How the seasonal shift will impact the spread of SARS-CoV-2 ?

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Winter is coming in the northern hemisphere and public health officials are asking how the seasonal shift will impact the spread of SARS-CoV-2, the virus that causes COVID-19?

A new study tested how temperatures and humidity affect the structure of individual SARS-Cov-2 virus-like particles on surfaces. They found that just moderate temperature increases broke down the virus’ structure, while humidity had very little impact.

In order to remain infectious, the SARS-Cov-2 membrane needs a specific web of proteins arranged in a particular order. When that structure falls apart, it becomes less infectious. The findings suggest that as temperatures begin to drop, particles on surfaces will remain infectious longer.

This is the first study to analyze the mechanics of the virus on an individual particle level, but the findings agree with large-scale observations of other coronaviruses that appear to infect more people during the winter months.

“You would expect that temperature makes a huge difference, and that’s what we saw. To the point where the packaging of the virus was completely destroyed by even moderate temperature increases,” said Michael Vershinin, assistant professor at the University of Utah and co-senior author of the paper.

“What’s surprising is how little heat was needed to break them down – surfaces that are warm to the touch, but not hot. The packaging of this virus is very sensitive to temperature.”

The paper published online on Nov. 28, 2020, in the journal Biochemical Biophysical Research Communications. The team also published a separate paper Dec. 14, 2020 in Scientific Reports describing their method for making the individual particle packaging.

The virus-like particles are empty shells made from the same lipids and three types of proteins as are on an active SARS-Cov-2 viruses, but without the RNA that causes infections. This new method allows scientists to experiment with the virus without risking an outbreak.

The SARS-CoV-2 is commonly spread by exhaling sharply, (e.g. sneezing or coughing), which ejects droplets of tiny aerosols from the lungs.

These mucus-y droplets have a high surface to volume ratio and dry out quickly, so both wet and dry virus particles come into contact with a surface or travel directly into a new host. The researchers mimicked these conditions in their experiments.

They tested the virus-like particles on glass surfaces under both dry and humid conditions. Using atomic force microscopy they observed how, if at all, the structures changed. The scientists exposed samples to various temperatures under two conditions: with the particles inside a liquid buffer solution, and with the particles dried out in the open.

In both liquid and bare conditions, elevating the temperature to about 93 degrees F for 30 minutes degraded the outer structure. The effect was stronger on the dry particles than on the liquid-protected ones. In contrast, surfaces at about 71 degrees F caused little to no damage, suggesting that particles in room temperature conditions or outside in cooler weather will remain infectious longer.

They saw very little difference under levels of humidity on surfaces, however the scientists stress that humidity likely does matter when the particles are in the air by affecting how fast the aerosols dry out. The research team is continuing to study the molecular details of virus-like particle degradation.

“When it comes to fighting the spread of this virus, you kind of have to fight every particle individually. And so you need to understand what makes each individual particle degrade,” Vershinin said. “People are also working on vaccines and are trying to understand how the virus is recognized?

All of these questions are single particle questions. And if you understand that, then that enables you to fight a hoard of them.”


The world has witnessed many epidemics in the past (McNeil, 1977). Other coronaviruses like SARS and MERS produced pandemics that started in 2002 and 2012, respectively (Peiris et. al., 2003; Ramadan and Shaib, 2019); and coronaviruses cause 15-20 % of all upper respiratory infections in humans, even in the absence of epidemics (Holmes, 1990).

Several other viruses, like those of relevance in biodefense (with mortality rates of 40% for Lassa virus and 53% to 92% for the Sudan and Zaire strains of Ebola virus, respectively [Jahrling, 1997]) cause higher mortality than SARS-Co V-2 (global mortality rate of COVID-19 averaged of 3.1% as of 22 September, 2020 [Johns’s Hopkins, 2020).

Rather what has been unusual were predictions made by computer modeling of 7 billion infections and 40 million deaths during 2020 alone if quarantine, lock-downs and other highly restrictive measures were not enforced (Walker et. al., 2020).

These predictions may have been instrumental (Sagripanti, 2020) in justifying 1168 quarantine and lock-down policies mandated by governments of 165 countries (Cheng, C. et. al., 2020) that confined indoors at-risk as well as healthy individuals, resulting in a political and social crisis without historical precedents.

It is well known that there is direct transmission of infectious virions by inhalation of contaminated aerosols exhaled, coughed, or sneezed from infected persons. Most measures mandated during COVID-19, from relatively benign (like wearing face masks or social distancing) to highly restrictive like quarantine, curfews, and stay-at-home orders or lock-downs, were intended to prevent person-to-person transmission of disease which has been a main component in models used to predict the progression of viral epidemics (Walker et.al., 2020).

Direct (person-to-person) transmission was shown to be important in transmission of SARS-Co V-2 between nearby individuals (Chan, J.F. et al., 2020). However, it is remarkable that the COVID-19 pandemic progressed at a sustained rate after 26 March, 2020, when 1.7 billion people worldwide were under some form of indoor confinement, figure which increased to 3.9 billion people by the first week of April, amounting to more than half of the world’s population in quarantine or in-house lock-downs (Kaplan et.al. 2020; Sandford, 2020). The COVID-19 pandemic progressed rapidly in spite of greatly hindered person-to-person transmission.

The amount of infectious virus present in the aerosolized droplets produced by symptomatic patients or non-symptomatic carriers is not well established for coronaviruses, but it has been reported that nasal secretions contain up to 107 infectious influenza viral particles per ml (Couch, 1995), from which aerosolized droplets generated by coughing, sneezing, and talking can contain several hundred infectious virions each (Gustin et.al., 2013).

These micro droplets can reach distances of 12.5 meters (over 40 feet; Reiling, 2000). Coronaviruses have been reported to persist on contaminated surfaces with risk of disease transmission for up 9 days (Kramer et.al., 2006; Kampf et.al., 2020).

SARS-CoV-2 persisted viable from 3 hours to 3 days depending on the type of surface on which it was deposited (vanDoremalen et.al., 2020). Influenza virus was readily re-aerosolized by sweeping floors without much loss in infectivity (Loosli et.al., 1943) and it should be assumed that SARS-CoV-2 will be reaerosolized in a similar manner.

These findings indicate that SARS-CoV-2 should be able to persist for long periods in contaminated environments with continued risk of infection and progression of COVID-19.

Three main physical factors generally considered with a potential effect on virus persistence outdoors, include temperature, humidity, and the contribution of the germicidal (UVB) component in sunlight radiation. Laboratory experiments have demonstrated (particularly when virus infectivity was corrected by aerosol losses and natural decay) a rather limited effect of changes in relative humidity and ambient temperature on environmental virus survival and disease transmission (Hemmes et.al., 1960; Schaffer et.al., 1976; Kormuth et.al., 2018). Epidemiological studies on influenza concluded that the mortality increase in winter was largely independent of ambient temperature and humidity (Tiller et.al., 1983; Reichert et.al., 2004).

Ultraviolet radiation in sunlight is the primary virucidal agent in the environment (Giese, 1976; Lytle and Sagripanti, 2005; Coohill and Sagripanti, 2009) and the relevance of sunlight in viral inactivation is documented (Mims, 2005; Sagripanti et.al., 2013).

In contrast, smallpox, Ebola virus, Lassa virus, and other viruses of relevance in biodefense persisted in darkness for many days on contaminated surfaces (Downie and Dumbell, 1947; Sagripanti et.al., 2010). Modeling of viruses suspended in the atmosphere indicates that the diffuse (scatter) component of sunlight may still have approximately 50% of the virucidal efficacy exerted by direct solar radiation (Ben-David and Sagripanti, 2010; Ben-David and Sagripanti, 2013); demonstrating that viral inactivation by sunlight continues outdoors (albeit at half the rate or less) even in the shade or in polluted air or partially cloudy days.

The UV sensitivity of coronaviruses, in general, and of SARS-CoV-2 in particular (Sagripanti and Lytle, 2020), indicates that 90% or more of SARS-CoV-2 virus should be inactivated after being exposed for 11-34 minutes of midday sunlight during summer in most world cities.

In contrast, the virus will persist infectious for a day or more in winter (December-March in the northern hemisphere), with continued risk of re-arosolization and transmission at the same locations. Considering that SARS-CoV-2 could be three-times more sensitive to UV than influenza A (Sagripanti and Lytle, 2020; Sagripanti and Lytle, 2007), it should be inferred that sunlight should have an effect on coronaviruses transmission at least similar to that previously established for the evolution of influenza epidemics (Tiller et. al., 1983; Reichert et. al., 2004; Mims, 2005).

An understanding of COVID-19 should account for a) the rapid progression of the pandemic in spite of highly hindered opportunity for person-to-person contagion, b) the role of environmental transmission by contaminated aerosols, surfaces and fomites, c) a potential seasonal inactivation of virus in the environment by germicidal sunlight, and d) should explain the new spikes or waves of infections recurring even during summer, when germicidal sunlight radiation is more potent. This article attempts addressing these topics.

reference link : https://www.medrxiv.org/content/10.1101/2020.12.06.20244780v1.full


More information: A. Sharma et al, Structural stability of SARS-CoV-2 virus like particles degrades with temperature, Biochemical and Biophysical Research Communications (2020). DOI: 10.1016/j.bbrc.2020.11.080

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