MadSci Network: Virology

Re: What exactly is encephalitis and how do you get it?

Date: Mon Dec 17 00:40:01 2001
Posted By: Joshua Chai, Medical student, Medical Sciences, University of Cambridge
Area of science: Virology
ID: 1008263142.Vi

Hi Amanda,

To answer your question I need to tell you something basic about 
pathology. Your teacher is absolutely right to tell you that, in short, 
encephalitis is an inflammation of the brain. Viral encephalitis is 
endemic in some parts of the world; it may occur epidemically or 
sporadically. But what is “inflammation” anyways? Often in everyday 
term “inflammation” is used as a blanket term to denote the type of 
tissue reaction you would expect when e.g. a wound get infected. Indeed, 
inflammation is the stereotyped tissue reaction against many different 
kinds of tissue insults. It could be acute or it could be chronic, 
depending not just on the time course but also in the range of cells 
involved in the process. No matter it is a physical injury e.g. burn, 
frost bite; chemical injury e.g. chemical burn; allergic reaction, 
bacterial, viral or parasitic infection, or the presence of foreign body 
or foci of necrosis (dead tissues) the tissues concerned respond locally 
in a stereotyped way (and normally backed up by systemic changes as 

Several different events operate in concert in acute inflammation to 
produce a sequence of events which is broadly similar regardless of the 
site in the body involved. In essence, this includes hyperaemia 
(increased local blood flow) largely due to local vasodilatation; 
exudation (accumulation of protein-rich fluid in the extracellular space 
to cause “swelling”, due to increased vascular permeability); and 
leukocyte emigration (mostly polymorphic neutrophils, but also cells from 
the monocyte/macrophage lineage). The purpose of acute inflammation is to 
generate an innate immediate defence against injury and to localise and 
eliminate e.g. bacterial infection. Most aspects of acute inflammation is 
in turn driven by chemical mediators, for e.g., mast cells release 
histamine, resident macrophages release prostaglandins, leukotrienes, 
platelet activating factors, interleukins, tumour necrosis factor-alpha 
and nitrous oxides, etc. What causes these cells to initiate the release 
then? Aha!! Many of these cells have surface receptor that could 
facilitate them to recognise invaders either directly or via the help of 
some serum proteins. 

Now back to your question. Viruses are obligate intracellular parasites 
and are distinguishable from all other biological entities by their lack 
of metabolic machinery. Different viruses could have different nucleic 
acids which constitute their genomes. This necessarily means that 
different viruses must use different strategies to invade the host. If 
you think logically, all invaders must have a route of entry and a route 
of exit, and these two routes to a large extent determine the 
transmission route. Using your example of encephalitis, a number of 
viruses and bacteria could cause encephalitis, a common sporadic type 
being herpes simplex viruses (nonetheless, encephalitis can also be part 
of an allergic response to a systemic viral infection). 

If we put all the above together, let’s say, a patient contracted a viral 
infection via the mucosa lining the conjunctiva (herpes simplex maybe, 
herpes can cause herpes encephalitis). The body immediate launches an 
acute inflammation in the hope to control the spread of the infection. 
Unfortunately, the virus this time is smart enough to escape host 
response and get into the blood (viraemia). The viruses thus get carried 
by the blood to all over the body. Different viruses have their 
preference target tissue and let’s say this virus XYZ expresses a surface 
receptor that facilitates them to invade nervous tissues (brain, spinal 
cord, etc.). This could result in the viruses causing an acute 
inflammatory response in the brain. Remember that the brain also has its 
vascular component (i.e. blood supplies) and resident surveillance cells 
(microglia – acts just like macrophages) and they can sense the presence 
of invaders and launch an inflammatory response just like your skin 
get “inflamed” after a superficial cut – hence encephalitis! So 
vasodilatation happens and local oedema occurs due to exudation (see 
above). But this is VERY bad if it happens in the brain because the brain 
is contained inside the cranium which cannot expand to accommodate the 
increased volume, instead the brain gets compressed by the cranium. The 
patient thus may feel headache at first, then drowsiness, and may 
progress to coma and finally death…

I am omitting all the details in the explanation because I think your 
teacher might have already explained the mechanism of viral infection and 
stuff. Moreover, general principles are far more important than specific 
details at this stage. So I am just trying to put them into context. 
However, if you are really into the details of virology, you can consult 
any of the standard virology textbook or general pathology textbooks in 
your school library. I hope this can help your revision and good luck 
with your test!!

Joshua Chai
Medical Student
University of Cambridge, UK

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