Lecture - Four (Clinical Virology)

Clinical Virology / Lecture Four/ Dr. B.
Al-Haidary
Protection & Treatment against Viral Infections:
Viral Vaccines:
Immunity to viral infections is based on the development of
an immune response to specific Ags located on the surface of virus
particles or virus-infected cells. For enveloped viruses the important Ags
are the surface glycoproteins. Although the infected animals may develop
Abs against virion core proteins or non-structural proteins involved in
viral replication, that immune response is believed to play little or no role
in the development of resistance to infection.
Vaccines are available for the prevention of several
significant human diseases. Certain general principles apply to most viral
vaccines for use in prevention of human dz. Neither vaccination nor
recovery from natural infection always results in total protection against
later infection with the same virus. This situation holds true for dzs
which successful control measures are available. Control can be achieved
by limiting the multiplication of virulent virus upon subsequent exposure
and preventing its spread to target organs where the pathogenic damage is
done, such as polio & measles viruses must be kept from the brain and
spinal cord & rubella virus must be kept from the embryo.
There are two types of viral vaccines; killed & live-
attenuated vaccines.
Killed-Virus Vaccines:-
Inactivated (killed virus) vaccines are made by purifying
viral preparation to certain extent and then inactivating viral infectivity in
a way that does minimal damage to the viral structural proteins; mild
formalin treatment is frequently used. Killed-virus vaccines prepared
from whole virion generally stimulate the development of circulating Ab
against the coat proteins of the virus conferring some degree of
resistance.
Attenuated Live-virus Vaccines:-

Live-virus vaccines utilize virus mutants that antigenically
overlap with wild-type virus, but are restricted in some step in the
pathogenesis of dz. The search for naturally attenuated strains or by
cultivation virus serially in various hosts and cultures in the hope of
deriving an attenuated an attenuated strain fortuitously is now being
approached by laboratory manipulations.
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Clinical Virology / Lecture Four/ Dr. B.Al-Haidary
Differences between Killed- & live-Virus Vaccines

Characteristics Killed-virus Vaccines Live-virus Attenuated
Vaccine
1. Immunity Brief & must be boosted Stimulate long-lasting I.R.
2. CMI Generally is poor Good cell-mediated response.
3. Type of Igs Stimulate circulating Stimulate s-IgA Ab.
IgG & IgM isotypes.
4. Safety Care is required during There is a risk for reversion to
preparation to avoid greater virulent strain.
presence of residual live
virus. No reversion.
5. Stability Usually stable Has a limited shelf-life
6. Cost Cheap Expensive
7. Side Effects Induce hypersensitivity No side effects
to subsequent infection
8. Route of Parenteral administration Orally
administration
9. Interference Not present Present by co-infection with
naturally wild-type virus
which may inhibit replication
of viral vaccine & decrease
its effectiveness
Future Prospects in Vaccination:

 Attenuation of viruses by genetic manipulation.
 Uses of Avirulent viral Vector.
 Purified proteins produced using Cloned genes.
 Synthetic peptides.
 Subunit Vaccines.
 Naked DNA vaccines.
 Local administration of vaccine.
 Conventional Vaccines.
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Anti-viral Chemotherapy:
Because viruses are obligate intra-cellular parasites, antiviral
agents must be capable of selectively inhibiting viral functions without
damaging the host. Furthermore an ideal drug would reduce dz symptoms
without modifying the viral infection so much as to prevent an immune
response in the host.
Compounds have been found that are value in treatment of
some viruses dzs. However, most antivirals are of use limited.
These agents are classified into:
A. Nucleoside Analogs:
The majority of this type is used for the treatment of HSV or
HIV with limited inhibition. They act to inhibit viral nucleic acid
replication by inhibition of enzymes of metabolic pathways for
nucleotides or by inhibition of Polymerases to nucleic acid replication.
In addition some analogs can be incorporated into the nucleic acid and
block further synthesis or alter its function such as Acyclovir,
Didanosine & Ribavirin.
B. Nucleotide Analog:
This analog is differ from nucleoside analogs in having an
attached phosphate group. Their ability to persist in cells for long
periods of time increases their potency. Cidofovir is an active
nucleotide analog against CMV & HSV. It inhibits viral DNA
polymerase and terminates the growing DNA chain.
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C. Non-nucleoside Reverse Transcriptase Inhibitors:

Nevirapine is the first member of the class of non-nucleoside
reverse transcriptase inhibitors. It inhibits the reverse transcriptase of
HIV. Resistant virus mutants arise rapidly so the drug is recommended
for use in combination therapy.
D. Protease Inhibitors:
Such as Indinavir, Ritonavir & Saquinavir, which used
against HIV infection. These drugs act to inhibit the viral protease that
required at the late stage of the replicative cycle to cleave the viral
structural protein to form mature virion core and activate reverse
transcriptase that will be used in the next round of infection. Inhibition
of protease results in non-infectious virus particles.
E. Interferon's
Interferon's (INFs) are host-coded proteins of the large
cytokine family that inhibit viral replication. They are extremely
potent that less than fifty molecules of INF / cell are sufficient to
induce antiviral state.

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Clinical Virology / Lecture Four/ Dr. B.

Protection & Treatment against Viral Infections:

Attenuated Live-virus Vaccines:-

Differences between Killed- & live-Virus Vaccines

Future Prospects in Vaccination:

C. Non-nucleoside Reverse Transcriptase Inhibitors:

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