Saturday 30 March 2019

Malevolent Design - A Virus to Help a Bacterium Make Us Sick!

Internalization of Pf bacteriophage within a mammalian cell.

Endocytosis of Pf by dendritic cells and other leukocytes triggers viral pattern recognition receptors, which suppress bacterial clearance. This three-dimensional image was generated by using confocal microscopy and z-stacked images (purple, actin stain; blue, DAPI (4′,6-diamidino-2-phenylindole) stain; green, Alexa Fluor 488–labeled Pf4).
Bacteria partners with virus to cause chronic wounds | News Center | Stanford Medicine

My admiration for the malevolent inventiness of creationism's putative Intelligent (sic) Designer, is growing by leaps and bounds.

Not content with designing a bacteria to infect wounds and prevent them healing, this supposed designer has given it a virus to enhance it's virulence.

We normally think in terms of viruses being parasites and there is a class of viruses known as bacteriophages (or phages) which often are parasitic on bacteria. Bacteria and viruses have been co-evolving for tens of billions of years so it shouldn't really be surprising that some have come to some sort of accommodation where the virus contributes something to the bacterium and the bacterium derives some benefit from being infected.

This example of a degree of symbiosis was however, surprising, and it could not have come about before there were more complex, multicellular organisms that could sustain damage that needed to heal.

A large team of researcher working at the Stanford University School of Medicine have found that the dangerous pathological bacterium, Pseudomonas aeruginosa, which commonly infects wound sites has weaponized one of its phage viruses so it fools the body's immune system to mount an antiviral response instead of an antibacterial response. This allows the bacterium to carry on feeding on the tissues and preventing healing.

The team published their findings in Science yesterday:

Structured Abstract


We have identified previously unsuspected, directly pathogenic roles for bacteriophage (phage) virions in bacterial infections. In particular, we report that internalization of phage by human and murine immune cells triggers maladaptive viral pattern recognition receptors and suppressed bacterial clearance from infected wounds.

Bacteriophage are abundant at sites of bacterial infection, but their effect on mammalian immunity is unclear. To investigate this, we studied Pseudomonas aeruginosa (Pa), a major human pathogen associated with chronic wounds and other infections, and Pf, a filamentous phage produced by Pa. Notably, Pf is lysogenic and its production does not typically destroy its bacterial host, unlike the lytic phage used in phage therapy for bacterial infections. Previous work had suggested that Pf phage are important in the pathogenesis of Pa infections, although the underlying mechanisms were unclear. Here, we have examined the impact of Pf on Pa wound infections in humans and in animal models.

We report that Pf bacteriophage were present in 25 of 37 (68%) Pa-infected wounds in our cohort. Furthermore, wounds infected with Pf-positive strains were significantly older than wounds infected with Pf-negative strains, and Pf was more commonly found in chronic, nonhealing wounds. Consistent with this finding, in a murine wound infection model, Pf-positive strains of Pa required an average of 50 times fewer bacteria than Pf-negative strains to establish wound infections. Additionally, mice infected with Pf-positive strains of Pa exhibited greater morbidity and mortality than mice infected with Pf-negative strains.

Mechanistically, these effects were associated with endocytosis of Pf phage by mammalian immune cells, both in vivo and in vitro. We found that uptake of Pf phage resulted in the production of phage RNA, which, in turn, triggered Toll-like receptor 3 (TLR3)– and TIR domain–containing adapter-inducing interferon-β (TRIF)–dependent type I interferon production, the inhibition of tumor necrosis factor production, and the suppression of phagocytosis. These data suggest that a natural (unmodified) bacteriophage may be able to produce mRNA within human cells.

Consistent with a pathogenic role for Pf phage, we report that a vaccine against Pf phage protects against Pa wound infections. Passive immunization of mice with monoclonal antibodies against Pf was likewise effective in protecting against Pa infection by enhancing the opsonization of Pa bacteria.

These results reveal direct, pathogenic roles for phage virions in bacterial infections. Building upon these insights, we report that vaccination against phage virions represents a potential therapeutic strategy for the prevention of infections by antibiotic-resistant Pa. These findings may have broad utility and impact beyond the pathophysiology of chronic wound infections. Pa is a major pathogen in other clinical settings as well, including lung infections in cystic fibrosis. Moreover, many other Gram-negative bacteria, including Klebsiella pneumoniae, Salmonella enterica, Vibrio cholerae, and Escherichia coli, have the capacity to harbor similar filamentous phage (genus Inovirus). Indeed, several of these phage are known to contribute to the virulence potential of their host bacteria. We propose that filamentous phage may be relevant to human interactions with a broad range of pathogenic and commensal bacteria and that these viruses may have profound, direct effects on human health and disease.

P. aeruginosa has been showing increasing drug resistance and in 2017 was named by the WHO as one of the critical priority pathogens posing the greatest risks to mankind. One of the most frequent causes of surgical amputation is infection by P. aeruginosa in diabetic ulcers. Although the phage virus normally lives inside the bacterial cell, it can be released from the cell surface when the conditions are right for it, like Herpes simplex viruses are released from the cells in a cold sore.

So, reviewing this from an ID perspective, we have:
  • A dangerous pathogen which has already been modified to give it drug resistance to overcome our medical science.
  • A virus which helps it circumvent the immune system, supposedly given to us by this same designer to help us avoid infections.
  • A purpose which appears to be either to make more dangerous pathogens complete with their complement of viruses, or to make us sick, or possibly both.

If an ID proponent can come up with a benevolent reason for all that, or even an intelligent reason for giving us an immune system then designing a bacterium to get around it, I would be pleased to hear it.

So far as I can see, if such a designer really exists, its only intelligent reason for doing this is because it changed its mind about wanting us to avoid becoming infected and now wants to make us sick. Changing its mind means it can't be omniscience and wanting us sick means it can't be benevolent but instead, is malevolent and sadistic, creating pain and suffering for the sake of it.

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