Viruses

Viruses contain proteins and a nucleic acid (DNA or RNA), and some viruses are membrane-limited. Also, they interact very specifically with living cells, often replicating themselves with lethal consequences for the host. They subvert the host's molecular machinery and force it to work according to their own instructions. In these respects, viruses resemble organisms and there is little doubt that they are related to organisms, so they are proper subjects for biologists. Nevertheless they are not alive.

Let us examine this claim, which some biologists might consider heterodox. (Others, such as Lynn Margulis, would agree with us.) First, viruses have no metabolism. They have no devices for making energy and materials available. When they infect a host cell their replication depends on the host's manufacturing and energy-supply systems. They have no internal transport processes and do not exhibit cellular homeostasis. Outside the host they are as quiescent as crystals. They have elaborate and distinctive structures; indeed, a virus can be distinguished from other viruses by its structure. But lacking metabolism, "cellular homeostasis" and transport, they have no internal states.

Second, their genomes are minute, comprising perhaps only half a dozen genes. Even the simplest bacteria have genomes more than a hundred times bigger. During infection the viral genes are transcribed in a prescribed order, but this depends on the host's protein synthesising equipment. Also, all the viral genes are expressed during infection; none is expressed outside the host cell; so there is no "pattern of gene expression" of the kind we discussed in chapters 8-9, susceptible to alteration in response to internal state changes and external stimuli.

Third, the only "stimulus" to which a virus responds is a receptor on the host cell surface. The virus binds to this and is either engulfed by the cell or injects its nucleic acid through the host membrane. There is no semblance of a signalling pathway. There is no processing of stimulus information.

Therefore, a virus has scarcely any of the main characteristics of the living state that we have identified. Viruses are sometimes called "the ultimate parasites". As we said earlier, parasites lack some components that would be needed for life outside the host, and viruses certainly lack the components needed for independent life. But the metaphor is misleading. Tapeworms, parasitic amoebae, malarial parasites and pathogenic bacteria all consist of one or more cells, and these cells have distinctive internal states and patterns of gene expression, though their stimulus-response repertoires might be limited. Parasites are unquestionably organisms. Viruses, on the other hand, do not have internal states, gene expression patterns or stimulus-response systems, so they are not organisms.

Can viruses be dubbed "potentially living", as plant spores are? Some authors take this position, but once again we consider the analogy flawed. A spore contains all the equipment necessary for the intricate choreography of internal state, gene expression and stimulus-response. It only awaits the signal to start the music. There is no such "suspended animation" in the case of a virus; the necessary equipment is not present. It must be supplied by the host.

When a virus infects a cell there are three possible consequences. First, the viral nucleic acid - or the whole infected cell - might be destroyed. From the virus's point of view this is a failure. Second, the host cell machinery might be subverted to replicating the virus. The end result is the destruction of the host cell and the release of several hundred new copies of the virus, each able to infect a new host cell. Third, the viral genome might be incorporated into the host genome. The host cell will continue to live, but it has been irreversibly if subtly altered. Assimilation of viral genes into the host genome has interesting evolutionary implications, which we shall discuss in a later chapter.

Some mammalian diseases known as spongiform encephalopathies have been attributed to the effects of an infectious "rogue protein", a prion. Nowadays, the most familiar of the spongiform encephalopathies is BSE, commonly known as "mad cow disease". The oldest known example is scrapie in sheep. These diseases cause slow, progressive destruction of the brain tissue and a deposition of tangled and highly resistant protein fibrils at the sites of damage. The disease is ultimately fatal. According to current beliefs, the prion closely resembles a normal brain protein. It enters the brain and subverts the organisation of this normal protein, thus producing many more copies of itself. If this account is correct, then a prion behaves very much like a virus. Indeed, these diseases were previously known as "slow virus diseases". But no one would suggest that a single protein molecule is "alive".

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