Why's my virus lingering?

In my previous post, written while in the gloomy grip of a viral illness I was eagerly awaiting the arrival of legions of lymphocytes and antibodies, all perfectly honed to deal with this particular virus. I am now at the “lingering” phase.

Disabling lassitude and gloom receded as my innate immune system retired from the field. My energy levels are nearly recovered but my sinuses are sensitive and my nasal passages and larynx are still decidedly damp.  And everyone I speak to who has had a winter virus seems to have the same complaint – it’s gone, in the main, but not yet forgotten. “It’s lingering” seems to be the common theme.

We should nod with respect to the complex interaction that helps us move into phase two. The innate system obviously “knows” when it can let up with those darn cytokines and let the adaptive system do its work. Hence the big leap forward after 4-7 days.

But why does the miraculous and ultimately effective adaptive immune system take so long to finally get rid of coughs and catarrh?

We have to imagine a numbers game. Viruses “breed” by invading cells and using material in those cells to make a new batch of viruses. The numbers produced are very, very large. Every time an infected cell bursts open they are releasing many thousands of virus particles with the potential to infect nearby cells.

The lymphocytes and antibodies are numerous too, but as they start to do their work, the virus production line is well-established so there is a massive amount of catching up to be done. It’s a bit like weeding a large patch of land on which the weeds are already producing seeds and the seedlings are sprouting almost as fast as the gardener can work. In the end the adaptive immune system always eliminates the last few viral particles. And the bonus prize is that it remembers the unique signature of the virus, so if you encounter it again next year it will be despatched without causing a single symptom.

I have just read a long and detailed account of the interaction between the immune system and the virus during flu (see link, below). As I sit here coughing I am slightly cheered by the thought that the sticky cough-inducing mucus in my larynx is the result of the wholesale death of infected cells.

This little episode has reminded me that influenza and other flu-like illnesses do nothing to enhance life. They can wipe out a week, or three while you wait for them to go. At least when it comes to influenza itself it’s easy to reduce the chances of picking it up by having a flu jab every autumn. It won’t prevent every possible virus – but it increases your chances of having a flu-free winter, and that’s worth having.
http://bit.ly/19yZ5jr

What is plasma treatment?

It’s reported in the press that a health care worker, recently diagnosed with Ebola, is being offered plasma treatment in a London hospital. This involves a transfusion of plasma from patients who have recovered from Ebola.

Plasma (blood with the cells removed) is a rich broth, full of antibodies and other immune proteins. The treatment should perhaps be re-named “antibody transfusion”.

When there's a new, unfamiliar infection the adaptive division of the immune system takes a while to set up a production line for the appropriate antibodies. First, a wandering immune cell detects the presence of a virus or bacterium and carries it to a lymph node where it's examined by passing lymphocytes. If a lymphocyte identifies it as a new threat it settles down in the lymph node, cloning a huge number of identical self-copies. These are then released (into the plasma) with the capacity to flood the body with millions of copies of the newly minted antibody. It is this lymphocyte-cloning process that takes several days.

The danger is, that in a disease like Ebola, a patient could die before their own antibodies can be produced in sufficient quantities to eliminate the virus. An infusion of antibodies from a recovered patient has the potential to keep them alive until their own production gets up to speed.

From the late 1890s plasma has been used to treat infections. Often the donor was a horse, which had been inoculated with a virus or bacterium causing it to form ample quantities of the antibody. The technique saved many lives but had its disadvantages – the need to keep large stables of horses and the risk of developing immune reactions to equine plasma proteins to name but two. The practice declined rapidly with the discovery of antibiotics and other modern drugs.

Plasma donated by human Ebola survivors has proved useful in previous outbreaks and is probably the best treatment currently available. As with any type of blood transfusion donors should be screened for viruses such as HIV. WHO has recently issued guidelines.

I’m sure we all hope that in this current UK case it will prove successful.

http://apps.who.int/iris/bitstream/10665/135591/1/WHO_HIS_SDS_2014.8_eng.pdf

Scientists synthesise antibodies

This week scientists at Yale University have announced one of those game-changing achievements that could change the future of medicine. And, probably, win a Nobel prize. They have synthesized mini-antibodies that can function within the body and attack both cancer cells and disease-causing agents.

An antibody is a highly complex macro-molecule, produced by the adaptive division of the immune system. It’s a powerful bespoke weapon that will only attack a single type of bacterium, a particular strain of virus or a cancer cell with a particular genetic signature. They lock on to receptors on the surface of the pathogens and disable them. Imagine them as tiny wheel clamps that are individually designed for each new make of car that comes on the market. One of the problems with antibody production is that it is not instant. It takes the immune system several days or weeks to get its production line up to speed and in a serious disease like Ebola, the patient can die before enough antibodies are produced. Once the antibody template has been produced, it can be used more swiftly whenever the particular threat re-appears.To work on cancer cells the immune system first has to identify them as alien.

Antibodies are tiny and these new synthetic antibodies even smaller. Picture a bespoke wheel clamp on a jumbo jet. But that might make them easier to produce.

Currently there are just a few ways in which medicine can use antibodies:

Vaccines – in which the body is induced to create a new type of antibody without becoming ill. New vaccines are hard to develop.

Extracting antibodies from blood of those previously infected. This is being tried currently to treat Ebola.

Snake bite serum – produced by injecting animals with small amount of venom and then extracting antibodies from blood serum.

Monoclonal antibodies – producing an individual antibody type in the lab, using a complex biological system.

If simpler synthetic antibodies could be produced by a less laborious process than monoclonal antibodies it would open the door to a wide range of options in treating infectious diseases and cancers.

A ground breaking moment in immunology without a doubt.

http://bit.ly/13kPg4T

Using Regulatory Immune Cells to Control Arthritis

For years now immunologists have been trying to understand auto-immune diseases, which occur when the immune system turns its weapons on the cells of its own body. This is no easy task because the immune system is extremely complex, consisting of many different types of immune cells and a host of complex chemicals. All of these interact and like the musicians in an orchestra they normally they produce a seamless performance. Orchestras need to play faster and more loudly at times but they also need to reverse this so as to play softly or slowly. In an autoimmune disease it’s as if one section of the orchestra is ignoring the conductor and just keeps playing louder and faster. The conductor’s job in the immune system is undertaken by regulatory T cells. These are a type of lymphocyte, also known as Tregs or CD8 cells, that calm things down after a period of inflammation. 

One of the most common autoimmune diseases is rheumatoid arthritis. In arthritis immune cells start attacking joints and the inflammation this causes runs out of control. For some reason the Tregs can't calm things down.

In some recently reported work, researchers injected some of Tregs into mice with arthritis and they worked – reducing the unwanted inflammation in the joints. They also used a technique to increase the number of Tregs produced by the mice and this also worked.

It is no easy task to tweak the workings of the immune system. Conventional drugs such as steroids can blunt more than one aspect of the immune system and cause other serious side effects throughout the body.

Experiments like these are beginning to give hope that one day the mountain of research papers in immunology will pay some real dividends in terms of treatments.

Article in Science Daily