presentation on herpes disease. complete description of disesse, drugs used against herpes, mode of action of drugs, potential drug targets.

1. HERPES
Presented by-
Rohit.

2. INTRODUCTION
• Herpes is a viral disease caused by HSV1 and HSV2.
• HSV1 causes oral herpes and HSV2 cause genetical herpies.
• HSV1 is highly contagious which is acquired orally and cause
cold sores on mouth lips or any other part of body exept
genetals which can be easily passed from person to person by
direct skin to skin contact.
• HSV2 is usually transmitted by having sex and affects the
genital area,that’s why it is called STD(Sexually Transmitted
Disease).

3. • HSV infection typically results in lifelong latent infection that
periodically give rise to clinical outbreaks, expressed as lesions.
Once you have it, there are chances that it will attack again and
again.
• After completion of infection cycle the viruses are transported
along sensory nerves to the sensory nerve cell bodies, where they
become latent and reside lifelong.
• HSV is one of the most difficult viruses to control because HSV1
when transmitted to genetical area causes genetical herpes and
HSV2 when transmitted to mouth can cause oral herpes. In short
the herpes virus changes its mode of action according to area
where it is transmitted.

4. HERPES SIMPLEX 1 HERPES SIMPLEX 2

5. STRUCTURE OF VIRUS

6. GENOME CHARACTERSTICS
• Herpes virus genomes range in length from 120 to 230 kbp
with base composition from 31% to 75% G+C content and
contain 60 to 120 genes.
• Herpesviruses can use both the host's transcription machinery
and DNA repair enzymes to support a large genome with
complex arrays of genes.
• Herpes virus genes, like the genes of their eukaryotic hosts, are
not arranged in operons and in most cases have individual
promoters.

7. Biological Properties
• The synthesis of viral genomes and assembly of capsids occurs
in the nucleus.
• Productive viral infection is accompanied by inevitable cell
destruction.
• Herpesviruses express a large number of enzymes involved in
metabolism
• Herpesviruses are able to establish and maintain a latent state
in their host and reactivate following cellular stress. Latency
involves stable maintanence of the viral genome in the
nucleus with limited expression of a small subset of viral
genes.

8. Strategies for Success
• The virion invades the host cell, turning off host protein
synthesis and releasing viral DNA into the nucleus, where
replication and virion production start immediately.
• Second tactics include inhibiting splicing of mRNA, blocking
presentation of antigenic peptides on the cell surface and
blocking the apoptosis (cell death) induced by viral gene
expression.
• Third important strategy shared by herpesviruses is their
ability to hide their bare

9. Signs and symptoms
HSV1
• Small, painful blisters filled with
fluid around any upper body
part or legs.
• Fever.
• Sore throat.
• Swollen lymph nodes in neck.
• Tingling or burning around the
face.
HSV2
• Tingling sensation in the
genitalia, buttocks, and thighs.
• Small red blisters or open sores
on genitals
• Fever, muscle aches.
• Painful urination and vaginal
discharge.
• Swollen lymph glands.

10. Risk factors
• Pregnant women who are infected with herpes simplex virus 2
have a higher risk for miscarriage, premature labor and
retarded fetal growth.
• May cause permanent Effects on the Brain and Central
Nervous System.
• May cause permanent blindness if spread to eye.
• Herpes simplex in any patient with a seriously compromised
immune system can cause serious and even life-threatening
complications including Inflammation of the esophagus and
brain, Liver damage, destruction of adrenel glands etc.

11. Treatment
• There is no cure for herpes, so the goals of treatment are to
reduce the number of outbreaks and to lessen symptoms and
make the virus dormant.
• In normal person the blisters goes away naturally but in case
immunocompromized patients and pregnant women, special
treatment is needed.
• Antiviral medicines like Acyclovir, Valtrex etc help shorten the
length of a herpes outbreak and cut down on recurring
outbreaks by inhibiting replication process of the virus.

12. Mode of action of drugs.

13. valtrex aciclovir
monophosphate
form
aciclo-GTPViral DNA pol
esterases
hepatic first-pass
metabolism
thymidine
kinase
cellular
kinases
phosphorylation
inhibition
Valtrex

14. Acyclovir

15. Drug targets
Riboneucleotide reductase
• Herpes simplex viruses encode their own RR.
• Converts ribonucleoside diphosphates to the corresponding
deoxyribonucleotides required for viral DNA synthesis.
• First anti-RR products to be identified belonged to the
thiosemicarbazone family.
• These peptides inhibit HSV RR activity in vitro by inducing
dissociation of the two subunits [58-60] and suppress the
replication of HSV-1, HSV-2.

16. Helicase-Primase
• The helicase–primase complex comprises three viral proteins
encoded by the UL5, UL8 and UL52 gene products.
• It unwinds double-stranded viral DNA and generates primers for
DNA synthesis by the viral DNA pol.
• The helicase primase complex plays an essential role in HSV
DNA replication and thus constitutes an excellent target for
antiviral therapy.

17. Polyamine pathway
• Potential cellular target.
• A recent report has demonstrated that the polyamine biosynthetic
pathway remains active in HSV.
• Two key enzymes of this pathway, S-adenosylmethionine
decarboxylase (SAMDC) and ornithine decarboxylase,is
upregulated.
• The use of methylglyoxal bis,(specific SAMDC inhibitor), reveals
that SAMDC activity is required for HSV-1 and HSV-2 replication
in cell culture.(in vitro).