Increasing Temperature and Relative Humidity Accelerates Inactivation of SARS-CoV-2 on Surfaces

Mitigating the transmission of SARS-CoV-2 in clinical settings and public spaces is critically important to reduce the number of COVID-19 cases while effective vaccines and therapeutics are under development. SARS-CoV-2 transmission is thought to primarily occur through direct person-to-person trans...

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Hlavní autori: Biryukov, Jennifer, Boydston, Jeremy A., Dunning, Rebecca A., Yeager, John J., Wood, Stewart, Reese, Amy L., Ferris, Allison, Miller, David, Weaver, Wade, Zeitouni, Nathalie E., Phillips, Aaron, Freeburger, Denise, Hooper, Idris, Ratnesar-Shumate, Shanna, Yolitz, Jason, Krause, Melissa, Williams, Gregory, Dawson, David G., Herzog, Artemas, Dabisch, Paul, Wahl, Victoria, Hevey, Michael C., Altamura, Louis A.
Médium: Journal Article
Jazyk:English
Vydavateľské údaje: United States American Society for Microbiology 01.07.2020
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ISSN:2379-5042, 2379-5042
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Abstract Mitigating the transmission of SARS-CoV-2 in clinical settings and public spaces is critically important to reduce the number of COVID-19 cases while effective vaccines and therapeutics are under development. SARS-CoV-2 transmission is thought to primarily occur through direct person-to-person transfer of infectious respiratory droplets or through aerosol-generating medical procedures. However, contact with contaminated surfaces may also play a significant role. In this context, understanding the factors contributing to SARS-CoV-2 persistence on surfaces will enable a more accurate estimation of the risk of contact transmission and inform mitigation strategies. To this end, we have developed a simple mathematical model that can be used to estimate virus decay on nonporous surfaces under a range of conditions and which may be utilized operationally to identify indoor environments in which the virus is most persistent. Coronavirus disease 2019 (COVID-19) was first identified in China in late 2019 and is caused by newly identified severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Previous studies had reported the stability of SARS-CoV-2 in cell culture media and deposited onto surfaces under a limited set of environmental conditions. Here, we broadly investigated the effects of relative humidity, temperature, and droplet size on the stability of SARS-CoV-2 in a simulated clinically relevant matrix dried on nonporous surfaces. The results show that SARS-CoV-2 decayed more rapidly when either humidity or temperature was increased but that droplet volume (1 to 50 μl) and surface type (stainless steel, plastic, or nitrile glove) did not significantly impact decay rate. At room temperature (24°C), virus half-life ranged from 6.3 to 18.6 h depending on the relative humidity but was reduced to 1.0 to 8.9 h when the temperature was increased to 35°C. These findings suggest that a potential for fomite transmission may persist for hours to days in indoor environments and have implications for assessment of the risk posed by surface contamination in indoor environments. IMPORTANCE Mitigating the transmission of SARS-CoV-2 in clinical settings and public spaces is critically important to reduce the number of COVID-19 cases while effective vaccines and therapeutics are under development. SARS-CoV-2 transmission is thought to primarily occur through direct person-to-person transfer of infectious respiratory droplets or through aerosol-generating medical procedures. However, contact with contaminated surfaces may also play a significant role. In this context, understanding the factors contributing to SARS-CoV-2 persistence on surfaces will enable a more accurate estimation of the risk of contact transmission and inform mitigation strategies. To this end, we have developed a simple mathematical model that can be used to estimate virus decay on nonporous surfaces under a range of conditions and which may be utilized operationally to identify indoor environments in which the virus is most persistent.
AbstractList ABSTRACTCoronavirus disease 2019 (COVID-19) was first identified in China in late 2019 and is caused by newly identified severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Previous studies had reported the stability of SARS-CoV-2 in cell culture media and deposited onto surfaces under a limited set of environmental conditions. Here, we broadly investigated the effects of relative humidity, temperature, and droplet size on the stability of SARS-CoV-2 in a simulated clinically relevant matrix dried on nonporous surfaces. The results show that SARS-CoV-2 decayed more rapidly when either humidity or temperature was increased but that droplet volume (1 to 50 μl) and surface type (stainless steel, plastic, or nitrile glove) did not significantly impact decay rate. At room temperature (24°C), virus half-life ranged from 6.3 to 18.6 h depending on the relative humidity but was reduced to 1.0 to 8.9 h when the temperature was increased to 35°C. These findings suggest that a potential for fomite transmission may persist for hours to days in indoor environments and have implications for assessment of the risk posed by surface contamination in indoor environments.IMPORTANCE Mitigating the transmission of SARS-CoV-2 in clinical settings and public spaces is critically important to reduce the number of COVID-19 cases while effective vaccines and therapeutics are under development. SARS-CoV-2 transmission is thought to primarily occur through direct person-to-person transfer of infectious respiratory droplets or through aerosol-generating medical procedures. However, contact with contaminated surfaces may also play a significant role. In this context, understanding the factors contributing to SARS-CoV-2 persistence on surfaces will enable a more accurate estimation of the risk of contact transmission and inform mitigation strategies. To this end, we have developed a simple mathematical model that can be used to estimate virus decay on nonporous surfaces under a range of conditions and which may be utilized operationally to identify indoor environments in which the virus is most persistent.
ABSTRACT Coronavirus disease 2019 (COVID-19) was first identified in China in late 2019 and is caused by newly identified severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Previous studies had reported the stability of SARS-CoV-2 in cell culture media and deposited onto surfaces under a limited set of environmental conditions. Here, we broadly investigated the effects of relative humidity, temperature, and droplet size on the stability of SARS-CoV-2 in a simulated clinically relevant matrix dried on nonporous surfaces. The results show that SARS-CoV-2 decayed more rapidly when either humidity or temperature was increased but that droplet volume (1 to 50 μl) and surface type (stainless steel, plastic, or nitrile glove) did not significantly impact decay rate. At room temperature (24°C), virus half-life ranged from 6.3 to 18.6 h depending on the relative humidity but was reduced to 1.0 to 8.9 h when the temperature was increased to 35°C. These findings suggest that a potential for fomite transmission may persist for hours to days in indoor environments and have implications for assessment of the risk posed by surface contamination in indoor environments. IMPORTANCE Mitigating the transmission of SARS-CoV-2 in clinical settings and public spaces is critically important to reduce the number of COVID-19 cases while effective vaccines and therapeutics are under development. SARS-CoV-2 transmission is thought to primarily occur through direct person-to-person transfer of infectious respiratory droplets or through aerosol-generating medical procedures. However, contact with contaminated surfaces may also play a significant role. In this context, understanding the factors contributing to SARS-CoV-2 persistence on surfaces will enable a more accurate estimation of the risk of contact transmission and inform mitigation strategies. To this end, we have developed a simple mathematical model that can be used to estimate virus decay on nonporous surfaces under a range of conditions and which may be utilized operationally to identify indoor environments in which the virus is most persistent.
Mitigating the transmission of SARS-CoV-2 in clinical settings and public spaces is critically important to reduce the number of COVID-19 cases while effective vaccines and therapeutics are under development. SARS-CoV-2 transmission is thought to primarily occur through direct person-to-person transfer of infectious respiratory droplets or through aerosol-generating medical procedures. However, contact with contaminated surfaces may also play a significant role. In this context, understanding the factors contributing to SARS-CoV-2 persistence on surfaces will enable a more accurate estimation of the risk of contact transmission and inform mitigation strategies. To this end, we have developed a simple mathematical model that can be used to estimate virus decay on nonporous surfaces under a range of conditions and which may be utilized operationally to identify indoor environments in which the virus is most persistent. Coronavirus disease 2019 (COVID-19) was first identified in China in late 2019 and is caused by newly identified severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Previous studies had reported the stability of SARS-CoV-2 in cell culture media and deposited onto surfaces under a limited set of environmental conditions. Here, we broadly investigated the effects of relative humidity, temperature, and droplet size on the stability of SARS-CoV-2 in a simulated clinically relevant matrix dried on nonporous surfaces. The results show that SARS-CoV-2 decayed more rapidly when either humidity or temperature was increased but that droplet volume (1 to 50 μl) and surface type (stainless steel, plastic, or nitrile glove) did not significantly impact decay rate. At room temperature (24°C), virus half-life ranged from 6.3 to 18.6 h depending on the relative humidity but was reduced to 1.0 to 8.9 h when the temperature was increased to 35°C. These findings suggest that a potential for fomite transmission may persist for hours to days in indoor environments and have implications for assessment of the risk posed by surface contamination in indoor environments. IMPORTANCE Mitigating the transmission of SARS-CoV-2 in clinical settings and public spaces is critically important to reduce the number of COVID-19 cases while effective vaccines and therapeutics are under development. SARS-CoV-2 transmission is thought to primarily occur through direct person-to-person transfer of infectious respiratory droplets or through aerosol-generating medical procedures. However, contact with contaminated surfaces may also play a significant role. In this context, understanding the factors contributing to SARS-CoV-2 persistence on surfaces will enable a more accurate estimation of the risk of contact transmission and inform mitigation strategies. To this end, we have developed a simple mathematical model that can be used to estimate virus decay on nonporous surfaces under a range of conditions and which may be utilized operationally to identify indoor environments in which the virus is most persistent.
Mitigating the transmission of SARS-CoV-2 in clinical settings and public spaces is critically important to reduce the number of COVID-19 cases while effective vaccines and therapeutics are under development. SARS-CoV-2 transmission is thought to primarily occur through direct person-to-person transfer of infectious respiratory droplets or through aerosol-generating medical procedures. However, contact with contaminated surfaces may also play a significant role. In this context, understanding the factors contributing to SARS-CoV-2 persistence on surfaces will enable a more accurate estimation of the risk of contact transmission and inform mitigation strategies. To this end, we have developed a simple mathematical model that can be used to estimate virus decay on nonporous surfaces under a range of conditions and which may be utilized operationally to identify indoor environments in which the virus is most persistent. Coronavirus disease 2019 (COVID-19) was first identified in China in late 2019 and is caused by newly identified severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Previous studies had reported the stability of SARS-CoV-2 in cell culture media and deposited onto surfaces under a limited set of environmental conditions. Here, we broadly investigated the effects of relative humidity, temperature, and droplet size on the stability of SARS-CoV-2 in a simulated clinically relevant matrix dried on nonporous surfaces. The results show that SARS-CoV-2 decayed more rapidly when either humidity or temperature was increased but that droplet volume (1 to 50 μl) and surface type (stainless steel, plastic, or nitrile glove) did not significantly impact decay rate. At room temperature (24°C), virus half-life ranged from 6.3 to 18.6 h depending on the relative humidity but was reduced to 1.0 to 8.9 h when the temperature was increased to 35°C. These findings suggest that a potential for fomite transmission may persist for hours to days in indoor environments and have implications for assessment of the risk posed by surface contamination in indoor environments. IMPORTANCE Mitigating the transmission of SARS-CoV-2 in clinical settings and public spaces is critically important to reduce the number of COVID-19 cases while effective vaccines and therapeutics are under development. SARS-CoV-2 transmission is thought to primarily occur through direct person-to-person transfer of infectious respiratory droplets or through aerosol-generating medical procedures. However, contact with contaminated surfaces may also play a significant role. In this context, understanding the factors contributing to SARS-CoV-2 persistence on surfaces will enable a more accurate estimation of the risk of contact transmission and inform mitigation strategies. To this end, we have developed a simple mathematical model that can be used to estimate virus decay on nonporous surfaces under a range of conditions and which may be utilized operationally to identify indoor environments in which the virus is most persistent.
Coronavirus disease 2019 (COVID-19) was first identified in China in late 2019 and is caused by newly identified severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Previous studies had reported the stability of SARS-CoV-2 in cell culture media and deposited onto surfaces under a limited set of environmental conditions. Here, we broadly investigated the effects of relative humidity, temperature, and droplet size on the stability of SARS-CoV-2 in a simulated clinically relevant matrix dried on nonporous surfaces. The results show that SARS-CoV-2 decayed more rapidly when either humidity or temperature was increased but that droplet volume (1 to 50 μl) and surface type (stainless steel, plastic, or nitrile glove) did not significantly impact decay rate. At room temperature (24°C), virus half-life ranged from 6.3 to 18.6 h depending on the relative humidity but was reduced to 1.0 to 8.9 h when the temperature was increased to 35°C. These findings suggest that a potential for fomite transmission may persist for hours to days in indoor environments and have implications for assessment of the risk posed by surface contamination in indoor environments. IMPORTANCE Mitigating the transmission of SARS-CoV-2 in clinical settings and public spaces is critically important to reduce the number of COVID-19 cases while effective vaccines and therapeutics are under development. SARS-CoV-2 transmission is thought to primarily occur through direct person-to-person transfer of infectious respiratory droplets or through aerosol-generating medical procedures. However, contact with contaminated surfaces may also play a significant role. In this context, understanding the factors contributing to SARS-CoV-2 persistence on surfaces will enable a more accurate estimation of the risk of contact transmission and inform mitigation strategies. To this end, we have developed a simple mathematical model that can be used to estimate virus decay on nonporous surfaces under a range of conditions and which may be utilized operationally to identify indoor environments in which the virus is most persistent.
Coronavirus disease 2019 (COVID-19) was first identified in China in late 2019 and is caused by newly identified severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Previous studies had reported the stability of SARS-CoV-2 in cell culture media and deposited onto surfaces under a limited set of environmental conditions. Here, we broadly investigated the effects of relative humidity, temperature, and droplet size on the stability of SARS-CoV-2 in a simulated clinically relevant matrix dried on nonporous surfaces. The results show that SARS-CoV-2 decayed more rapidly when either humidity or temperature was increased but that droplet volume (1 to 50 μl) and surface type (stainless steel, plastic, or nitrile glove) did not significantly impact decay rate. At room temperature (24°C), virus half-life ranged from 6.3 to 18.6 h depending on the relative humidity but was reduced to 1.0 to 8.9 h when the temperature was increased to 35°C. These findings suggest that a potential for fomite transmission may persist for hours to days in indoor environments and have implications for assessment of the risk posed by surface contamination in indoor environments. Mitigating the transmission of SARS-CoV-2 in clinical settings and public spaces is critically important to reduce the number of COVID-19 cases while effective vaccines and therapeutics are under development. SARS-CoV-2 transmission is thought to primarily occur through direct person-to-person transfer of infectious respiratory droplets or through aerosol-generating medical procedures. However, contact with contaminated surfaces may also play a significant role. In this context, understanding the factors contributing to SARS-CoV-2 persistence on surfaces will enable a more accurate estimation of the risk of contact transmission and inform mitigation strategies. To this end, we have developed a simple mathematical model that can be used to estimate virus decay on nonporous surfaces under a range of conditions and which may be utilized operationally to identify indoor environments in which the virus is most persistent.
Coronavirus disease 2019 (COVID-19) was first identified in China in late 2019 and is caused by newly identified severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Previous studies had reported the stability of SARS-CoV-2 in cell culture media and deposited onto surfaces under a limited set of environmental conditions. Here, we broadly investigated the effects of relative humidity, temperature, and droplet size on the stability of SARS-CoV-2 in a simulated clinically relevant matrix dried on nonporous surfaces. The results show that SARS-CoV-2 decayed more rapidly when either humidity or temperature was increased but that droplet volume (1 to 50 μl) and surface type (stainless steel, plastic, or nitrile glove) did not significantly impact decay rate. At room temperature (24°C), virus half-life ranged from 6.3 to 18.6 h depending on the relative humidity but was reduced to 1.0 to 8.9 h when the temperature was increased to 35°C. These findings suggest that a potential for fomite transmission may persist for hours to days in indoor environments and have implications for assessment of the risk posed by surface contamination in indoor environments.IMPORTANCE Mitigating the transmission of SARS-CoV-2 in clinical settings and public spaces is critically important to reduce the number of COVID-19 cases while effective vaccines and therapeutics are under development. SARS-CoV-2 transmission is thought to primarily occur through direct person-to-person transfer of infectious respiratory droplets or through aerosol-generating medical procedures. However, contact with contaminated surfaces may also play a significant role. In this context, understanding the factors contributing to SARS-CoV-2 persistence on surfaces will enable a more accurate estimation of the risk of contact transmission and inform mitigation strategies. To this end, we have developed a simple mathematical model that can be used to estimate virus decay on nonporous surfaces under a range of conditions and which may be utilized operationally to identify indoor environments in which the virus is most persistent.Coronavirus disease 2019 (COVID-19) was first identified in China in late 2019 and is caused by newly identified severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Previous studies had reported the stability of SARS-CoV-2 in cell culture media and deposited onto surfaces under a limited set of environmental conditions. Here, we broadly investigated the effects of relative humidity, temperature, and droplet size on the stability of SARS-CoV-2 in a simulated clinically relevant matrix dried on nonporous surfaces. The results show that SARS-CoV-2 decayed more rapidly when either humidity or temperature was increased but that droplet volume (1 to 50 μl) and surface type (stainless steel, plastic, or nitrile glove) did not significantly impact decay rate. At room temperature (24°C), virus half-life ranged from 6.3 to 18.6 h depending on the relative humidity but was reduced to 1.0 to 8.9 h when the temperature was increased to 35°C. These findings suggest that a potential for fomite transmission may persist for hours to days in indoor environments and have implications for assessment of the risk posed by surface contamination in indoor environments.IMPORTANCE Mitigating the transmission of SARS-CoV-2 in clinical settings and public spaces is critically important to reduce the number of COVID-19 cases while effective vaccines and therapeutics are under development. SARS-CoV-2 transmission is thought to primarily occur through direct person-to-person transfer of infectious respiratory droplets or through aerosol-generating medical procedures. However, contact with contaminated surfaces may also play a significant role. In this context, understanding the factors contributing to SARS-CoV-2 persistence on surfaces will enable a more accurate estimation of the risk of contact transmission and inform mitigation strategies. To this end, we have developed a simple mathematical model that can be used to estimate virus decay on nonporous surfaces under a range of conditions and which may be utilized operationally to identify indoor environments in which the virus is most persistent.
Author Yolitz, Jason
Wood, Stewart
Williams, Gregory
Yeager, John J.
Ferris, Allison
Reese, Amy L.
Freeburger, Denise
Hooper, Idris
Herzog, Artemas
Hevey, Michael C.
Miller, David
Ratnesar-Shumate, Shanna
Dabisch, Paul
Dawson, David G.
Zeitouni, Nathalie E.
Wahl, Victoria
Altamura, Louis A.
Biryukov, Jennifer
Krause, Melissa
Weaver, Wade
Boydston, Jeremy A.
Phillips, Aaron
Dunning, Rebecca A.
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  orcidid: 0000-0002-9598-3876
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  organization: National Biodefense Analysis and Countermeasures Center (NBACC), Operated by Battelle National Biodefense Institute (BNBI) for the U.S. Department of Homeland Security Science and Technology Directorate, Fort Detrick, Maryland, USA
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  givenname: Jeremy A.
  surname: Boydston
  fullname: Boydston, Jeremy A.
  organization: National Biodefense Analysis and Countermeasures Center (NBACC), Operated by Battelle National Biodefense Institute (BNBI) for the U.S. Department of Homeland Security Science and Technology Directorate, Fort Detrick, Maryland, USA
– sequence: 3
  givenname: Rebecca A.
  surname: Dunning
  fullname: Dunning, Rebecca A.
  organization: National Biodefense Analysis and Countermeasures Center (NBACC), Operated by Battelle National Biodefense Institute (BNBI) for the U.S. Department of Homeland Security Science and Technology Directorate, Fort Detrick, Maryland, USA
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  givenname: John J.
  surname: Yeager
  fullname: Yeager, John J.
  organization: National Biodefense Analysis and Countermeasures Center (NBACC), Operated by Battelle National Biodefense Institute (BNBI) for the U.S. Department of Homeland Security Science and Technology Directorate, Fort Detrick, Maryland, USA
– sequence: 5
  givenname: Stewart
  surname: Wood
  fullname: Wood, Stewart
  organization: National Biodefense Analysis and Countermeasures Center (NBACC), Operated by Battelle National Biodefense Institute (BNBI) for the U.S. Department of Homeland Security Science and Technology Directorate, Fort Detrick, Maryland, USA
– sequence: 6
  givenname: Amy L.
  surname: Reese
  fullname: Reese, Amy L.
  organization: National Biodefense Analysis and Countermeasures Center (NBACC), Operated by Battelle National Biodefense Institute (BNBI) for the U.S. Department of Homeland Security Science and Technology Directorate, Fort Detrick, Maryland, USA
– sequence: 7
  givenname: Allison
  surname: Ferris
  fullname: Ferris, Allison
  organization: National Biodefense Analysis and Countermeasures Center (NBACC), Operated by Battelle National Biodefense Institute (BNBI) for the U.S. Department of Homeland Security Science and Technology Directorate, Fort Detrick, Maryland, USA
– sequence: 8
  givenname: David
  surname: Miller
  fullname: Miller, David
  organization: National Biodefense Analysis and Countermeasures Center (NBACC), Operated by Battelle National Biodefense Institute (BNBI) for the U.S. Department of Homeland Security Science and Technology Directorate, Fort Detrick, Maryland, USA
– sequence: 9
  givenname: Wade
  surname: Weaver
  fullname: Weaver, Wade
  organization: National Biodefense Analysis and Countermeasures Center (NBACC), Operated by Battelle National Biodefense Institute (BNBI) for the U.S. Department of Homeland Security Science and Technology Directorate, Fort Detrick, Maryland, USA
– sequence: 10
  givenname: Nathalie E.
  orcidid: 0000-0001-5525-6976
  surname: Zeitouni
  fullname: Zeitouni, Nathalie E.
  organization: National Biodefense Analysis and Countermeasures Center (NBACC), Operated by Battelle National Biodefense Institute (BNBI) for the U.S. Department of Homeland Security Science and Technology Directorate, Fort Detrick, Maryland, USA
– sequence: 11
  givenname: Aaron
  surname: Phillips
  fullname: Phillips, Aaron
  organization: National Biodefense Analysis and Countermeasures Center (NBACC), Operated by Battelle National Biodefense Institute (BNBI) for the U.S. Department of Homeland Security Science and Technology Directorate, Fort Detrick, Maryland, USA
– sequence: 12
  givenname: Denise
  surname: Freeburger
  fullname: Freeburger, Denise
  organization: National Biodefense Analysis and Countermeasures Center (NBACC), Operated by Battelle National Biodefense Institute (BNBI) for the U.S. Department of Homeland Security Science and Technology Directorate, Fort Detrick, Maryland, USA
– sequence: 13
  givenname: Idris
  surname: Hooper
  fullname: Hooper, Idris
  organization: National Biodefense Analysis and Countermeasures Center (NBACC), Operated by Battelle National Biodefense Institute (BNBI) for the U.S. Department of Homeland Security Science and Technology Directorate, Fort Detrick, Maryland, USA
– sequence: 14
  givenname: Shanna
  orcidid: 0000-0001-5181-7772
  surname: Ratnesar-Shumate
  fullname: Ratnesar-Shumate, Shanna
  organization: National Biodefense Analysis and Countermeasures Center (NBACC), Operated by Battelle National Biodefense Institute (BNBI) for the U.S. Department of Homeland Security Science and Technology Directorate, Fort Detrick, Maryland, USA
– sequence: 15
  givenname: Jason
  surname: Yolitz
  fullname: Yolitz, Jason
  organization: National Biodefense Analysis and Countermeasures Center (NBACC), Operated by Battelle National Biodefense Institute (BNBI) for the U.S. Department of Homeland Security Science and Technology Directorate, Fort Detrick, Maryland, USA
– sequence: 16
  givenname: Melissa
  surname: Krause
  fullname: Krause, Melissa
  organization: National Biodefense Analysis and Countermeasures Center (NBACC), Operated by Battelle National Biodefense Institute (BNBI) for the U.S. Department of Homeland Security Science and Technology Directorate, Fort Detrick, Maryland, USA
– sequence: 17
  givenname: Gregory
  surname: Williams
  fullname: Williams, Gregory
  organization: National Biodefense Analysis and Countermeasures Center (NBACC), Operated by Battelle National Biodefense Institute (BNBI) for the U.S. Department of Homeland Security Science and Technology Directorate, Fort Detrick, Maryland, USA
– sequence: 18
  givenname: David G.
  surname: Dawson
  fullname: Dawson, David G.
  organization: National Biodefense Analysis and Countermeasures Center (NBACC), Operated by Battelle National Biodefense Institute (BNBI) for the U.S. Department of Homeland Security Science and Technology Directorate, Fort Detrick, Maryland, USA
– sequence: 19
  givenname: Artemas
  surname: Herzog
  fullname: Herzog, Artemas
  organization: Censeo Consulting Group Inc., Washington, DC, USA
– sequence: 20
  givenname: Paul
  orcidid: 0000-0002-3181-6825
  surname: Dabisch
  fullname: Dabisch, Paul
  organization: National Biodefense Analysis and Countermeasures Center (NBACC), Operated by Battelle National Biodefense Institute (BNBI) for the U.S. Department of Homeland Security Science and Technology Directorate, Fort Detrick, Maryland, USA
– sequence: 21
  givenname: Victoria
  orcidid: 0000-0002-6588-4308
  surname: Wahl
  fullname: Wahl, Victoria
  organization: National Biodefense Analysis and Countermeasures Center (NBACC), Operated by Battelle National Biodefense Institute (BNBI) for the U.S. Department of Homeland Security Science and Technology Directorate, Fort Detrick, Maryland, USA
– sequence: 22
  givenname: Michael C.
  surname: Hevey
  fullname: Hevey, Michael C.
  organization: National Biodefense Analysis and Countermeasures Center (NBACC), Operated by Battelle National Biodefense Institute (BNBI) for the U.S. Department of Homeland Security Science and Technology Directorate, Fort Detrick, Maryland, USA
– sequence: 23
  givenname: Louis A.
  orcidid: 0000-0001-7389-295X
  surname: Altamura
  fullname: Altamura, Louis A.
  organization: National Biodefense Analysis and Countermeasures Center (NBACC), Operated by Battelle National Biodefense Institute (BNBI) for the U.S. Department of Homeland Security Science and Technology Directorate, Fort Detrick, Maryland, USA
BackLink https://www.ncbi.nlm.nih.gov/pubmed/32611701$$D View this record in MEDLINE/PubMed
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Issue 4
Keywords COVID-19
SARS-CoV-2
transmission
temperature
coronavirus
humidity
fomite
half-life
contamination
Language English
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Citation Biryukov J, Boydston JA, Dunning RA, Yeager JJ, Wood S, Reese AL, Ferris A, Miller D, Weaver W, Zeitouni NE, Phillips A, Freeburger D, Hooper I, Ratnesar-Shumate S, Yolitz J, Krause M, Williams G, Dawson DG, Herzog A, Dabisch P, Wahl V, Hevey MC, Altamura LA. 2020. Increasing temperature and relative humidity accelerates inactivation of SARS-CoV-2 on surfaces. mSphere 5:e00441-20. https://doi.org/10.1128/mSphere.00441-20.
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SSID ssj0001626676
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Snippet Mitigating the transmission of SARS-CoV-2 in clinical settings and public spaces is critically important to reduce the number of COVID-19 cases while effective...
Coronavirus disease 2019 (COVID-19) was first identified in China in late 2019 and is caused by newly identified severe acute respiratory syndrome coronavirus...
ABSTRACTCoronavirus disease 2019 (COVID-19) was first identified in China in late 2019 and is caused by newly identified severe acute respiratory syndrome...
ABSTRACT Coronavirus disease 2019 (COVID-19) was first identified in China in late 2019 and is caused by newly identified severe acute respiratory syndrome...
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SubjectTerms Aerosols
Air Pollution, Indoor
Applied and Environmental Science
Cell culture
Contamination
coronavirus
Coronavirus Infections - prevention & control
Coronavirus Infections - transmission
Coronavirus Infections - virology
Coronaviruses
COVID-19
Culture media
Disease transmission
Drug development
Editor's Pick
Environmental conditions
Estimates
fomite
Fomites
Fomites - virology
Generalized linear models
Half-Life
Humans
Humidity
Indoor environments
Mathematical models
Models, Theoretical
Observation
Pandemics - prevention & control
Personal protective equipment
Plastics
Pneumonia, Viral - prevention & control
Pneumonia, Viral - transmission
Pneumonia, Viral - virology
Porosity
Relative humidity
Saliva - chemistry
Saliva - virology
SARS Virus
SARS-CoV-2
Severe acute respiratory syndrome coronavirus 2
Severe acute respiratory syndrome-related coronavirus - physiology
Stainless Steel
Standard deviation
Surface Properties
Temperature
Variance analysis
Virus Inactivation
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Title Increasing Temperature and Relative Humidity Accelerates Inactivation of SARS-CoV-2 on Surfaces
URI https://www.ncbi.nlm.nih.gov/pubmed/32611701
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