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When viruses and bacteria unite!

The views expressed are those of the author and are not necessarily those of Scientific American.


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Illnesses have a tendency to clump together. An attack of the flu can bring on bacterial lung infections; in the USA almost half of all cases of bacterial sepsis occur following viral infections in the lungs. This is a problem at the best of times as it means that patients spend longer in hospitals, but in times of a viral pandemic it becomes incredibly deadly.

One clear reason for this can be fairly easily deduced. A viral lung infection leads to raw red areas, at the very least around the side of the nose! Anywhere that the outer layer of skin is compromised is going to be a site for easy bacterial entrance. And the mouth, throat and nasal areas are pretty much crawling with bacteria anyway which need very little excuse to break in.

That is a *very* big hankie

Virus heading out, bacteria heading in! Image from wikimedia commons via mcfarlandmo's photostream.

The immunology behind the connection between viral and bacterial infections is slightly harder to pin down. The immune system is a highly complicated network of responses, but for both bacteria and viruses it starts by recognising common proteins and glycoproteins found in microorganisms.

Common bacterial cell-wall particles are recognised by a set of receptors called the NOD-like receptors, the most important two for the purposes of this post are called Nod1 and Nod2. Nod1 receptors tend to be more specific to Gram negative bacteria, whereas Nod2 can recognise both Gram negative and Gram positives. Once they recognise the bacterial glycoproteins, these receptors activate the innate immune response, which recruits white blood cells that specialise in eating foreign particles (macrophages) and leads to inflammation around the affected area.

Possibly the easiest figure I've had to draw!

A "blobological" diagram of Pathogen Receptor Molecules. NOD proteins work in a similar way, but they are completely INTRACELLULAR and only recognise bacterial proteins that have been broken down inside the cell. (c) me.

Although this immune response is important to help clear the infection, over activating the innate immune system can lead to severe problems including septic shock and multi-organ failure. It could be that it is simply the combined effect of both a viral and a bacterial infection that overloads the innate immune response. But researchers (in ref. 2) have found a more specific connection. Infection by viruses specifically increases the Nod1 and Nod2 response to the secondary bacterial infection, leading to a lethal immune response.

How does this work? The researcher’s argument is that the viral infection produces certain immune system chemicals which help to make the Nod1 and Nod2 hypersensitive. Biochemically this can be shown by adding these chemicals into a cell system and watching the Nod1 and Nod2 response increase. On a larger level, mice infected with a bacterial infection (following infection by viruses – you do feel rather sorry for the mice in this paper!) actually survived far better when they had both of their Nod proteins knocked out.

Quite why this is an evolutionary advantage within a body is unclear. It could be argued that at a time when your body is suffering from a viral infection it is a wise idea to have the cells hypersensitive towards any other invading infectious species. After all, there are many cases of people who don’t die after a viral-and-bacterial infection, and in that case the extra immunity might help. Some of the chemicals that the viruses used to augment the Nod response are also produced when certain types of bacteria invade the body, so this system may also act as a positive feedback loop to help clear bacterial infections.

Whatever the reason, it’s always good to have as much information about the interplay between viral and bacterial infections as possible. Diseases do not happen in a vacuum, and sometimes it is the interaction between two infections, rather than their separate effects, that produces the most dangerous outcome.

Ref 1 = Beadling, C., & Slifka, M. (2004). How do viral infections predispose patients to bacterial infections? Current Opinion in Infectious Diseases, 17 (3), 185-191 DOI: 10.1097/00001432-200406000-00003
Ref 2 = Kim YG, Park JH, Reimer T, Baker DP, Kawai T, Kumar H, Akira S, Wobus C, & Núñez G (2011). Viral infection augments nod1/2 signaling to potentiate lethality associated with secondary bacterial infections. Cell host & microbe, 9 (6), 496-507 PMID: 21669398
Ref 3 = Brundage, J. (2006). Interactions between influenza and bacterial respiratory pathogens: implications for pandemic preparedness The Lancet Infectious Diseases, 6 (5), 303-312 DOI: 10.1016/S1473-3099(06)70466-2

S.E. Gould About the Author: A biochemist with a love of microbiology, the Lab Rat enjoys exploring, reading about and writing about bacteria. Having finally managed to tear herself away from university, she now works for a small company in Cambridge where she turns data into manageable words and awesome graphs. Follow on Twitter @labratting.

The views expressed are those of the author and are not necessarily those of Scientific American.





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  1. 1. Kevbonham 11:03 am 07/22/2011

    Great post!

    I wonder what the effect of viral infection on the normal flora in your lungs are. Since NODs are so critical to modulating gut flora (NOD knockouts get way worse colitis), is interesting that in this model the subsequent pathology is better in the NOD knockouts in the lung.

    Also, immunology pedantry warning: NOD’s are intracellular receptors, not transmembrane :-)

    Link to this
  2. 2. Kevbonham 11:04 am 07/22/2011

    effects*… are

    Link to this
  3. 3. S.E. Gould in reply to S.E. Gould 6:17 am 07/23/2011

    Ah dammit they are intracellular aren’t they. I think I got them mixed up with the plant versions, which definitely are transmembrane. Thanks for the comment (and thanks for joining the network!) I will make a correction under the figure.

    Link to this

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