PATHOGENESIS OF VIRAL DISEASE.

Viral pathogenesis can be defined as the methods by which viruses produce diseas
e in the host The fast majority of viral infection are subclinical (symptomless)
and go almost unrecognized, One individual may succumb to disease with an infec
tion by a virus, while another may be entirely asymptomatic when infected by the
identical strain of virus; genetic factors, immunity, nutrition and other facto
rs influence the results of infection. The study of viral pathogenesis can be co
nsidered at two levels. First, at the level of the virus (parasite) and, second
, at the level of the host.
Entry of viral infection.
As in bacterial infections, viruses gain entry into the host by:
Inoculation (via the skin and mucosa)
Inhalation (via the respiratory tract)
Ingestion (via the gastrointestinal tract).
See figure 5.1. (Note: although in this section viruses are considered separatel
y, very similar host defence mechanisms operate to prevent the entry of all othe
r pathogens through these portals.)
Skin and mucosa.
The skin is an effective barrier against viral infection as the dead cells of th
e stratum corneum cannot support viral replication. Breach of skin integrity occ
urs:
During accidental abrasions or needlestick injuries (durin vacination, virus is
inoculated into the skin liberately)
Via the bites of arthropod vectors, e.g. mosquitoes and ticks (these infect the
host either because their saliva is infected as a result of viral multiplication
within the arthropod e.g. yellow fever virus in mosquitoes, or because their mo
uthparts are contaminated with the virus)
As a result of deep inoculation into the subcutaneous tissue and muscle, which c
an follow hypodermic needle injections, tattoing, acupuncture, ear-piercing or a
nimal bites. Once a virus has reached the dermis it has access to blood and lymp
hatic vessels as well as to macrophages, so the infection may spread readily (Fi
g. 5.2).
Oropharynx and intestinal tract.
Natural defence mechanisms of the mouth and the gastrointestinal tract that prev
ent viral entry are:
Continuous desquamation of the epithelium
The presence of saliva, the mucous layer of the intestine, gastric acid, bile an
d proteolytic enzymes, all of which nonspecifically inhibit viral entry
Mechanical movements of tongue, cheek, peristalsis, etc
Immune mechanisms (see Ch. 10).
Respiratory tract.
A number of defence mechanisms operate to prevent viral entry through the respir
atory tract. These include:
Secretion of mucus by goblet cells; this, propelled by the action of ciliated ep
ithelial cells, clears inhaled foreign material (the mucociliary escalator)
IgA present in respiratory secretions
Alveolar phagocytic cells.
To gain access to the respiatory tract, viruses need to be primarily in the form
of aerosol particles or droplets. Other factors that affect viral respiratory i
nfection include the humidity and air temperature (e.g. influenza is more common
in the winter months) and the physical and chemical properties and structure of
the virus particle.
Genitourinary tract.
The vagina and urethra can be portals for entry of viral infection. The host fac
tors that can influence viral entry via these routes include :
Natural mucosal desquamation

Vaginal secretion and cervical mucus, which contain both specific and non-specif
ic defence factors
Intermittent flushing action of urine.
Sexual activity may cause tears or abrasions of the vaginal epithelium or trauma
to the urethra , allowing viral ingress. Sexually transmitted viruses in humans
include HIV, herpesviruses, human papillomaviruses, and most hepatitis viruses.