PRESENTATION ON

-HERPES SIMPLEX VIRUS 1& 2

-VARICELLA ZOSTER VIRUS

BY LALRUATTLINGA ROLL-17
SAMUEL C.L. TLUANGA ROLL-25 GROUP-11
Content:
❖ Introduction of Herpes virus
❖ Morphology
❖ Replication & Resistance
❖ Classification
❖ Herpes Simplex Virus
- Introduction
- Cultural characteristics
- Pathogenicity
- Lab. Diagnosis
-Treatment and Prophylaxis
❖ Varicella Zoster Virus
-Introduction
-cultural characteristics
-pathogenesis
-lab diagnosis
Treatment & prophylaxis
 HERPES VIRUS
INTRODUCTION:
Herpes are included in family Herpesviridae containing 100 species of
DNA virus.
Characterise by the ability to established life-long latent infections.
MORPHOLOGY:

Herpesvirus is 100-200 nm in diameter containing icosahedral capsid

having 162 capsomeres, enclosing linear double stranded DNA.
Capsid is surrounded by lipid envelope containing peplomers [about
8mm]
Between capsid and envelope is “tegument” which contain several
proteins.
CLASSIFICATION
8 different types of herpesvirus are known which are sub-divided into
3.
-Alphaherpesvirinae
-Betaherpesvirinae
-Gammaherpesvirinae

Herpes family has no common antigen and so no cross reaction except

HSV-1 & HSV-2.
 REPLICATION & RESISTANCE

-Herpes virus multiply in nuclei of infected cells and produced Cowdry type A
intranuclear inclusion bodies.
-They are susceptible to fats solvents like alcohol, bile salts, chloroform, ether etc.

HERPES SIMPLEX VIRUS

HSV occur naturally in human but can produce experimental infection in lab
animals.
There are 2 types HSV-1and HSV-2 .
HSV-1is usually associated with oral and ocular lesin and transmission is by direct
contact or droplet spread.
HSV-2 is responsible for genital lesion and transmitted by sexual means.
 CULTURAL CHARACTERISTICS
-The virus grows in a variety of primary and continuous cell culture(monkey,
rabbit, human amnion etc),resulting in cytopathic changes eg. Giant cell formation.

-On Chick embryo CAM white shiny non necrotic pocks

are produced. large pocks are produced in case of
HSV-2 and smaller pocks in HSV-1

-CAM and inoculation in mice is not sensitive and are

replace by tissue culture for virus isolation. Human
embryonic kidney and amnion and many other
are susceptible but fibroblast are preferred drug
susceptibility test can also be done
in cell culture.
 Differentiating features of HSV-1 & HSV-2
-In CAM HSV-2 form larger pock as compare to HSV-1 form.
-HSV-2 replicate well in fibroblast while HSV-1 does not.
-Type are more neurovirulent than type 1 in lab animals.
-Infectivity of type 2 is more temp sensitive than type.
-Type are more resistant to antiviral like IUDR cytarabine culture.
➢ PATHOGENICITY
HSV is the one of the most viral infections in humans , about 60-90% of adults shows
detectable antibody. Primary infections occurs during childhood , and human are the
only natural host.
Sources of infection are saliva, skin lesions or droplet spread
Asymtomatic carrier are most imp sources of infection especially in genital herpes.
 Route of infection
The disease transmitted by close contact or by sexually in case of genital herpes.
The virus enter through the defect in skin , mucous membrane and multiply locally resulting
in vesicle formation.
After primary infections the virus travel by retrograde intraaxonal flow to sensory root
ganglia and settle in the neurons(ganglia) trigeminal in HSV-1 and sacral in case of HSV-2
They settle in host cell genome and get reactivated by stimuli eg. common cold, stress,
pneumonia etc.
 CLINICAL FEATURES
Clinical manifestation depends on the site of infection,age,immune status of the
host and antigenic type of the virus.
-Cutaneous infection : Most common site - cheeks, chin, forehead etc the typical is
the fever blister due to reactivation of the virus
-Mucosal: Buccal mucosa is the most common affected site eg. gigivostomatitis
-Opthalmic : HSV is the most common cause of corneal blindness in developed
countries.eg. Acute keratoconjuctivitis which can occur by itself or extension
from facial herpes.
-Genital herpes: Categorised as veneral diseases in men, lesions occur mainly in the
penis and or in the urethra. In women cervix, vagina, vulva and perineum are
affected.
-Congenital: Transplacental infection with HSV-1 & HSV-2 can lead to congenital
malformation but rare , infection occur during birth, particularly if the mother has
genital herpes.



 Infection cause by HSV-1 & HSV-2
HSV-1
-acute gingivomatitis
-pharyngotonsillitis
-herpes labialis
-keratoconjuctivitis
-eczema herpeticum
-encephalitis
-dendritic keratistis
HSV-2
-genital herpes( penis, cervix, vagina, urethra)
-neonatal herpes
-aseptic meningitis
Cutaneous lesion of herpes’skin above waist’usually occur in HSV-1 and ‘skin below waist’ in
HSV-2.
 Herpetic whitlow is an occupational hazard of health workers , who
acquired
infections from saliva and respiratory secretion of patients.

IMMUNITY : Antibodies produced may not prevent reccurrences, but can

reduce the severity of the diseases.
 LABORATORY DIAGNOSIS
1.Specimen:Vesicle fluid,skin swab,saliva,CSF,brain biopsy etc according to
site of involvement.
2.Direct Examination:
-Smear prepared from scraping of the base of vesicles stained with toluidine blue TZANCK
smear Tzanck cells are present in positive smear.
-cowdry type A intranuclear inclusion bodies may be seen in Giemsa stain.
-It can also be demonstrated by Electron Microscopy.
-Viral antigen can also be demonstrated by immunofluorescent staining.
3.Tissue Culture: Virus are isolated min human fibroblast,Hep-2,Vero cells etc.
diagnosis can be confirmed by immunofluorescent staining of infected cells.
4.Serology:primary infection can be diagnosed by detection of virus specific IgM antibody
immunofluorescence, RIA, ELISA have been employed for antibody detection but
serology is not widely used.
5.Polymerase Chain Reaction: PCR can be used for detection of HSV DNA IN CSF.
Nowadays, they are the most preffered diagnostic tool in virology.
 TREATMENT AND PROPHYLAXIS
HSV infection cab be treated by ancyclovir(ancycloguanase)it interfere viral dna synthesis
by inhibiting viral DNA depend DNA-polymerase.HSV-2 is more resistant to treatment.
Valaciclovir and Famciclovir are more effective oral agents.When drug resistant are
developed Trisodium phosphonoformate(foscarnet) may be useful.
 Currently there is no vaccine approved available for HSV infection.

Additional info.
Moderna’s HSV vaccine candidate (mRNA – 1608) mRNA vaccine targeted against
HSV-2 which could provide cross-protection against HSV-1. Moderna’s aim to induce a
strong antibody response with neutralizing and effector functionally combined cell-
mediated immunity as stated on 18th Feb 2022.
 VARICELLA ZOSTER VIRUS
 Varicella (chickenpox) & herpes (shingles) are caused by single
virus called Varicella Zoster Virus.
 Chickenpox follows primary infection in a non-individual,
whereas herpes zoster is a reactivation of the latent virus.
 Contact with either chickenpox or zoster may only lead to
chickenpox but not zoster.
 MORPHOLOGY

 The structural morphology is similar to that of herpes

simplex virus
 CULTURAL CHARACTERISTICS :
 Varicella zoster does not grow in experimental animals & chick embryo.
 It was first isolated by Weller in human embryonic tissue culture.
 It can be grown in cultures of human fibroblasts, human amnion cells or HeLa cells.
 Cytopathic effects are similar, but less marked than herpes simplex virus.
 In cultures, the virus remains cell associated & does not appears in free medium.
It is possible to distinguish between herpes virus type 1&2 and varicella zoster
viruses by using highly specific antisera.
 Only one antigenic type of Varicella zoster virus is known
 VARICELLA (CHICKENPOX)
o Chickenpox is one of the mildest and most common of childhood infections.
o The adult chickenpox is more serious, rather common in tropical areas.
o Source of infection – Chickenpox & herpes zoster virus.
- Infectivity is maximum during the early stage of the disease, as the virus is
abundant at the upper respiratory part.
- The buccal lesions which appears in early stage of the disease & vesicular
fluid are rich in virus content.
- There are no animal reserviours.
o The disease mostly occurred during December – Spring
PATHOGENECITY OF VARICELLA :
 The portal entry of the virus is respiratory tract & conjunctiva.
 Incubation period – about 2 weeks ( 7-23 days).
 The patient is considered to be infectious 2 days before & 5 days after the
onset of the lesions.
 In children, the disease is first
noticeable when the lesion
appears, evolution of the rash is
rapid. The rash is centripetal in
distributon during the fisrt 3-4 days
& begin to crush within 48 hrs.
 In adult, the symptoms maybe
severe , the rash maybe
haemoraghic & occasionaly
bullous lesion appears &
pneumonia is more common in
adults.
Chickenpox in pregnancy:
 Chickenpox in pregnancy can be dangerous for both mother and the baby.
 It can incresae the risk of pneumonia.
HERPES ZOSTER (SHINGLES/ZONA)
 While varicella is a childhood disease, herpes zoster is of old age
(50+ years). But can occur at any age.
 It usually occurs in a person who had chickenpox several years
earlier . because, virus remains latent in the sensory ganglia.
 When the host immunity is severely weakened, VZV maybe
reactivated resulting in herpes zoster / shingles
 Pathogenicity:
 Lesions are identical to Varicella lesions, but they are locally
distributed which heals in about two weeks.
 Pain & paresthesia at the effected area may persists for weeks or
months.
 Other complications are Lower motor neuron paralysis.
Difference between Chickenpox & Shingles :
 IMMUNITY :
 Although VZV is responsible for both the disease, One attack of
chickenpox provide life-long immunity.
 But, antibody fails to eliminate the virus from dorsal root ganglia. Hence,
zosters occurs in person who have immunity to varicella
Laboratory Diagnosis:
1 ) Direct Microscopy :
o Stain smear from early vesicle shows type-A
intranuclear inclusion bodies.
o The virus can also be viewed under electron
microscopy.

2 ) Virus Isolation :
o Virus can be isolated in human fibroblast cells,
HeLa cells or vero cells etc.
o Virus antigen can be detected by immune
fluorescence (monoclonal antibody).
3 ) Polymerase Chain Reaction (PCR) :
o DNA can be extracted from specimen and amplified by PCR
o Most preferred for detection of VZV in CFS & other body fluids.

4 ) Serology :
o VZV specific IgM antibody in patient serum can be detected by ELISA, CFT,
Immunofluorescence.
Treatment & Prophylaxis :
 Acyclovir & Vidarabine are effective in the treatment of severe varicella and
zoster.

 VZV immunoglobulins from patients of zosters gives passive protection in

immunecompromised children (not useful in treatment)
 Life attenuated varicella vaccine (Oka strain) modified lyophilised form of
vaccine is now available.
 Is safe and effective, but not in pregnant women.

Additional Info. : Moderna expected varicella zoster vaccine candidate mRNA-1468,

designed to express VZV glycoprotein E (gE) to reduce the rate of shingles, as stated on
18th February 2022.

Reference : Textbook of Microbiology – Dr. C.P. Baveja (6th editon)

Textbook of Microbiology – Ananthanarayan & Paniker’s (9th edition)
Textbook of Microbiology & Immunology – Subhash Chandra Parija
(2nd edition)
THANK YOU