ORCID Profile
0000-0002-7756-9831
Current Organisations
University of Southampton
,
National Institute of Allergy and Infectious Diseases
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Publisher: Springer Science and Business Media LLC
Date: 29-03-2023
DOI: 10.1038/S41586-023-05772-8
Abstract: Optimal growth and development in childhood and adolescence is crucial for lifelong health and well-being 1–6 . Here we used data from 2,325 population-based studies, with measurements of height and weight from 71 million participants, to report the height and body-mass index (BMI) of children and adolescents aged 5–19 years on the basis of rural and urban place of residence in 200 countries and territories from 1990 to 2020. In 1990, children and adolescents residing in cities were taller than their rural counterparts in all but a few high-income countries. By 2020, the urban height advantage became smaller in most countries, and in many high-income western countries it reversed into a small urban-based disadvantage. The exception was for boys in most countries in sub-Saharan Africa and in some countries in Oceania, south Asia and the region of central Asia, Middle East and north Africa. In these countries, successive cohorts of boys from rural places either did not gain height or possibly became shorter, and hence fell further behind their urban peers. The difference between the age-standardized mean BMI of children in urban and rural areas was .1 kg m –2 in the vast majority of countries. Within this small range, BMI increased slightly more in cities than in rural areas, except in south Asia, sub-Saharan Africa and some countries in central and eastern Europe. Our results show that in much of the world, the growth and developmental advantages of living in cities have diminished in the twenty-first century, whereas in much of sub-Saharan Africa they have lified.
Publisher: Proceedings of the National Academy of Sciences
Date: 12-10-2020
Abstract: Viruses have coevolved with their hosts and developed strategies to d en, evade, or subvert the host immune response to provide an advantage to the virus. We show that ectromelia virus (ECTV) encodes a TNF receptor (TNFR) homolog, which provides an advantage to the host and virus by d ening TNF levels and inflammation. Infection of ECTV-resistant mice with a mutant virus lacking viral TNFR (vTNFR) caused significant lung pathology and death due to secretion of excessive levels of TNF and other inflammatory cytokines. In vitro, recombinant vTNFR from ECTV and other orthopoxviruses bound to membrane-associated TNF and down-regulated inflammatory gene expression through reverse signaling. vTNFR benefits the host by enabling survival, potentially facilitating virus spread, which should advantage the virus.
Publisher: Cold Spring Harbor Laboratory
Date: 25-02-2020
DOI: 10.1101/2020.02.24.963520
Abstract: Ectromelia virus (ECTV) causes mousepox, a surrogate mouse model for smallpox caused by variola virus in humans. Both viruses encode tumor necrosis factor receptor (TNFR) homologs termed cytokine response modifier (Crm) proteins, containing a TNF-binding domain and a chemokine-binding domain termed smallpox virus-encoded chemokine receptor (SECRET) domain. Infection of ECTV-resistant C57BL/6 mice with an ECTV CrmD deletion mutant resulted in uniform mortality due to excessive TNF secretion and dysregulated inflammatory cytokine production but viral load was not affected. CrmD d ened lung pathology, leukocyte recruitment and inflammatory cytokines including TNF, IL-6, IL-10 and IFN-γ. Blockade of IL-6, IL-10R or TNF function with monoclonal antibodies reduced lung pathology and provided 60-100% protection from an otherwise lethal infection. IFN-γ caused lung pathology only when both the TNF-binding and SECRET domains were deleted but it was neither necessary nor sufficient to cause pathology when only the CrmD SECRET domain was expressed by virus.
Location: United Kingdom of Great Britain and Northern Ireland
Location: United States of America
No related grants have been discovered for SERGIO PONTEJO.