Chinese scientists find all the genetic building blocks of SARS in a single population of horseshoe bats.

After a detective hunt across China, researchers chasing the origin of the deadly SARS virus have finally found their smoking gun. In a remote cave in Yunnan province, virologists have identified a single population of horseshoe bats that harbours virus strains with all the genetic building blocks of the one that jumped to humans in 2002, killing almost 800 people around the world.

The killer strain could easily have arisen from such a bat population, the researchers report in PLoS Pathogens1 on 30 November. They warn that the ingredients are in place for a similar disease to emerge again.

In late 2002, cases of a mystery pneumonia-like illness began occurring in Guangdong province, southeastern China. The disease, dubbed severe acute respiratory syndrome (SARS), triggered a global emergency as it spread around the world in 2003, infecting thousands of people.

Scientists identified the culprit as a strain of coronavirus and found genetically similar viruses in masked palm civets (Paguma larvata) sold in Guangdong’s animal markets. Later surveys revealed large numbers of SARS-related coronaviruses circulating in China’s horseshoe bats (Rhinolophus)2 — suggesting that the deadly strain probably originated in the bats, and later passed through civets before reaching humans. But crucial genes — for a protein that allows the virus to latch onto and infect cells — were different in the human and known bat versions of the virus, leaving room for doubt about this hypothesis.

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Mantenere il giusto grado di umidità e un adeguato ricambio d’aria evita la propagazione del virus negli ambienti al chiuso, specialmente dove il rischio è più alto, come ospedali e studi medici. Lo conferma uno studio internazionale condotto, tra gli altri, da ricercatori Cnr-Isac e pubblicato sull’International Journal of Environmental Research and Public Health.

È risaputo che il Sars-Cov-2 non si trasmette solo per contatto diretto, ma può diffondersi attraverso l’aria tramite “droplet”, le goccioline di saliva nebulizzata. “Sebbene il virus, di per sè, abbia dimensioni dell’ordine di un centinaio di nanometri (il diametro di un capello è di 50.000-180.000 nanometri), è verificato che una persona infetta, attraverso la respirazione, la vocalizzazione, la tosse, gli starnuti, può emettere un aerosol contenente potenzialmente il SARS-CoV-2”, spiega Francesca Costabile, ricercatrice dell’Istituto di scienze dell’atmosfera e del clima del Consiglio nazionale delle ricerche (Cnr-Isac).
Uno studio pubblicato sull’International Journal of Environmental Research and Public Health da Cnr-Isac, in collaborazione con il tedesco Leibniz Institute for Tropospheric Research, il CSIR-National Physical Laboratory indiano e il 2B Technologies- Boulder (USA), suggerisce opportune strategie di prevenzione e mitigazione del rischio di trasmissione aerea del virus.

Mentre il mondo affronta la seconda ondata di COVID-19, che trova le sue radici profonde nei nostri impatti sulla natura (come già anticipato nel report WWF  “Pandemie, l’effetto boomerang della distruzione degli ecosistemi” e rilanciato dal recente report IPBES  Escaping the ‘Era of Pandemics’) è sempre più chiaro come un’altra delle emergenze globali stia mettendo sempre più a rischio la nostra salute e la nostra stessa sicurezza: il cambiamento climatico.

Oggi come non mai siamo in grado di valutare quanto sia importante essere pronti ad affrontare le emergenze sanitarie globali. Proprio per questa ragione è necessario prevedere i rischi legati al cambiamento climatico in atto anche nelle politiche sanitarie nazionali. Proprio in questi giorni la rivista Scientific American ha lanciato un appello per l’istituzione di un Istituto Nazionale su Clima e Salute negli USA (We Need a National Institute of Climate Change and Health - Scientific American). Anche l’Europa e l’Italia devono prepararsi a impatti che non potremo più evitare, oltre che fare di tutto per evitare gli impatti peggiori.

Abstract

Lactoferrin (Lf) is an iron-binding glycoprotein of the transferrin family, which is expressed in most biological fluids with particularly high levels in mammalian milk. Its multiple activities lie in its capacity to bind iron and to interact with the molecular and cellular components of hosts and pathogens. Lf can bind and sequester lipopolysaccharides, thus preventing pro-inflammatory pathway activation, sepsis and tissue damages. Lf is also considered a cell-secreted mediator that bridges the innate and adaptive immune responses. In the recent years much has been learned about the mechanisms by which Lf exerts its activities. This review summarizes the recent advances in understanding the mechanisms underlying the multifunctional roles of Lf, and provides a future perspective on its potential prophylactic and therapeutic applications.

https://www.nature.com/articles/aps2013200

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