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      Solar ultraviolet radiation sensitivity of SARS-CoV-2

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      a , b , c
      The Lancet Microbe
      The Author(s). Published by Elsevier Ltd.

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          Abstract

          Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), can be life-threatening; the outbreak of this disease was characterised as a pandemic by WHO on March 11, 2020. 1 COVID-19 is currently a global health issue and governments are taking a series of measures to reduce the spread of the virus among communities. Factors affecting the survival of SARS-CoV-2 need to be clarified and the effect of solar ultraviolet radiation is one subject under discussion. 2 The output of both the popular and scientific press have included hopeful speeches by politicians or scientists suggesting that the transmission of SARS-CoV-2 will be contained within the coming months because of increasing temperatures and solar ultraviolet radiation during the summer season in countries in the northern hemisphere. However, solar ultraviolet radiation and ultraviolet germicidal irradiation (UVGI) are not the same. To evaluate effectiveness of ultraviolet radiation, we need to consider the virology of SARS-CoV-2, an enveloped, single stranded RNA virus. SARS-CoV-2 is a novel betacoronavirus and showed 88% genome similarity with two SARS-like coronaviruses (SL-CoV) found in bats: SL-CoV-ZC45 and SL-CoVZXC21. 3 Human-to-human transmission occurs via droplets (by direct or indirect contact) 4 and viral droplets can survive on various surfaces for several hours, despite reductions in the viral load. 2 This information shows that, despite their enveloped structure, SARS-CoV-2 is quite resistant to environmental conditions. During epidemics and pandemics, disinfection of environments is crucial, particularly for airborne diseases. 5 The advantages offered by ultraviolet radiation make UVGI (ultraviolet disinfection) a very effective disinfection tool. 6 Ultraviolet light can be classified into three subtypes by radiation wavelengths: ultraviolet A (320-400 nm), ultraviolet B (280–320 nm) and ultraviolet C (200–280 nm). 7 The commonly used wavelength for UVGI is ultraviolet C because its germicidal effectiveness peak wavelength is 260–265 nm, which is equivalent to the peak of ultraviolet radiation absorption of nucleic acids. 7 It is known that as the ultraviolet wavelength decreases, the germicidal effect of ultraviolet radiation increases. 8 Therefore, ultraviolet wavelengths below 320 nm are classed as actinic—ie, causing photochemical reactions. Since ultraviolet A radiation is insufficiently absorbed by viral nucleic acid, ultraviolet A radiation is not considered germicidal. 7 Unfortunately, ultraviolet A is the major ultraviolet component of sunlight reaching the ground. 8 Ultraviolet B radiation can also have a small germicidal effect, 7 but only a small portion of it reaches the Earth's surface as most is absorbed by the atmosphere. 8 Ultraviolet radiation that is totally absorbed by the ozone layer is accepted as having the optimum germicidal wavelength—ie, ultraviolet C radiation. 8 Unifying all these principles, it is clear that sunlight reaching the ground lacks germicidal ultraviolet C radiation.7, 8 Studies show that UVGI methods can be used effectively to eliminate viruses—eg, in health-care facilities, schools, indoors, etc—by using special ultraviolet radiation systems (ultraviolet C lamps, chambers). Also, it is known that the ultraviolet absorption peak of RNA viruses is around 250 nm wavelength. 7 Therefore, the germicidal effectiveness of ultraviolet C radiation is limited to such applications and sunlight is not an alternative. However, some studies based on SARS-CoV, have shown that at least 60°C (which the earth does not reach to this temperature) and a minimum of 90 min are required to inactivate SARS-CoV-2. 9 In the absence of scientific evidence showing ultraviolet B radiation's germicidal effectiveness on SARS-CoV-2, both politicians and scientists should avoid voicing assumptions on the effect of sunlight on viral transmission. Such uninformed statements can promoted misunderstanding and offer unrealistic hope to communities. This misunderstanding can also cause lethargy with regard to the government measurements in place in the community. Further studies should be done by simulating complex environmental conditions, in which a number of variables will test the effectiveness of ultraviolet B radiation against environmental SARS-CoV-2.

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          Aerosol and Surface Stability of SARS-CoV-2 as Compared with SARS-CoV-1

          To the Editor: A 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.
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            Molecular immune pathogenesis and diagnosis of COVID-19

            Coronavirus disease 2019 (COVID-19) is a kind of viral pneumonia with an unusual outbreak in Wuhan, China, in December 2019, which is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The emergence of SARS-CoV-2 has been marked as the third introduction of a highly pathogenic coronavirus into the human population after the severe acute respiratory syndrome coronavirus (SARS-CoV) and the Middle East respiratory syndrome coronavirus (MERS-CoV) in the twenty-first century. In this minireview, we provide a brief introduction of the general features of SARS-CoV-2 and discuss current knowledge of molecular immune pathogenesis, diagnosis and treatment of COVID-19 on the base of the present understanding of SARS-CoV and MERS-CoV infections, which may be helpful in offering novel insights and potential therapeutic targets for combating the SARS-CoV-2 infection.
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              Differences and similarities between Severe Acute Respiratory Syndrome (SARS)-CoronaVirus (CoV) and SARS-CoV-2. Would a rose by another name smell as sweet?

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                Author and article information

                Contributors
                Journal
                The Lancet Microbe
                The Author(s). Published by Elsevier Ltd.
                2666-5247
                2666-5247
                11 May 2020
                May 2020
                11 May 2020
                : 1
                : 1
                : e8-e9
                Affiliations
                [a ]Department of Medical and Clinical Microbiology, Cyprus International University, Nicosia, 99258, Cyprus
                [b ]Department of Medical Microbiology, Celal Bayar University, Manisa, Turkey
                [c ]Experimental Health Sciences Research Institute, Near East University, Nicosia, Cyprus
                Article
                S2666-5247(20)30013-6
                10.1016/S2666-5247(20)30013-6
                7212978
                32835321
                67dcdc5b-c612-417b-9e67-39fcc6df6031
                © 2020 The Author(s). Published by Elsevier Ltd. This is an Open Access article under the CC BY 4.0 license.

                Since January 2020 Elsevier has created a COVID-19 resource centre with free information in English and Mandarin on the novel coronavirus COVID-19. The COVID-19 resource centre is hosted on Elsevier Connect, the company's public news and information website. Elsevier hereby grants permission to make all its COVID-19-related research that is available on the COVID-19 resource centre - including this research content - immediately available in PubMed Central and other publicly funded repositories, such as the WHO COVID database with rights for unrestricted research re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for free by Elsevier for as long as the COVID-19 resource centre remains active.

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