Virus? ...simply a piece of bad news wrapped up in protein.

—Jean and Peter Medawar

by Christoph
 

In the middle of the first major pandemic of my lifetime I feel the need, as a microbiologist, to make occasional contributions that may help individuals and society approach the pandemic in a reasonably informed way. Today, I'd like to contribute with a small dose of 'microbial literacy,' as called for by Ken Timmis and colleagues well before "the coronavirus" hit. Here is the question: are viruses alive? Short answer: No. Long answer: it's complicated because of biology (see part 2, next Monday).
 

Short answer: No, viruses are not alive

(Click to enlarge)
Figure 1. See below for legend Source. Frontispiece: SARS-CoV-2 by @dsgoodsell

In a paper published on March 17th in The New England Journal of Medicine (NEJM), a team of 13 NIAID research­ers analyzed the "Aerosol and Surface Stability of SARS-CoV-2 as Compared with SARS-CoV-1." They state that "SARS-CoV-2 remained viable in aerosols throughout the duration of our experiment (3 hours), with a reduction in infectious titer from 10^3.5 to 10^2.7 TCID₅₀ per liter of air." And they conclude "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..." (My emphases in both cases.) What they actually did was expose different surfaces under carefully controlled conditions to aerosolized virus par­ticles, and measure their time-dependent decay rate by tissue-culture infection of Vero E6 cells (a standard cell line used in virology). This last experimental step, the infection of tissue culture, was the only one during which the virus multiplied (Figure 1).
 

Unfortunately, virologists habitually speak of the "viability" of viruses when they actually mean (and measure) their "infectivity." This talk of viral viability extends to the World Health Organiza­tion (WHO) in their Q&A on coronaviruses (COVID-19): "...the virus that causes COVID-19 survives on surfaces," and "...simple disinfectant to kill the virus..." (My emphases.) One can thus hardly blame the press to continue along those lines, like in this headline in The Economist: "How long can the novel coronavirus survive on surfaces and in the air?"
 

Why is a distinction between "viability" and "infectivity" relevant and not just merely semantic? Because the therapeutic and hygienic measures required to treat and contain viral diseases are different from those required for bacterial diseases. It is difficult enough to convey to the public − and to governments, by the way − that antibiotics are not effective against viruses (spoiler: an­ti­virals are). But there's something more basic here. Viruses only multiply within cells after they have infected them, and, once released from the cells, stay infectious only for a while. That is, un­less they're brought again into contact with other host cells, they decay. Bacterial human patho­gens, on the other hand, not only simply survive outside human hosts but can usually grow and multiply in various non-human environments ('natural reservoirs' is the technical term). Vibrio cholerae, for example, thrive happily on chitinous surfaces of marine invertebrates (forming bio­films) and in coastal waters (planktonic). Or take Staphylococcus aureus (MRSA), which are per­manent guests in animal breeding facilities and waste water.
 

People from all cultural backgrounds identify living beings by their ability to grow, reproduce and eventually die. (I am of course fully aware that this is the lowest common denominator, and peo­ple from different cultures add other ingredients to this 'basic recipe,' usually metaphysical or re­ligious). So, for the sake of your 'microbial literacy' you can rely on the fact that viruses have the ability to reproduce (within host cells), but do not grow (host cells do), and cannot die (host cells eventually can). No, viruses are not living beings because they only fulfill one of the three basic conditions.
 

There's nothing wrong with this naïve, intuitive way to understand what "life" is when it comes to dealing with the coronavirus, SARS-CoV-2. But don't take the quote of the Medawars in the title of this post as a quip, take it literally − "bad news" refers to you! Continue with the practices of phy­si­cal distancing and frequent thorough hand washing − 20 sec minimum, with soap − as rec­om­mend­ed by the WHO. Soap does not "kill" the virus, but breaks it down neatly into its then harm­less individual components (Lizah van der Aart made a fancy poster about this). And do not touch your face − avoid picking your nose or biting your finger nails, and remember Stanley Falkow's cartoons. It can also be helpful to wear a self-sewn face mask − you don't prevent the inhalation of aerosolized virus particles but you reduce it; more importantly, you reduce the exhalation of virus particles by wearing a face mask if you are infected but asymptomatic, that is, you do not show any of the symptoms typical of COVID-19.
 

 
 

Legend to Figure 1. Viability of SARS-CoV-1 and SARS-CoV-2 in Aerosols and on Various Surfaces. As shown in Panel A, the titer of aerosolized viable virus is expressed in 50% tissue-culture infectious dose (TCID₅₀) per li­ter of air. Viruses were applied to copper, cardboard, stainless steel, and plastic maintained at 21 to 23°C and 40% relative humidity over 7 days. The titer of viable virus is expressed as TCID50 per milliliter of collection medium. All samples were quantified by end-point titration on Vero E6 cells. Plots show the means and stan­dard errors (bars) across three replicates. As shown in Panel B, regression plots indicate the predicted decay of virus titer over time; the titer is plotted on a logarithmic scale. Points show measured titers and are slightly jittered (i.e., their horizontal positions are modified by a small random amount to reduce overlap) along the time axis to avoid overplotting. Lines are random draws from the joint posterior distribution of the exponen­tial decay rate (negative of the slope) and intercept (initial virus titer) to show the range of possible decay pat­terns for each experimental condition. There were 150 lines per panel, including 50 lines from each plotted replicate. As shown in Panel C, violin plots indicate posterior distribution for the half-life of viable virus based on the estimated expo­nen­­tial decay rates of the virus titer. The dots indicate the posterior median estimates, and the black lines indicate a 95% credible interval. Experimental conditions are ordered according to the pos­­terior median half-life of SARS-CoV-2. The dashed lines indicate the limit of detection, which was 3.33× 10^0.5 TCID₅₀ per liter of air for aerosols, 10^0.5 TCID₅₀ per milliliter of medium for plastic, steel, and card­board, and 10^1.5 TCID₅₀ per milliliter of medium for copper.