Herpes Simplex Virus: Herpesviridae Family

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HERPES SIMPLEX VIRUS

INTRODUCTION
Herpesviridae Family

photo lifted from Research Gate https://www.researchgate.net/figure/Classification-of-


human-herpesviruses_tbl1_337246305

The virus envelope contains at least 10


glycoproteins that are useful for the
attachment and penetration of the virus.
The structure of herpes viruses consists of a
relatively large double-stranded, linear DNA
genome encased within an icosahedral protein
cage called the capsid, which is wrapped in a
lipid bilayer called the envelope, and the
envelope joined to the capsid by means of a
tegument.
This complete particle is known as the virion.

photo lifted from Science Direct https://www.sciencedirect.com/topics/immunology-and-


microbiology/simplexvirus

Herpes Simplex Virus


 member of the Alphaherpesvirinae subfamily of the Herpesviridae family
 double-stranded DNA virus
 HSV infection is generally divided into two categories—primary (first or initial
infection) and recurrent (reactivation of the latent virus).
 Infections are generally spread by contact with contaminated secretions.
 two types, HSV-1 and HSV-2
 HSV-1 and HSV-2 produce a wide variety of illnesses, including mucocutaneous
infections, central nervous system (CNS) infections, and occasionally, infections of
the visceral organs.
 As the first human herpesvirus to be discovered, HSV is one of the most extensively
studied viruses. Not only have these studies shed light on basic viral processes but
HSV has often served as a probe for investigating fundamental cellular processes as
well.

BIOLOGY 

HERPES VIRUS STRUCTURE - GENERAL


 Envelope

 surrounding an icosahedral capsid


 100nm in diameter 
 dsDNA genome
 "fried-egg" appearance.

 Tegument

 Glycoprotein "spikes" on the HSV surface


 10 nm in length
 Between the capsid and the envelope is an ill-defined
layer of proteins

 Capsid

 doughnut shaped capsomere


  100-200 nm in diameter
 162 capsomeres

 Genome
 double stranded DNA. 
 The size of the genomes differs with cytomegalovirus having the largest
genome
 Encoding 70-200 proteins 

REPLICATION 
 DNA released in the cytoplasm 
 DNA migrates to the nucleus 
 mRNA (transcription) synthesis takes place in the nucleus by using host RNA
polymerase
 mRNA transported to the cytoplasm 
 New viral proteins made and migrate to nucleus 
 Genomic DNA (replication) synthesis takes place in the nucleus by using viral DNA
polymerase.

TRANSMISSION 
 HSV 1:transmitted by saliva and vaginal secretion
 HSV 2: transmitted by sexual contact
 Oral- genital sexual activity:
HSV-1 infections of the genitals
HSV-2 lesions in the oral cavity

EPIDEMIOLOGY 
 60-95% human adults
 No animals or reservoirs or vectors 
 children 6 months to 3 years of age
 70-90% of persons thus acquire type 1 antibodies by adulthood 
 Primary infection by HSV-2 (young adult)

PATHOPHYSIOLOGY

HERPES SIMPLEX VIRUS 1


- Associated with Orofacial / Orolabial Diseases
- It spread through direct contact with contaminated saliva or other infected
bodily secretions.

 HERPETIC GINGIVOSTOMATITIS
 Causative agent is Herpes Simplex Virus Type 1 (HSV-1).
 Characterized by high grade fever and painful oral lesions.
 Typically occurs in children younger than the age of 5 Years, but can also occur in
adolescents and adults.
 The main symptoms are : Pain, swollen gums, blisters and sores.
 HERPES LABIALIS (Cold Sores)
 Infection by the Herpes Simplex Virus 1.
 Affects primarily the lips.
 Fever blisters or cold sores is the milder, recurrent form.
 KERATOCONJUNCTIVITIS
 Caused by Herpes Simplex Virus 1
 Superficial inflammation of the Cornea (Keratitis) and Conjunctiva of the eye.
 Recurrences Can lead to scarring and blindness.
 ENCEPHALITIS
 When Herpes Simplex Virus enters the brain.
 Necrotic lesion in one temporal lobe.
 Symptoms are: Fever, Headache, vomiting, seizures, and altered mental status.
 HERPETIC WHITLOW
 pustular lesion of the skin of the finger or hand.
 It can occur in Medical Personnel’s as a result in contact with patients lesions.
 HERPES GLADIATORUM
 Caused by Herpes Simplex Virus 1z
 common skin condition in Wrestlers.
PATHOPHYSIOLOGY
HERPES SIMPLEX VIRUS 2
 is a sexually transmitted infection that causes genital herpes
 is almost exclusively transmitted through genital-to-genital contact during sex,
causing infection in the genital or anal area.
 Infection with HSV-2 increases the risk of acquiring and transmitting HIV infection.

 GENITAL HERPES OF FEMALE


 The infection manifests itself in females as vesicles on the mucosa of the labia,
vagina, or both.
 Cause acute cervicitis with local minor ulceration which although usually
asymptomatic, may result in a vaginal discharge.
 GENITAL HERPES OF MALE
 The shaft, glans, and prepuce of the penis are the most commonly affected
sites.
 HERPES SIMPLEX VIRUS PROCTITIS
 is thought to progress from the perianal skin into the anal canal and then into
the rectum. 
 Patients with HSV proctitis may complain of anorectal pain, discharge,
tenesmus, or rectal bleeding.
 HERPES SIMPLEX NEONATORUM
 Is the transmission of either HSV-1 or HSV-2 from the mother to child during
gestation via the placenta, during delivery via vaginal secretions, or perinatally
via direct contact with active lesions.
 Infection can be acquired in utero, intranatally (during birth), or postnatally
(after birth)
 Cesarean delivery or suppressive antiviral therapy at delivery significantly
reduces the risk of transmission
 HERPES SIMPLEX VIRUS ENCEPHALITIS
 Occur in neonates, however, brain involvement is generalized, and the usual
cause is HSV-2, which is acquired at the time of delivery
 HERPETIC WHITLOW
 pustular lesion of the skin of the finger or hand
 The occurrence of herpetic whitlow due to HSV-2 is increasingly recognized,
probably due to digital-genital contact in sexually active individuals.
GENITAL HERPES OF FEMALE

GENITAL HERPES OF MALE HERPES SIMPLEX VIRUS


PROCTITIS

HERPES SIMPLEX NEONATORUM


HERPES SIMPLEX VIRUS ENCEPHALITIS

HERPETIC WHITLOW

LABORATORY TECHNIQUES

 Cytopathology - (Tzanck preparation)


- scrapings from base of lesion
-wrights or Giemsa stain
-formation of multinucleated giant cells
 Virus Isolation
- growth inside the cell lines
- typical cytopathic effect occurs in 1-3 days
 Viral Antigen Detection
- by Neutralization test or Immunofluorescence staining with specific antiserum.

 HSV DNA detection by PCR


- most sensitive and can differentiate between HSV1 and HSV2.

 Antibody Detection by ELISA


-antibodies appear in 4-7 days after infection; reach a peak in 2-4 weeks.

PREVENTION and CONTROL


Herpes simplex virus type 1 (HSV-1) and type 1 (HSV-2)
 People with active symptoms of herpes:
 Should avoid oral contact with others.
 Should not share objects that have contact with saliva.
 Should abstain from sexual activity while experiencing any of the symptoms.
 The consistent and correct use of condoms can help to prevent the spread of genital
herpes.
 Pregnant women with symptoms of genital herpes should inform their health care
providers.
 People with symptoms suggestive of genital HSV infection should also receive HIV
testing.
 Treatment (These can help to reduce the severity and frequency of symptoms, but
cannot cure the infection.)
 Antiviral medications
 Acyclovir
 Famciclovir
 Valacyclovir

 Antiviral chemotherapy 
 First Clinical Episode of Genital Herpes (for newly acquired genital herpes)

 Acyclovir 400 mg orally three times a day for 7–10 days


OR
 Valacyclovir 1 g orally twice a day for 7–10 days
OR
 Famciclovir 250 mg orally three times a day for 7–10 days

 Suppressive Therapy for Recurrent Genital Herpes

 Acyclovir 400 mg orally twice a day


OR
 Valacyclovir 1 g orally once a day
OR
 Famiciclovir 250 mg orally twice a day

 Episodic Therapy for Recurrent Genital Herpes

 Acyclovir 400 mg orally three times a day for 5 days


OR
 Valacyclovir 1 g orally once a day for 5 days
OR
 Famciclovir 1 gram orally twice daily for 1 day

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