Posts Tagged ‘Virus’

If a virus is not alive, how does it die?

March 24, 2020

You can’t strictly kill a virus since it is not alive.

Outside living cells, some viruses remain potentially active for thousands of years. A virus recovered from permafrost was able to infect an amoeba. Influenza and corona viruses are thought to stay active for a few hours or days. But the smallpox virus can remain active for years

These days there are many reports about how long the coronavirus remains “alive” or “viable” or “active” on surfaces.  For example this is an abstract of a new paper (yet to be published):

Aerosol and surface stability of HCoV-19 (SARS-CoV-2) compared to SARS-CoV-1

Abstract
HCoV-19 (SARS-2) has caused >88,000 reported illnesses with a current case-fatality ratio of ~2%. Here, we investigate the stability of viable HCoV-19 on surfaces and in aerosols in comparison with SARS35 CoV-1. Overall, stability is very similar between HCoV-19 and SARS-CoV-1. We found that viable virus could be detected in aerosols up to 3 hours post aerosolization, up to 4 hours on copper, up to 24 hours on cardboard and up to 2-3 days on plastic and stainless steel. HCoV-19 and SARS-CoV-1 exhibited similar half-lives in aerosols, with median estimates around 2.7 hours. Both viruses show relatively long viability on stainless steel and polypropylene compared to copper or cardboard: the median half-life estimate for HCoV-19 is around 13 hours on steel and around 16 hours on polypropylene. Our results indicate that aerosol and fomite transmission of HCoV-19 is plausible, as the virus can remain viable in aerosols for multiple hours and on surfaces up to days.

But then I also read that viruses are not “alive”. They are just a bunch of chemicals, non-bacterial pathogens,  which, by unknown mechanisms, just happen to have

  1. long molecules of DNA or RNA that encode the structure of the proteins by which the virus acts;
  2. a protein coat, the capsid, which surrounds and protects the genetic material; and
  3. in some cases an outside envelope of lipids

Scientific American:

For about 100 years, the scientific community has repeatedly changed its collective mind over what viruses are. First seen as poisons, then as life-forms, then biological chemicals, viruses today are thought of as being in a gray area between living and nonliving: they cannot replicate on their own but can do so in truly living cells and can also affect the behavior of their hosts profoundly. The categorization of viruses as nonliving during much of the modern era of biological science has had an unintended consequence: it has led most researchers to ignore viruses in the study of evolution. Finally, however, scientists are beginning to appreciate viruses as fundamental players in the history of life. …..

What exactly defines “life?” A precise scientific definition of life is an elusive thing, but most observers would agree that life includes certain qualities in addition to an ability to replicate. For example, a living entity is in a state bounded by birth and death. Living organisms also are thought to require a degree of biochemical autonomy, carrying on the metabolic activities that produce the molecules and energy needed to sustain the organism. This level of autonomy is essential to most definitions.

Viruses, however, parasitize essentially all biomolecular aspects of life. That is, they depend on the host cell for the raw materials and energy necessary for nucleic acid synthesis, protein synthesis, processing and transport, and all other biochemical activities that allow the virus to multiply and spread. One might then conclude that even though these processes come under viral direction, viruses are simply nonliving parasites of living metabolic systems. But a spectrum may exist between what is certainly alive and what is not.

A rock is not alive. A metabolically active sack, devoid of genetic material and the potential for propagation, is also not alive. A bacterium, though, is alive. Although it is a single cell, it can generate energy and the molecules needed to sustain itself, and it can reproduce. But what about a seed? A seed might not be considered alive. Yet it has a potential for life, and it may be destroyed. In this regard, viruses resemble seeds more than they do live cells. They have a certain potential, which can be snuffed out, but they do not attain the more autonomous state of life. Another way to think about life is as an emergent property of a collection of certain nonliving things. Both life and consciousness are examples of emergent complex systems. They each require a critical level of complexity or interaction to achieve their respective states. A neuron by itself, or even in a network of nerves, is not conscious—whole brain complexity is needed. Yet even an intact human brain can be biologically alive but incapable of consciousness, or “brain-dead.” Similarly, neither cellular nor viral individual genes or proteins are by themselves alive. The enucleated cell is akin to the state of being braindead, in that it lacks a full critical complexity. A virus, too, fails to reach a critical complexity. So life itself is an emergent, complex state, but it is made from the same fundamental, physical building blocks that constitute a virus. Approached from this perspective, viruses, though not fully alive, may be thought of as being more than inert matter: they verge on life.

But how then do they die? Clearly there has to be a chemical change. Is it just a case of going from active to inactive as chemistry changes?

And that begs the question as to what that chemical change might be.


 

If you can’t kill the virus, kill the cells that contain the virus

August 11, 2011

An ingenious way of getting around the problem of attacking viruses. An MIT press release desribes a development that could transform how viral infections are treated. A team of researchers at MIT’s Lincoln Laboratory has designed a drug that can identify cells that have been infected by any type of virus, then kill those cells to terminate the infection.

Rider TH, Zook CE, Boettcher TL, Wick ST, Pancoast JS, et al. (2011) Broad-Spectrum Antiviral Therapeutics. PLoS ONE 6(7): e22572. doi:10.1371/journal.pone.0022572

Todd Rider invented the PANACEA and DRACO antiviral therapeutics, and previously invented the CANARY (Cellular Analysis and Notification of Antigen Risks and Yields) sensor for rapid pathogen detection and identification: Image MIT

In a paper published July 27 in the journal PLoS One, the researchers tested their drug against 15 viruses, and found it was effective against all of them — including rhinoviruses that cause the common cold, H1N1 influenza, a stomach virus, a polio virus, dengue fever and several other types of hemorrhagic fever.

The drug works by targeting a type of RNA produced only in cells that have been infected by viruses. “In theory, it should work against all viruses,” says Todd Rider, a senior staff scientist in Lincoln Laboratory’s Chemical, Biological, and Nanoscale Technologies Group who invented the new technology.

Because the technology is so broad-spectrum, it could potentially also be used to combat outbreaks of new viruses, such as the 2003 SARS (severe acute respiratory syndrome) outbreak, Rider says.

Other members of the research team are Lincoln Lab staff members Scott Wick, Christina Zook, Tara Boettcher, Jennifer Pancoast and Benjamin Zusman.


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