What is Swine flu?

Swine flu is splashed all over the news and the Internet. I thought I should illuminate readers on how it actually works, because it is rather interesting.

Firstly, what's the big deal with influenza? Why don't we see similar pandemic outbreaks with let's say the Rabies virus, or the Measles virus? The answer lies in the structure.

Influenza virus is a spherical virus having two kinds of receptors on its surface coat which help it to infect a host: Haemagglutinin (H) & Neuraminidase (N). Think of it as a sphere with two kinds of embedded rods in it.

Accordingly, different strains of the virus are called H1N1, H3N2 etc. depending on the type of H and N rods they have. Inside this sphere, there is the nuclear material (RNA) of the virus. Here's the catch. Most bacteria and viruses have a single piece of DNA/RNA as their nuclear material. Influenza's nuclear material is split into 8 pieces or segments. These segments code for, amongst other things, those H and N rods. (Nucleic acids code for proteins remember?)

This 8-segmented genome property of influenza allows it to undergo a process called 'Antigenic shift' which is responsible for these sudden pandemics.

Here's how antigenic shift works:

Firstly, it occurs often in pigs, because pigs can be infected with two influenza strains at the same time (which is why we have 'swine' flu).

So lets say we have a pig 'The Empress' (nod to Wodehousians). The Empress has been infected with two strains of influenza, H1N4 and H4N1. Both the strains infect cells in the pig. They do this by

1) Using their H 'rods' to bind to the lung cells.

2) Entering the cells.

3) Releasing their RNA into the cells.

4) The RNA is multiplied to make many copies.

5) These many copies of RNA serve two purposes: One, they make new H and N rods and new coats. Two, they get packaged into these new coats (eight segments each) to make new complete viruses.

6) The cell bursts releasing new viruses that infect more cells

Now here's the awesome part:

Strain A (H1N4) and Strain B (H4N1) BOTH release their RNA. The viruses multiply in the cell and make four types of receptors: H1, N4 AND H4, N1. All these are floating in the cell. During the packaging, there's a mix up. The RNA segments of both strains mix up and get packed into the wrong coats i.e. of the OTHER strain.

This gives a new strain with H type 1 (from strain A) and N type 1 (from strain B). It is thus called H1N1.

All the vaccines for influenza were specific for H1N4 and H4N1. Similarly all the natural immunity we have is specific for those two only because we may have been exposed to it before. No vaccine is for H1N1 because it didn't exist before! So now, for the moment, the virus is invincible.

Well not exactly, some drugs still work for this new 2009 strain. Eg: Oseltamivir (Tamiflu) and Zanamivir (Relenza) though it is resistant to Amantidine & Rimantidine.

Vaccines for the same are in development. The problem is viral vaccines take a month or so to make and then they have to pass a rigorous set of safety tests.


Addendum 1: Influenza isn't the only virus that has multiple segments. So do HIV and the Rotavirus (common cause of infantile diarrhoea, you must have seen the vaccine ad). However in Rotavirus the phenomenon is called 'reassortment' and in HIV 'recombination'. 'Antigenic shift' is a term solely for influenza. Now in rotavirus and HIV infection/reassortment/recombination doesn't occur between very genetically diverse strains, thus minimising the damage done by the recombined strains. This is because the new strain is still significantly similar to the two parent strains and is thus susceptible to a certain extant to previously used vaccines/drugs. I don't know why it doesn't occur. A probable guess is viral receptor interference.

Addendum 2: Whether the packaging is specific (taking one segment of each of the eight types) or random (randomly any 8 fragments are taken) is unknown. In the random process one would get only 1 functional virus for every 400 assembled. However, recent evidence indicates that the process might be partially specific.

Addendum 3: A little bit on how the drugs work. Oseltamivir and Zanamivir are neuraminidase inhibitors. You see, once the complete spherical viruses are ready to leave the cell, the H receptor still anchors them to the host cell. Here's where Neuraminidase (N) kicks in. It breaks the bond between H and the host cell, so that the virus can be free and infect neighbouring cells. Now these two drugs bind to N and inactivate it. So viruses remain attached to one cell and cant infect others.
Thus Oseltamivir & Zanamivir don't kill the virus, they just limit its spread. Something like 'damage control'

On the other hand Amantidine & Rimantidine bind to a protein called M2 on the virus. This protein is required for the virus to release its RNA into the cell. However, mutations in M2 that prevent the drug from binding to it can make a virus resistant to the same.

Well, that's about all that I know. I might have made some mistakes, if you spot them, do tell me.

Cheers,