Hogga's perfect Easter - surrounded by broads.

Norfolk Broads that is. The medieval digging for peat in this area has left ditches and sunken areas which have filled with water; these are interlinked by the major rivers and canals around, forming a space of reed-fringed waterways that extends through Norfolk in a North-South band passing a few miles to the East of Norwich. And from April through to September these waterways are liberally covered with a great profusion of boats. Families hire the boats - often large cabin cruisers - and chug slowly around, stopping here and there to visit local villages and, more importantly, local pubs.

It's a strange old week at work right now. School holidays of course - so many people have taken off for sunnier climates leave anyway. The weather in Norfolk is still a little cool for what is essentially spring - in fact last week someone was taking bets on us having a White Easter - and so I decided that I'd not take any extra leave. More likely mid-year when I'll head to SA for a visit. Nevertheless there still remained a few days to fill with something unusual, so we headed for a little town called Acle and hopped aboard the "Pearl Horizon 2", which is a 32-foot cruiser with a breakneck top speed of around 7 knots (and that is too fast for the Broads, where speed cops patrol in little rubber duck Zephyrs).


My cruising companion helped me with the tricky task of mooring stern-on in a vast wallowing tub of aboat with absolutely no rearward visibility - and as you can see I did a passable job, albeit with much salty nautical language and indeed some military oaths not often heard in these parts. Here we are moored in Ranworth Broad, a little offshoot of the river Bure between Acle and Horning. Lots of bird life, including a confused looking black swan in between loads of white ones. No mammals spotted except of course the familiar squat and tattooed forms of Homo Touristensis.

One amazing thing here in Norfolk is the large amount of hippies, gypsies, fen people and general Woodstock refugees that pop out of the reeds and marshes on bank holidays. Men wearing earrings, gold rings on most fingers, greying ponytails and a mix of denim and camouflage. Of course it is my considered belief that anyone who has been obliged to wear camouflage for a living will never be able to wear it as a fashion statement. Nevertheless, we seem to have a strange subculture here that I've not seen anywhere else in England.


Still, a nice time was had by all. A couple of beaut sunsets, some relaxed cruising and lots of bacon and eggs. So much so, in fact, that I am obliged to once again endure the rigours of the Atkins Diet lest I become unable to fit through the door of my new cottage. Hopefully the present uneasiness and general state of worry in our restructuring HR department will soon be over and we can all get back to working and, in my case, waddling to and from the gym.

Lipid Mosaic

Ha ha so somewhere out there in the land of my readers is a secret virus anorak... wanting to know about the attachment of the virus to the cell indeed. Well Ok Mici, let's see what I can do.

I suppose firstly we need to look at the structure of a flu virus (from the Orthomyxovirus family, name derived from the Greek word myxa meaning mucus), and the structure of a normal cell. Of course any mammalian cell with a nucleus will do, or even avian cells. Nucleated - that's the key.

So - let's start with the structure of a cell with a nucleus. And what keeps the nucleus and associated little organelles from spilling into the street is a membrane holding it all together. For ease of understanding how this membrane looks, we can use the now somewhat outdated Singer Nicholson model of a double layer of lipids (fat molecules if you prefer) with islands of protein floating around randomly in this little fatty sea. More bookish anoraks are referred to http://scienceweek.com/2005/sw051223-3.htm where the latest thinking is contained.

The virus however, is slightly different. We already know that the influenza virus has a spiky coat (and just to complicate things the viral genome or set of instructions for making more influenza viruses is split into 8 pieces, and all of these need to be present at once for infection to occur). But never mind all that Dan Brown stuff, let's focus on the way the little bugger gets into the cell.

Mr. Flu is a spiky little bugger, as I will remind you, and looks rather like this http://www-ermm.cbcu.cam.ac.uk/01003465h.htm or like this -
















and also with a bilayered membrane (lipid envelope) surrounding it. The lipids in this bilayer are probably nicked from the previous host cell's membrane (imagine the little baby viruses bursting through the cell walls like that creature in Alien exiting the chest of a hapless crew member - and becoming coated with a layer of fatty slime in the process) but the protein bits are all viral. Not that the cell bursts, you understand - in this particular kind of flu infection and because of the way the viruses leave the cell by "budding" through the membrane, cell integrity is maintained. Viruses that don't need the lipid coat feel quite free to burst the cell as they leave, and can cause spectacular damage.

But I am getting ahead of myself here. First the virus must attach to the surface of the cell membrane. This is unaffected by temperature, but strongly sensitive to pH (occurring best at neutral pH), implying some sort of electrostatic binding between the amino groups on the virus protein spikes and the acidic phospholipids of the cell membrane. In fact, as is common with many viruses, the binding occurs with something called sialic acid (also known as 5-N-acetyl neuraminic acid and I just know that many of you will be spotting the link to the viral spike neuraminidase already..).

So the virus kinda drifts up against a cell - attracted by electrostatic forces to the appropriate sites on the cell membrane where exactly the right bits lock together. Haemagglutinin (thus named because it can cause clumping or agglutination of red blood cells, a useful trick for a virus to have) locks onto the correct receptor site of sialic acid and then, perhaps assisted by our old friend neuraminidase here although evidence is sketchy, the cell's membrane becomes a little more flexible and the virus slips through by a process called endocytosis. That means the whole virus enters the cell, not just the RNA instructions (some other viruses operate in this second way, injecting their replicating code into the cell while leaving their capsule outside). But the important point is that the fatty cell membrane becomes more easily penetrated and the virus sinks into it and then through into the cell.

In some cases the flu virus may, for reasons best known to itself, decide not to infect the cell after attachment. This is when the neuraminidase spikes come in useful - neuraminidase as mentioned before is an enzyme and has the specific function of cleaving neuraminic acid, so the virus can then disengage and drift off again. Usually, however, the process unfolds normally, virus enters cell, the little packages of RNA instruct the cell to stop making its own proteins and start making the building blocks of more viruses, the blocks drift together and assemble into finished examples of Orthomyxoviridae, loosen the cell membrane from the inside now with judicious applications of neuraminidase and then pop out through this Singer Nicholson lipid mosaic membrane that started the whole rambling blog entry...

Sheesh. It's been a long time since Microbiology III (23 years to be precise) and I must admit to needing to refresh my knowledge a little. Useful sites include http://www-ermm.cbcu.cam.ac.uk/01003465h.htm and
http://www.pnas.org/cgi/content/full/100/25/14610

I didn't go into any detail on which body locations have cells with more or less receptors for different kinds of H spikes - but you're welcome to check that out yourselves. Of course different species will have different receptor concentrations so infection may occur by inhalation, ingestion or other methods depending on where in the body the cells are with the most amount of the right receptors for that kind of virus...

Have fun and try not to cuddle any chickens

Bird Flu in England

"werl, not really a problem for me izzit? I mean this bird flu stuff. Why? Cos I'm a bloke, of course."

Watching the TV as I sweated away on an exercise cycle in the gym this morning, it struck me how dumbed down the news in the UK really is. And how patronising are the various "experts" called on to explain that there really is no danger. I guess they're forgetting the last epidemic, five short years ago, when a variety of similar experts and boneheaded bureaucrats laid waste to vast areas of the country and burned much of the national herd trying to combat the spread of another virus amongst animals.

The influenza virus is a sneaky little bugger. It has a protein coat with spikes on - two kinds of spike actually. The one kind, haemagglutinin (abbreviated to H) has 16 variants of which three have been seen in cases of human infection so far (H1, H2 and H3) and the rest have been implicated in animal infections.

The other protein, neuraminidase (I suppose technically it's an enzyme, ending in -ase as it does) has 9 variants, of which two have thus far been seen in human infections (N1 and N2) and the rest in animal infections.

So there are hundreds of different possible variations in the "spike pattern" on the virus coat. If it's a H1N1 pattern then there is a fair chance it can infect a human, and so on. In fact there is a relatively high level of residual immunity in the world population to some of these variants, due to repeated infections.

Each time a virus infects a cell, it essentially commandeers that cell's assembly line for making useful proteins and converts it over to making more viruses. These are eventually released (often by rupturing the cell) and bumble off to infect other cells. As with any rush production line, the replicating process can, over time, cause some slight changes in the nature of the spikes even though broadly they still remain the same kinds of H and N as they were. Some people believe this is due to the malign nature of the virus, ascribing a level of cunning to it, while others look at it as typical of any knock-off factory in Asia with a high tolerance for defects in its mass production.

This slight alteration in the pattern on the protein coat of the virus (called antigenic drift, which is the slow change in the spikes which make them become slightly different "strains" of 'flu and allow them to sneak past the very literal-minded antibodies guarding our systems, kind of like Peter Sellers disguising himself with a false nose in the "Pink Panther" movies) is why we sometimes have only partial immunity to a strain of the disease.

A more fundamental change in the spikes (antigenic shift) can also happen. This is when, with a snap and a crackle (like a hedgehog rolling into a ball) a new set of spikes appear, new H and N proteins that the human body does not recognise at all and consequently is not immune to. Sometimes this is associated with interspecies transmission of the virus - and that's what we're worrying about here.

The birds dying of Avian Flu at the moment are contracting an H5N1 strain of the virus. Traditionally this is not a concern for humans, unless of course you are a poultry farmer and see your livelihood expiring in small sneezing lumps of feathers around you, but for some strange reason it seems that humans are occasionally able to contract this strain of H5N1 from birds, although mercifully as yet the virus expires with the patient and is not transmitted onwards to another human.

If, however, the H5N1 virus undergoes an antigenic shift as a result of its travels from bird to human, and then becomes a different strain that can cause infection from human to human, why then dear readers we are in deep doo-doo. Because already if a human catches H5N1 avian 'flu, they often die. And all that is saving us right now is that the little bugger of a virus has not yet worked out how to reconfigure its spikes so as to pass from person to person.

So no real point in rushing off to your doctor for a 'flu vaccination (unless you're in the traditional "at risk" category of elderly or infirm and want to avoiud catching normal 'flu). Why? Well, the H5N1 variant that is transmissible from human to human does not yet exist, and so it is not yet possible to get some in a syringe and inject it into chicken eggs (strangely enough that is how we make vaccines, and I am sure I'd be laughed at if I pointed out a correlation between this method of growing viruses to be later killed and made into vaccines and the rise of bird to human transmision of viruses).

So then, all you ever wanted to know about flu. Not complicated. But sadly enough, too many big words for Sky News and so all we get is more and more impossibly-coiffed presenters asking dumb questions of nerdy scientists. And a blanket reassurance that we have more chance of winning the lottery than of catching bird flu. Tell you what, though, someone does win the lottery quite often. And if that winning ability was able to be spread from human to human, why we'd be millionaires quite soon in this overcrowded little island.

See ya.