Some science behind the scenes
A bacteriophage is a virus that infects and replicates within a bacterium. The term is derived from "bacteria" and the Greek: φαγεῖν (phagein), "to devour". The word devour is misleading. Generally speaking, the viruses do not actually harm their host, but co-exist, using them like a Trojan horse to enter other organisms. In effect the bacteria, perhaps being one less likely to be attacked by the immune system because it is one naturally found in the host, is used as a hiding place in the host – a place in which the virus can breed and spread its little phages.
Bacteriophages are composed of proteins that encapsulate a DNA or RNA genome. They may be released via
- Cell lysis - Lysis, by tailed phages, is achieved by an enzyme called endolysin, which attacks and breaks down the cell wall peptidoglycan.
- Extrusion - An altogether different phage type, the filamentous phages, make the host cell continually secrete new virus particles. Released virions are described as free, and, unless defective, are capable of infecting a new bacterium
- Budding - Budding is associated with certain Mycoplasma phages.
In contrast to virion release, phages displaying a lysogenic cycle do not kill the host but, rather, become long-term residents.
Nowhere near enough research has been done on phages. There are a large number of bacteria which appear to do no harm to about 98% of their hosts, but in 2% of cases are virulent and exceptionally destructive, and the reason may be the phages and not the bacteria. In effect we are blaming bacteria for a host of diseases which may actually be virus related - phage related.
The clue is often the response of the bacteria to antibiotics. There are some antibiotics that appear to be effective against certain bacteria. The illness goes on medication. But there are an increasing number of illnesses which do not respond to antibiotics even though the infection is bacterial, and the reason may be the spread of the viruses in a weakened and innocent bacteria population.
The destructive nature of virus phages in nature in general is already known, the research questions still to be tackled is not if it happens but to which bacteria does it apply, for example
Disease is an increasing threat to reef-building corals. One of the few identified pathogens of coral disease is the bacterium Vibrio coralliilyticus. In Vibrio cholerae, infection by a bacterial virus (bacteriophage) results in the conversion of non-pathogenic strains to pathogenic strains and this can lead to cholera pandemics. PMID: 26644037
This question has become of far greater importance now that research is actually centring on the use of phages as a form of antibiotic. We could be opening up a pandora’s box of troubles here, as the ‘good bacteria’ are killed off in their billions and the viruses actually causing the disease multiply in their trillions - and those same viruses are killing us. So we are faced with the bleak future of extinction by viruses we have let loose.
It looks like the planet in the future will be owned by viruses, if science has its way.
Some good research has been ongoing about just how dependent these viruses are on the bacteria, and the answer appears to be – not at all. A fair number look like they can live without the bacteria they have used as their Trojan horse, which makes the prospect of their use even more alarming because we cannot remove them using conventional antibiotics.
All viruses are obligate intracellular parasites and depend on certain host cell functions for multiplication. However, the extent of such dependence and the exact nature of the functions provided by the host cell remain poorly understood.
Here, we investigated if nonessential Bacillus subtilis genes are necessary for multiplication of bacteriophage SPP1.
Screening of a collection of 2,514 single-gene knockouts of nonessential B. subtilis genes yielded only a few genes necessary for efficient SPP1 propagation. Among these were genes belonging to the yuk operon, which codes for the Esat-6-like secretion system, including the SPP1 receptor protein YueB. In addition, we found that SPP1 multiplication was negatively affected by the absence of two other genes, putB and efp. The gene efp encodes elongation factor P, which enhances ribosome activity by alleviating translational stalling during the synthesis of polyproline-containing proteins. PutB is an enzyme involved in the proline degradation pathway that is required for infection in the post-exponential growth phase of B. subtilis, when the bacterium undergoes a complex genetic reprogramming. The putB knockout shortens significantly the window of opportunity for SPP1 infection during the host cell life cycle. This window is a critical parameter for competitive phage multiplication in the soil environment, where B. subtilis rarely meets conditions for exponential growth. Our results in combination with those reported for other virus-host systems suggest that bacterial viruses have evolved toward limited dependence on nonessential host functions.
A successful viral infection largely depends on the ability of the virus to hijack cellular machineries and to redirect the flow of building blocks and energy resources toward viral progeny production. However, the specific virus-host interactions underlying this fundamental transformation are poorly understood. Here, we report on the first systematic analysis of virus-host cross talk during bacteriophage infection in Gram-positive bacteria. We show that lytic bacteriophage SPP1 is remarkably independent of nonessential genes of its host, Bacillus subtilis, with only a few cellular genes being necessary for efficient phage propagation. We hypothesize that such limited dependence of the virus on its host results from a constant "evolutionary arms race" and might be much more widespread than currently thought. PMID: 25540376
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