5 Introduction to Host Response
Each vertebrate host is a multicellular organism composed of tens of millions of cells.
Most cells form tissues and organs but each cell has at some stage of its life a nucleus which
contains a set of chromosomes specific to each organism — the genotype. The genes (made
up of DNA) are located on the chromosomes and contain the ‘blueprint’ for all the pro-
tein molecules that are assembled into an individual.
Every cell type has an outer surface membrane, the structure of which is unique.
Cells identify/recognise each other by their surface membranes, ie they can distinguish
self from non-self. A normal healthy individual will attempt to maintain its integrity by
eliminating any foreign (non-self) cells. An invading parasite fits this category, that is as
far as the host is concerned a parasite, no matter how well adapted it is to the host or
how tolerant the host is of the parasite, is identified by the host’s surveillance mechanism
as non-self or foreign.
In order to maintain integrity and keep out or destroy infectious parasites, verteb-
rates have evolved a protective system. This system is based upon:
n having a protective outer layer — the skin — which maintains a barrier to all other
non-self organisms.
n having a mechanism for detecting any non-self organism that has managed to breach
this protective layer. This system is based upon having cells whose prime function is
detection and destruction of non-self material (in a primary infection) and then
‘remembering’ the infectious material, to be able react more rapidly during a secondary
infection.The mechanism that operates against a primary infection, in a host with no previous
contact with the parasite, reacts in a similar manner no matter what the infectious
organism may be and is referred to as the innate immune system.
If the parasite is not destroyed by the innate immune response and survives to become
a chronic infection, then a complex adaptive immune response comes into operation. This
mechanism leads to the host developing a memory of the infection and becoming pro-
grammed to react much more rapidly during a secondary infection.