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1. Prevention of viral infection
Osama khider

2. • Prevention and control of viral disease can be
achieved by the use of vaccines that induce
active immunity , or by administration of
performed antibodies that provides passive
immunity .
• vaccination is the most effective method
of prevention of serious viral infection.

3. Vaccination
• Control of many viral diseases has been
accomplished by vaccination .
• there are two types of vaccines that
induce active immunity .
• live attenuated vaccines
• killed vaccines

4. • live attenuated vaccines
• That contain live viruses whose pathogenecity
has been attenuated ( weakened, unable to
cause disease) but retain its immunogenicity
and can induce protection.
• killed vaccines
vaccines that contain killed or inactivated viruses
these vaccines are made by purifying the viral
preparation , then inactivating their infectivity .

5. Vaccine
Disease
Attenuated -Live
Yellow fever
Attenuated –Live& Inactivated
Poliomyelitis
Attenuated -Live
Measles
Attenuated -Live
Mumps
Attenuated -Live
Rubella
Inactivated
Hepatitis B
Inactivated
Influenza
Attenuated -Live
Smallpox
Attenuated -Live
Chickenpox
Inactivated
Hepatitis A
Inactivated
Rabies
Attenuated -Live
Rotavirus

6. Immune prophylaxis and therapy
• Immune prophylaxis is used to functionally
prevent serious viral infection in immune or
compromised patient .
• it is possible to confer limited protection by the
intramuscular inoculation of human
immunoglobulin .
• Pooled human immunoglobulin contains
antibody against all common viruses .

7. • Immune prophylaxis should be considered an
emergency procedure .
• passive immunization is occasionally effective
as therapy for viral infection.
• therapy with immune serum for some
hemorrhagic fever , such as Lassa fever , has
reduced mortality.

8. Situation
Disease
Prophylaxis
Traveler to developing country
Hepatitis A
Newborns of infected mothers or
unimmunized laboratory following
needle stick
Hepatitis B
Following bite by potentially rabid
animal
Rabies
Unimmunized close contact of
patient
Measles
Newborns of infected mothers at
time of delivery
Varicella
Infants younger than 2yrs with
underling lung disease
Respiratory syncytial virus
Therapy
At time of disease to decrease
severity
Lassa fever

9. Antiviral chemotherapy

10. • A successful anti-viral drug should:
(i) interfere with a virus-specific function (either
because the function is unique to the virus or the
similar host function is much less susceptible to
the drug)
or
)ii) interfere with a cellular function so that the
virus cannot replicate. To be specific, the anti-
viral drug must only kill virus-infected cells. This
could be done by restricting drug activation to
virus-infected cells .

11. • An ideal drug should be:
• Water-soluble
• Stable in the blood stream
• Easily taken up by cells
• An ideal drug should NOT be:
• Toxic
• Carcinogenic
• Allergenic
• Mutagenic
•

12. Achilles' heel

13. POSSIBLE PHASES OF LIFE CYCLE ON
WHICH ANTI-VIRAL ATTACK
• Attachment of the virus to the cell surface,
perhaps as a result of competition with a specific
viral receptor .
• Uptake into intracellular vesicles (endosomes(
• Uncoating of virus (loss of protein coat, fusion of
lipid membrane with endosome/lysosome).
Note: the endosome/lysosome compartment is
acidic and inhibition of acidification of this
compartment might be a good target .
• Integration of the viral DNA into chromosomal
DNA of the host cell

14. • Transcription of genome to new RNA or DNA
(polymerases are the target(
• mRNA transcription
• mRNA processing (poly adenylation, methylation,
capping, splicing(
• Translation to protein
• Post-translational modification of proteins (glycosylation,
phosphorylation, fatty acylation, proteolysis). Some of
these are essential for functional, infective viral progeny .
• Assembly of the components into the whole virus

15. • Compared with antibiotics used against bacterial
infection the number and use of antiviral drugs is
very small..
• The major possible reasons for this:
• Difficulty in obtaining selective toxicity against
viruses without affecting the cells of the host
their replication is intimately involved with the
normal synthetic process of the cell "obligatory
intra cellular pathogen"

16. • Relatively ineffective, because many cycles of
viral replication occur during the incubation
period , by the time the clinical symptoms
appear, the virus will spread throughout the
body and it is too late to control.
• Some viruses, e.g. herpes viruses, become
latent within the cell and no current antiviral
drug can eradicate them.

17. • Emergence of drug – resistant, viral mutants
• at present, this is not major clinical
significance. e.g. mutants of HSV – resistant to
a acyclovir have been recorded from patients
but they don't interfere with recovery.

18. BINDING TO RECEPTOR OR UPTAKE
INTO INTRACELLULAR VESICLES
• Maraviroc
• For HIV to infect a cell, it must bind both to CD4 antigen
and to a co-receptor, a chemokine receptor
• It blocks the interaction between chemokine receptor
CCR5 and HIV gp120

19. • FUSION OF VIRAL AND HOST CELL
MEMBRANE
• Agents that block fusion of HIV with the host
cell by interacting with gp41 e.g.
Enfuvirtide

20. Examples of antiviral drugs:
• Antiviral drugs act by inhibiting any of viral
replication stages:
(1) Inhibition of early events:
• Amantadine: is a tricyclic compound that is used
to prevent influenza A infections.
• It inhibits uncoating of the virus by blocking the
ion – channel activity of matrix protein in the
virion.
• The drug doesn't work against influenza B or C
viruses

21. NUCLEIC ACID SYNTHESIS
• The best anti-viral drugs that we have are
of this type .They are selective because:
• the virus may use its own enzyme to
activate the drug
• the viral polymerases may be much more
sensitive to the drug than the
corresponding host enzymes
• Thymidine kinase substrates

22. (2) Inhibition of viral NA synthesis:
(a) Inhibition of herpes viruses:
• Sugar modifications
• Nucleosides inhibitors: these drugs are analog
of nucleosides that inhibit the DNA polymerase
of many members of herpes virus group
• Acyclovir (zovirax): inhibits the DNA
polymerase of HSV-1 and 2 and varicella
zoster virus but not CMV. It is very effective
against these diseases

23. • Ganciclovir (cytogene): structurally similar to
acyclovir but is more active against CMV. It is
effective in treatment of retinitis caused by
CMV in AIDS patients.
• cidofavir: effective against CMV as above and
in severe papilloma virus infections

24. Inhibitors of retroviruses:
• Nucleoside inhibitors
• Azidothymidine [zidovadine, Retrovir (ATZ)]:
nucleoside analogue that causes chain
termination during DNA synthesis by RT of HIV
and inhibits growth of the virus in cell culture. It
is currently the drug of choice in patients with
AIDS. It's side effect B.M suppression and
Myopathy.

25. • Dideoxycytidine (Zalcitabine, Hivid): it causes
chain termination during DNA synthesis by
reverse transcriptase synthesis of HIV. It is used
to treat patients with advanced AIDS who are
resistant to AZT.
• Side effect: pancreatitis and peripheral
neuropathy

26. • Inhibitors of other viruses:
• Ribavirin (virazole) :is a nucleoside analog that
inhibits the synthesis of guanine nucleotides
which are essential for both DNA and RNA
viruses. Ribavirin aerosol is used clinically to
treat pneuomonitis caused by RSV in infants
and severe influenza B infections.

27. • Inhibitors of virus poly peptide precursors:
• Saquinavir (cinvirase) and retinovir are
inhibitors of protease encoded by HIV. These
drugs inhibit production of infectious virions
but don't affect the integrated proviral DNA and
therefore don't cure infection. Always used in
combination with RT inhibitors like ATZ.

28. • Inhibitors of viral protein synthesis:
• Interferons: recombinant interferon alpha IFN-α
is effective in the treatment of some patients
with chronic HB and HC infections, also cause
regression of the lesions of Kaposi's sarcoma
caused by human herpes virus-8.

29. • Fomivirsen (Vitravene) :
• Is an antisense DNA that blocks replication of
CMV. It binds to the viral mRNA within the
infected cells which prevent sit from being
translated viral protein. It is very good as
intraocular treatment of CMV retinitis.

30. Inhibitors of release of viruses
• Zanamivir (Relenza) , (Tami flu) inhibit the
neuramindase of influenza virus and thus
prevent the release the of virus from infected
cells.
• These drugs are also effective against both
influenza (A&B)