CoV‐2 infection [relative risk (RR) = 0.74, 95% credible interval (CrI) = 0.58–0.93, τ = 0.41]. Data for former smokers were inconclusive (RR = 1.05, 95% CrI = 0.95–1.17, τ = 0.17), but favoured there being no important association (21% probability of RR ≥ 1.1). Former compared with never smokers were at somewhat increased risk of hospitalization (RR = 1.20, CrI = 1.03–1.44, τ = 0.17), greater disease severity (RR = 1.52, CrI = 1.13–2.07, τ = 0.29) and mortality (RR = 1.39, 95% CrI = 1.09–1.87, τ = 0.27). Data for current smokers were inconclusive (RR = 1.06, CrI = 0.82–1.35, τ = 0.27; RR = 1.25, CrI = 0.85–1.93, τ = 0.34; RR = 1.22, 95% CrI = 0.78–1.94, τ = 0.49, respectively), but favoured there being no important associations with hospitalization and mortality (35% and 70% probability of RR ≥ 1.1, respectively) and a small but important association with disease severity (79% probability of RR ≥ 1.1).Conclusions: Compared with never smokers, current smokers appear to be at reduced risk of SARS‐CoV‐2 infection, while former smokers appear to be at increased risk of hospitalization, increased disease severity and mortality from COVID‐19. However, it is uncertain whether these associations are causal.

1 April 2020 in International Journal of Infectious Diseases
Verified
Journal Article
Open access
NKNathan Kapata
Nathan Kapata
CIChikwe Ihekweazu
Chikwe Ihekweazu
FNFrancine Ntoumi
Francine Ntoumi
TRTajudeen Raji
Tajudeen Raji
PCPascalina Chanda-Kapata
Pascalina Chanda-Kapata
AZAlimuddin Zumla
Alimuddin Zumla

29 May 2022 in International Journal of Infectious Diseases
Verified
Journal Article
Open access
Najmul HaiderNajmul Haider
Najmul Haider
JGJavier Guitian
Javier Guitian
DSDavid Simons
David Simons
DADanny Akhere Asogun
Danny Akhere Asogun
RARashid Ansumana
Rashid Ansumana
AZAlimuddin Zumla
Alimuddin Zumla
We explain research gaps on Monkeypox (MPX) virus epidemiology in endemic countries and present hypotheses for the recent increase of MPX cases in West Africa as a possible explanation for the current epidemic in Europe, America, and Australia. The detection of >400 MPX cases in less than a month in May 2022, across many countries underscores the epidemic potential of MPX in humans and demonstrates several important research gaps. First, the true burden of MPX in West and Central Africa is poorly understood, although it is critical for prevention and control of future outbreaks. Second, the diversity and extent of the animal reservoir remain unknown. We hypothesize that the synanthropic rodent population has increased in recent years in Africa leading to more human-rodent interactions and thus increased transmission of MPXV. We further hypothesise that nearly 45 years after the end of routine smallpox vaccination, the larger and more interconnected immune-naïve population has crossed a threshold resulting in more sustainable human-to-human transmission of MPXV. The current epidemic in the Western World is possibly a consequence of increased local transmission of MPXV in Africa. A new estimation of the basic and effective reproduction rate (R0 and Re) in different populations is required. National, regional, and international collaborations are needed to address research gaps related to MPX outbreaks.

22 November 2022 in International Health
Verified
Journal Article
Open access
PDF file
DSDavid Simons
David Simons
Background: Lassa fever is a viral haemorrhagic fever endemic to eight West African countries. Symptomatic disease is expected to occur in 20% of those infected and transmission typically occurs from viral spillover from rodent hosts. The combination of limited access to diagnostics and healthcare means the true burden of this disease is unknown. Methods: The case fatality rate among confirmed, probable and possible cases of Lassa fever in endemic regions is expected to be ≈15%. Here, annual reported cases and deaths have been used to estimate the case fatality rate, using three subsets of available data, to understand the scale of underreporting of severe human cases. Results: The literature review produced 38 records of cases and fatalities, comprising 5230 reported cases and 1482 reported deaths in seven countries. The estimated case fatality rate ranges from 16.5 to 25.6% (standard deviation 11.5–32.2). The expected number of severe cases between 2012 and 2022 is 8995, with current reported numbers 58% of what is expected. Conclusion: This analysis highlights current uncertainty and systemic underreporting of the morbidity and mortality burden of Lassa fever in its endemic region and must be considered when discussing the epidemiology of this neglected tropical disease.