In a recent post I talked about a metabolic poison that can decouple electron transport and oxidative phosphorylation.  You may be interested to know that this process is a known mechanism in infants.  This is not mediated by the same metabolic poison as I mentioned before, but rather by a naturally produced protein called thermogenin.  This protein causes the uncoupling of electron transport and oxidative phosphorylation in a cell’s mitochondria.  Check back a few posts for the mechanism if you’re interested.

So where does this take place?  If it took place in all cells (like if someone were to take that metabolic poison) the infant would be unable to survive.  Infants have specialized cells called brown adipose tissue or “brown fat” where this takes place.  These cells have many small fat vacuoles and mitochondria.  The normal fat found in adults is referred to as white fat.  Adults don’t have much (if any) brown fat.  By decoupling electron transport and oxidative phosphorylation the cell redirects the metabolic energy.  This results in the generation of heat and infants don’t need to shiver.  Neat, huh?

Dengue is a medically relevant virus that is common in tropical climates. The virus itself is a single stranded RNA virus. It is spread by the mosquito Aedes aegypti. It causes two diseases, dengue fever and dengue hemorrhagic fever. One cannot contract the second without having had the first. This is a very interesting component of dengue infection that relies on the host’s immune response. It is also why vaccination for dengue is seen as a risky proposition.

There are four different strains of dengue virus. These strains are very similar; so similar in fact that the immune system recognizes all of them after seeing only one. But recognition is not protection. Human T-cells each are programmed to recognize a specific pattern (or antigen). In the first infection virus particles will be captured and processed by so-called antigen presenting cells. These viruses will be presented to T-cells causing them to become activated. And likewise B-cells will encounter their antigen free floating and become activated. B-cells produce antibodies. Antibodies are used (among other things) to tag the viruses to encourage their uptake by macrophages (called opsonization) and inactivate them.

This first infection is known as dengue fever and will last 6 or 7 days. Its symptoms are much like a severe flu. Most people get over it without incident. If one becomes infected again things could go wrong. There are four strains of Dengue, all of which are all very similar. If you are infected with a different strain than you encountered the first time, you will contract dengue hemorrhagic fever.

But why does this happen? As it turns out, the antibodies from the first infection will attach to the virus particles but will not inactivate them. The strains are just different enough to remain active in the presence of another strain’s antibodies. These are referred to as “non-neutralizing antibodies”. These antibodies will still cause opsonization. So Macrophages willingly take up infectious viruses. This accelerates the course on infection to such a degree that hemorrhagic symptoms are seen. It’s one of those interesting times when our immune systems fail us. Imagine if people were vaccinated for dengue. What if someone missed one of the four vaccines or one was innactivated by improper storage? They would be quite prone to dengue hemorrhagic fever.