Herpesvirus

Herpesvirus
Sunil Bhandari
Balkumari College
©sunilbhandariv@gmail.com

Herpesvirus family:
General introduction:
• Most important human pathogens with both broad and specific
host range.
• Ability to establish lifelong persistence with periodic
reactivation.
• Frequent reactivation occurs in immunocompromised patients.
Common human pathogens:
1. Herpes simplex virus type 1 and type 2
2. Vericella-zoster virus
3. Cytomeghalovirus
4. Epstein-Barr virus
5. Herpes virus type-6
8. Herpes B-virus of monkey can infects human.

Classification of Herpesvirus Family
3 Broad categories
*Lymphoreticular system: spleen, lymphnodes, lymphatic vessels, thymus, and bone marrow.

Morphology:
1. Core:
Single linear DNA (ds) in
the form of torus.
2. Capsid:
surrounds core:
Icosahedral, 100nm dm,
constructed of 160
capsomeres.
3. Teguments:
• Between capsid and
envelope
• Amorphous or
asymmetrical features
• Consists of viral
enzymes needed for
cellular process and some
against hosts cells
immediate responses.
3. Envelope:
• Outer layer of virion
• Composed of altered hosts N-membrane
• Consists dozen of unique viral glycoproteins which
appears as short spikes embedded in envelopes.

Herpes simplex virus
 Herpes simplex virus causes disease by direct cytopathologic
effects.
 The infection is initiated by direct contact and depends on the
infected tissues whether oral, genital, or brain, etc.
 The infection occurs by inoculation of virus into susceptible mucosal
surfaces, such as the oropharynx, conjunctiva, or cervix or
through small abrasions on the skin.
Persists in three different ways:
1. Neuroinvasiveness (the ability of virus to invade the brain)
2. Neurotoxicity (ability to multiply in the brain and destroy the brain)
3. Latency (ability to remain in a nonreplicating stage in the dorsal root
ganglia of the central nervous system, or CNS) are the properties of HSV.

 The virus replicates in the infected cells and infects the
innervating neuron.
 Subsequently, the viruses travel by retrograde transport
(axonal transport) to the ganglion, such as the trigeminal
ganglion (brain) for HSV-1 and the sacral ganglion(spine) for
HSV-2.
 The virus then returns back to the initial site of infection and
produce vesicular lesions.
 Thin walled umbilicated vesicles—the roof of which breaks down,
leaving tiny superficial ulcers—are the typical lesions caused by
HSV. The vesicle fluid contains infectious virions.

Herpes Simplex Virus

Viral Replication

Pathogenesis of HSV

Clinical syndrome of HSV infections:
Both HSV-1 and HSV-2 cause many clinical entities, and infections
may be primary or recurrent.
The clinical manifestations depend on
(a) The age of patient
(b) Immune status of the host
(c) Previous immunity of the patient to autologous or heterologous viruses
(d) Antigenic type of the virus
(e) Anatomical site of involvement.
• Generally, HSV-1 produces the lesions above the waist, and HSV-2
produces lesions below the waist.
• HSV-1 infection is normally associated with orofacial infections and
encephalitis, whereas HSV-2 is associated with genital infections.

Clinical syndrome of HSV-2 infections:
1. Genital herpes:
- Most primary genital infections are asymptomatic.
- In symptomatic men, the herpetic vesicles appear in the glans
penis, the prepuce, shaft of the penis, and sometimes on the
scrotum, thighs, and buttocks.
- In women, the vesicles appear on the external genitalia, labia
majora, labia minora, vaginal vestibule, and introitus.
- The vesicles subsequently rupture, leaving behind extremely
painful ulcers.
- In both gender, the primary infection may be associated with
constitutional symptoms, such as fever, headache, malaise, and
myalgia.

2. Neonatal infection:
Neonatal infection is a most serious and usually fatal disease
caused mostly by HSV-2.
It usually occurs due to:
• Shedding of HSV-2 from the cervix during vaginal delivery.
• An ascending in-utero infection during a primary infection of
the mother.
• Can be acquired postnatally from family members or hospital
staff.
 Since CMI is poorly developed in neonates, the virus
causes a disseminated disease with involvement of
liver, lung, as well as the organs of the CNS. The
condition has a high mortality of 80%.
 Progression of the infection to the CNS results in
mental retardation or neurological disabilities even
with treatment, or may finally lead to death.

3. Aseptic meningitis:
Aseptic meningitis may occur as a complication of genital HSV-2
infection.
• Meningitis is an inflammation of the membranes (meninges)
surrounding your brain and spinal cord.
• The swelling from meningitis typically triggers symptoms such as
headache, fever and a stiff neck.

3. Direct antigen detection
Direct enzyme immunoassay and direct fluorescent antibody test are useful to
demonstrate HSV antigens directly in vesicular fluid, tissue smear, or biopsy.

5. Serodiagnosis :
• Antibodies appears in 4-7 days after infection.
• They reach a peak in 2-4 weeks.
• Immunofluorescence, ELISA, Neutralization test (Nt-test)
6. Molecular Diagnosis:
Specimens: vesicular fluid, skin scraping, CSF, and other
specimens
• DNA probe and PCR are useful for demonstration of viral
genome.
• PCR shows a higher sensitivity (95%) for detection of HSV-1 DNA
in the CSF specimen.
• PCR is also used to detect asymptomatic shedding or HSV in skin
lesions, but is not cost-effective
• The DNA maps of restriction enzyme fragments of HSV-1 and
HSV-2 are unique. ©sunilbhandariv@gmail.com

Treatment of HSV-infection:
• Several antiviral drugs have proved effective against HSV infections,
including:
Acyclovir, Valacyclovir, and Vidarabine, Famciclovir
• All are inhibitors of viral DNA synthesis.
• Acyclovir: It is a synthetic acyclic purine nucleotide analog, which
is most commonly used to treat HSV infection. Acyclovir is useful:
■ To diminish shedding of viruses,
■ To decrease rate of clinical recurrences
■ To suppress recurrent genital infections.
• Oral therapy with acyclovir is usually recommended for primary orolabial and
genital HSV infections
• Intravenous acyclovir is recommended for life-threatening and serious HSV
infections, such as encephalitis, infections in immunocompromised patients.

Herpesvirus

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