Πραγματικά τρομακτικά είναι τα αποτελέσματα μελέτης που πραγματοποιήθηκε στις ΗΠΑ, με χρηματοδότηση της αμερικανικής κυβέρνηση, σχετικά με τον νέο κορονοϊό.

Σύμφωνα με τα αποτελέσματα αυτής της έρευνας, ο νέος κορονοϊός επιβιώνει για πολλές ώρες έξω από το ανθρώπινο σώμα.

Συγκεκριμένα, στις πλαστικές ή μεταλλικές επιφάνειες ο ιός επιβιώνει για 2 έως 3 μέρες και επάνω στο χαρτόνι για 24 ώρες.

Για τον αέρα, η έρευνα λέει πως η διάρκεια και δυνατότητα επιβίωσής του είναι παρόμοια με τον SARS την περίοδο 2002 - 2003.

ια να διαπιστωθεί η μετάδοση και η διάρκεια ζωής του στον αέρα, οι επιστήμονες χρησιμοποίησαν νεφελοποιητή ώστε να τον διασπείρουν. Βρήκαν στη συνέχεια ότι μπορούσε να εντοπιστεί στον αέρα τρεις περίπου ώρες μετά την διασπορά του.

Αναφορικά με αυτό, ορισμένοι άλλοι επιστήμονες επιχειρηματολόγησαν ενάντια στη χρήση νεφελοποιητή καθώς, σύμφωνα με αυτούς, δεν είναι παρόμοιος με το βήχα ή το φτέρνισμα, και αυξανει την διάρκεια ζωής του ιού.

ι ίδιοι επιστήμονες τονίζουν πως ο βήχας και το φτάρνισμα προκαλούν τον "θάνατο" του ιού μετά από μερικά δευτερόλεπτα.

Βέβαια, δεν απαντούν στο ερώτημα, αν ισχύει η δική τους προσέγγιση, γιατί είναι απαραίτητο να φοράμε μάσκα ώστε να μην ερχόμαστε σε επαφή με τα σταγονίδια τα οποία περιέχουν τον ιό, αν όντως ο ιός "πεθαίνει" δευτερόλεπτα μετά την έξοδό του από το σώμα

[caption id="attachment_6551" align="alignright" width="300"] Η διάρκεια ζωής του νέου κορονοϊού στον αέρα και σε διάφορες επιφάνειες[/caption]

Τέλος, η έρευνα αναφέρει πως η ταχύτερη εξάπλωση της επιδημίας από το SARS, ίσως να οφείλετε στην μετάδοση του ιού εύκολα από έναν φαινομενικά "υγιή" φορέα (χωρίς συμπτώματα) στον υπόλοιπο πληθυσμό.

Αυτό γινεται εμφανές από το γεγονός πως ο νέος κορονοϊός έχει προσβάλει σχεδόν 200.000 ανθρώπους με 8.000 περίπου νεκρούς ενώ ο SARS είχε μολύνει περίπου 8.000 και είχε στοιχίσει τη ζωή σε περίπου 800.

Ανάλογες μελέτες για τον κορονοϊό που προκαλεί το SARS είχαν δείξει πως η δυνατότητα επιβίωσής του εκτός του ανθρώπινου σώματος βρισκόταν σε παρόμοια επίπεδα.

Η έρευνα δημοσιεύθηκε στο επιστημονικό περιοδικό New England Journal of Medicine (NEJM) και σε αυτήν έλεβαν μέρος επιστήμονες από τα Πανεπιστήμια του Los Angeles και του Prinston μαζί με επιστήμονες από το CDC (Κέντρο Ελέγχου και Πρόληψης Ασθενειών).

Όλη η έρευνα στα αγγλικά ΕΔΩκαι ΕΔΩ

"

novel human coronavirus that is now named severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) (formerly called HCoV-19) emerged in Wuhan, China, in late 2019 and is now causing a pandemic.1 We analyzed the aerosol and surface stability of SARS-CoV-2 and compared it with SARS-CoV-1, the most closely related human coronavirus.2

We evaluated the stability of SARS-CoV-2 and SARS-CoV-1 in aerosols and on various surfaces and estimated their decay rates using a Bayesian regression model (see the Methods section in the Supplementary Appendix, available with the full text of this letter at NEJM.org). SARS-CoV-2 nCoV-WA1-2020 (MN985325.1) and SARS-CoV-1 Tor2 (AY274119.3) were the strains used. Aerosols (<5 μm) containing SARS-CoV-2 (105.25 50% tissue-culture infectious dose [TCID50] per milliliter) or SARS-CoV-1 (106.75-7.00 TCID50 per milliliter) were generated with the use of a three-jet Collison nebulizer and fed into a Goldberg drum to create an aerosolized environment. The inoculum resulted in cycle-threshold values between 20 and 22, similar to those observed in samples obtained from the upper and lower respiratory tract in humans.

Our data consisted of 10 experimental conditions involving two viruses (SARS-CoV-2 and SARS-CoV-1) in five environmental conditions (aerosols, plastic, stainless steel, copper, and cardboard). All experimental measurements are reported as means across three replicates.

SARS-CoV-2 remained viable in aerosols throughout the duration of our experiment (3 hours), with a reduction in infectious titer from 103.5 to 102.7 TCID50 per liter of air. This reduction was similar to that observed with SARS-CoV-1, from 104.3 to 103.5 TCID50 per milliliter (Figure 1A).

SARS-CoV-2 was more stable on plastic and stainless steel than on copper and cardboard, and viable virus was detected up to 72 hours after application to these surfaces (Figure 1A), although the virus titer was greatly reduced (from 103.7 to 100.6 TCID50 per milliliter of medium after 72 hours on plastic and from 103.7 to 100.6 TCID50 per milliliter after 48 hours on stainless steel). The stability kinetics of SARS-CoV-1 were similar (from 103.4 to 100.7 TCID50 per milliliter after 72 hours on plastic and from 103.6 to 100.6 TCID50 per milliliter after 48 hours on stainless steel). On copper, no viable SARS-CoV-2 was measured after 4 hours and no viable SARS-CoV-1 was measured after 8 hours. On cardboard, no viable SARS-CoV-2 was measured after 24 hours and no viable SARS-CoV-1 was measured after 8 hours (Figure 1A).

Both viruses had an exponential decay in virus titer across all experimental conditions, as indicated by a linear decrease in the log10TCID50 per liter of air or milliliter of medium over time (Figure 1B). The half-lives of SARS-CoV-2 and SARS-CoV-1 were similar in aerosols, with median estimates of approximately 1.1 to 1.2 hours and 95% credible intervals of 0.64 to 2.64 for SARS-CoV-2 and 0.78 to 2.43 for SARS-CoV-1 (Figure 1C, and Table S1 in the Supplementary Appendix). The half-lives of the two viruses were also similar on copper. On cardboard, the half-life of SARS-CoV-2 was longer than that of SARS-CoV-1. The longest viability of both viruses was on stainless steel and plastic; the estimated median half-life of SARS-CoV-2 was approximately 5.6 hours on stainless steel and 6.8 hours on plastic (Figure 1C). Estimated differences in the half-lives of the two viruses were small except for those on cardboard (Figure 1C). Individual replicate data were noticeably “noisier” (i.e., there was more variation in the experiment, resulting in a larger standard error) for cardboard than for other surfaces (Fig. S1 through S5), so we advise caution in interpreting this result.

We found that the stability of SARS-CoV-2 was similar to that of SARS-CoV-1 under the experimental circumstances tested. This indicates that differences in the epidemiologic characteristics of these viruses probably arise from other factors, including high viral loads in the upper respiratory tract and the potential for persons infected with SARS-CoV-2 to shed and transmit the virus while asymptomatic.3,4 Our results indicate that aerosol and fomite transmission of SARS-CoV-2 is plausible, since the virus can remain viable and infectious in aerosols for hours and on surfaces up to days (depending on the inoculum shed). These findings echo those with SARS-CoV-1, in which these forms of transmission were associated with nosocomial spread and super-spreading events,5 and they provide information for pandemic mitigation efforts.

Neeltje van Doremalen, Ph.D.

enton Bushmaker, B.Sc.

tional Institute of Allergy and Infectious Diseases, Hamilton, MT

Dylan H. Morris, M.Phil.

inceton University, Princeton, NJ

Myndi G. Holbrook, B.Sc.

tional Institute of Allergy and Infectious Diseases, Hamilton, MT

Amandine Gamble, Ph.D.

iversity of California, Los Angeles, Los Angeles, CA

Brandi N. Williamson, M.P.H.

tional Institute of Allergy and Infectious Diseases, Hamilton, MT

Azaibi Tamin, Ph.D.

nnifer L. Harcourt, Ph.D.

talie J. Thornburg, Ph.D.

san I. Gerber, M.D.

nters for Disease Control and Prevention, Atlanta, GA

James O. Lloyd-Smith, Ph.D.

iversity of California, Los Angeles, Los Angeles, CA, Bethesda, MD

Emmie de Wit, Ph.D.

ncent J. Munster, Ph.D.

tional Institute of Allergy and Infectious Diseases, Hamilton, MT

[email protected]

Supported by the Intramural Research Program of the National Institute of Allergy and Infectious Diseases, National Institutes of Health, and by contracts from the Defense Advanced Research Projects Agency (DARPA PREEMPT No. D18AC00031, to Drs. Lloyd-Smith and Gamble), from the National Science Foundation (DEB-1557022, to Dr. Lloyd-Smith), and from the Strategic Environmental Research and Development Program of the Department of Defense (SERDP, RC-2635, to Dr. Lloyd-Smith).

Disclosure forms provided by the authors are available with the full text of this letter at NEJM.org.

The findings and conclusions in this letter are those of the authors and do not necessarily represent the official position of the Centers for Disease Control and Prevention (CDC). Names of specific vendors, manufacturers, or products are included for public health and informational purposes; inclusion does not imply endorsement of the vendors, manufacturers, or products by the CDC or the Department of Health and Human Services.

This letter was published on March 17, 2020, at NEJM.org.

Dr. van Doremalen, Mr. Bushmaker, and Mr. Morris contributed equally to this letter."