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Herpesviruses
DR.HAMISI MKINDI,MD.
TO DOWNLOAD CONTACT:
hermyc@live.com
Important herpesvirus
• There are nearly 100 viruses of the herpes group that
infect many different animal species.
• Official name of herpesviruses that commonly infect
human is Humans herpesvirus (HHV)
– herpes simplex virus types 1 (HHV 1)
– Herpes simplex virus type 2 (HHV 2)
– Varicella-zoster virus (HHV 3)
– Epstein-Barr virus, (HHV 4)
– Cytomegalovirus (HHV 5)
– Human herpesvirus 6 (HHV 6)
– Human herpesvirus 7 (HHV 7)
– Human herpesvirus 8 (HHV 8) (Kaposi's sarcoma-associated
herpesvirus).
• Herpes B virus of monkeys can also infect humans.
General characteristics
• exhibit a spectrum of diseases. Some have a wide host-cell range,
whereas others have a narrow host-cell range.
• ability to establish lifelong persistent infections in their hosts and to
undergo periodic reactivation.
• Reactivation in immunosuppressed patients causes serious health
complications.
• Reactivated infection may be clinically quite different from the disease
caused by the primary infection.
• Herpesviruses possess a large number of genes, susceptible to
antiviral chemotherapy.
• There is little antigenic relatedness among members of the herpesvirus
group.
• Only herpes simplex viruses type 1 and type 2 share a significant
number
• Structure/Biological characteristics
– Icosahedral core surrounded by lipoprotein
envelope, 120 – 200 nm in diameter,
– 2nd in size only to poxvirus
– Linear DS DNA, no virion polymerase
– More than 35 protein in virion
– Replicate in the nucleus, budding from the
nuclear membrane
– Envelope contain glycoprotein, Fc receptors
• Pathogenesis
• Ability to cause latent infection
• Acute disease followed by asymptomatic
period of latent state
• Exposure to inciting agent and
immunosuppresion trigger reactivation
• Subsequent symptoms may be similar to
first episode
• Three categories based on types of cell
most often infected and the site of latency
Classification of Human
category types Cell infected Latent
infection
site
Alpha
herpesviruses
HSV 1, HSV 2,
VZV
Epethelial cells neurons
Beta
herpesviruses
Cytomegaloviru
ses, HHV 6
Variety of tissue Variety of tissue
Gamma
herpesvirues
EBV, HHV 8, Lymphoid cells Lymphoid cells
Varicella-zoster virus (VZV)
Varicella-zoster virus (VZV)
• Important properties
• Structure and morphology identical to other but different
antigen
• Single serotype
• Human is the natural hosts
• Epidemiology
• Transmitted in respiratory droplet or direct contact
• Highly contiguous in children
• Occur worldwide
pathogenesis
– Infect mucosa of upper respiratory tract,
spread via blood to skin
– Multinucleated giant cell at base of the lesion
– After recover, the virus become latent in the
dorsal root of ganglia
– Viral DNA in cytoplasm during latent period
– Varicella is followed by long lasting immunity
Clinical features
• (1) Varicella or chicken pox – primary infection
• (2) herpes zoster or shingles – sensory infection
• Chicken pox
– This is a common childhood infection and severe in adult
– The incubation period is 14 - 21 days
– mild febrile illness associated with a generalized vesicular rash.
– papulovesicular rash appear in crops on trunk and spread to head and
extremities
– The lesions progress from macule to papule to vesicle to pustule to
crusts.
– Itching is a prominent symptom when vesicle are present
– Varicella pneumonia and encephalitis are the major rare complication in
adult
– Reyes’s syndrome (encephalopathy, liver degeneration) in children
given aspirin
Zoster
• Reactivation lesion of VZV
• the virus establishes a latent infection in sensory ganglia.
Reactivation usually occurs many years after primary
infection and is often associated with immunosuppresion
of the host.
• The virus travels down the axon and re-infects the
dermatome supplied by the sensory ganglia to produce
painful vesicles on the skin.
• Common sites include the thoracic dermatomes and
those supplied by the trigeminal nerve.
• Post herpetic neuralgia is a common complication.
Herpes Zoster
Herpes Zoster
Laboratory diagnosis
• In stained smears of scrapings or swabs of the
base of vesicles (Tzanck smear) -
multinucleated giant cells
• Intracellular viral antigens can be demonstrated
by immunofluorescence staining of similar
smears
• Cell culture – produce typical cytopathic effect,
identified with specific antiserum
• Electron microscopy
• Rising antibody used in chicken pox
treatment
• Varicella in normal children is a mild disease and
requires no treatment
• Neonates and immunocompromised patients with severe infections
should be treated Treatment
• Gamma globulin of high varicella-zoster virus antibody titer
(varicella-zoster immune globulin)
• Several antiviral compounds provide effective therapy for
varicella, acyclovir, famciclovir
• Acyclovir can prevent the development of systemic disease in
varicella-infected immunosuppressed patients
• Acyclovir Nucleoside analogue of Guanosine viral DNA polymerase
incorporates Acyclovir. This interferes with viral DNA synthesis by:
Binding irreversibly and blocking the viral DNA polymerase, and
causes chain termination of the viral DNA

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7. herpersvirus VCV.ppt

  • 2. Important herpesvirus • There are nearly 100 viruses of the herpes group that infect many different animal species. • Official name of herpesviruses that commonly infect human is Humans herpesvirus (HHV) – herpes simplex virus types 1 (HHV 1) – Herpes simplex virus type 2 (HHV 2) – Varicella-zoster virus (HHV 3) – Epstein-Barr virus, (HHV 4) – Cytomegalovirus (HHV 5) – Human herpesvirus 6 (HHV 6) – Human herpesvirus 7 (HHV 7) – Human herpesvirus 8 (HHV 8) (Kaposi's sarcoma-associated herpesvirus). • Herpes B virus of monkeys can also infect humans.
  • 3. General characteristics • exhibit a spectrum of diseases. Some have a wide host-cell range, whereas others have a narrow host-cell range. • ability to establish lifelong persistent infections in their hosts and to undergo periodic reactivation. • Reactivation in immunosuppressed patients causes serious health complications. • Reactivated infection may be clinically quite different from the disease caused by the primary infection. • Herpesviruses possess a large number of genes, susceptible to antiviral chemotherapy. • There is little antigenic relatedness among members of the herpesvirus group. • Only herpes simplex viruses type 1 and type 2 share a significant number
  • 4. • Structure/Biological characteristics – Icosahedral core surrounded by lipoprotein envelope, 120 – 200 nm in diameter, – 2nd in size only to poxvirus – Linear DS DNA, no virion polymerase – More than 35 protein in virion – Replicate in the nucleus, budding from the nuclear membrane – Envelope contain glycoprotein, Fc receptors
  • 5.
  • 6. • Pathogenesis • Ability to cause latent infection • Acute disease followed by asymptomatic period of latent state • Exposure to inciting agent and immunosuppresion trigger reactivation • Subsequent symptoms may be similar to first episode • Three categories based on types of cell most often infected and the site of latency
  • 7. Classification of Human category types Cell infected Latent infection site Alpha herpesviruses HSV 1, HSV 2, VZV Epethelial cells neurons Beta herpesviruses Cytomegaloviru ses, HHV 6 Variety of tissue Variety of tissue Gamma herpesvirues EBV, HHV 8, Lymphoid cells Lymphoid cells
  • 9. Varicella-zoster virus (VZV) • Important properties • Structure and morphology identical to other but different antigen • Single serotype • Human is the natural hosts • Epidemiology • Transmitted in respiratory droplet or direct contact • Highly contiguous in children • Occur worldwide
  • 10. pathogenesis – Infect mucosa of upper respiratory tract, spread via blood to skin – Multinucleated giant cell at base of the lesion – After recover, the virus become latent in the dorsal root of ganglia – Viral DNA in cytoplasm during latent period – Varicella is followed by long lasting immunity
  • 11. Clinical features • (1) Varicella or chicken pox – primary infection • (2) herpes zoster or shingles – sensory infection • Chicken pox – This is a common childhood infection and severe in adult – The incubation period is 14 - 21 days – mild febrile illness associated with a generalized vesicular rash. – papulovesicular rash appear in crops on trunk and spread to head and extremities – The lesions progress from macule to papule to vesicle to pustule to crusts. – Itching is a prominent symptom when vesicle are present – Varicella pneumonia and encephalitis are the major rare complication in adult – Reyes’s syndrome (encephalopathy, liver degeneration) in children given aspirin
  • 12.
  • 13. Zoster • Reactivation lesion of VZV • the virus establishes a latent infection in sensory ganglia. Reactivation usually occurs many years after primary infection and is often associated with immunosuppresion of the host. • The virus travels down the axon and re-infects the dermatome supplied by the sensory ganglia to produce painful vesicles on the skin. • Common sites include the thoracic dermatomes and those supplied by the trigeminal nerve. • Post herpetic neuralgia is a common complication.
  • 14.
  • 16. Laboratory diagnosis • In stained smears of scrapings or swabs of the base of vesicles (Tzanck smear) - multinucleated giant cells • Intracellular viral antigens can be demonstrated by immunofluorescence staining of similar smears • Cell culture – produce typical cytopathic effect, identified with specific antiserum • Electron microscopy • Rising antibody used in chicken pox
  • 17. treatment • Varicella in normal children is a mild disease and requires no treatment • Neonates and immunocompromised patients with severe infections should be treated Treatment • Gamma globulin of high varicella-zoster virus antibody titer (varicella-zoster immune globulin) • Several antiviral compounds provide effective therapy for varicella, acyclovir, famciclovir • Acyclovir can prevent the development of systemic disease in varicella-infected immunosuppressed patients • Acyclovir Nucleoside analogue of Guanosine viral DNA polymerase incorporates Acyclovir. This interferes with viral DNA synthesis by: Binding irreversibly and blocking the viral DNA polymerase, and causes chain termination of the viral DNA