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HERPES VIRUS
INTRODUCTION
The herpes viruses derived their name from the greek word ‘herpein’, meaning to
creep(sneak).
Herpes viruses have been isolated from a various range of hosts that include
mammals, birds, reptiles,fish,amphibians and molluscs.
A notable characteristic of herpesviruses is that, once they have infected the host,
they often remain as persistant infection for the lifetime of the host.
CLASSIFICATION OF HSV
There are 3 groups of herpes viruses isolated routinely from humans:-
1. Alpha herpesviruses
2. Beta herpesviruses
3. Gamma herpesviruses
Out of 100 only 8 herpesviruses have been isolated from humans:-
1.HSV-1 2.HSV-2 3.Varisella-zoster virus 4.Cytomegalovirus
5.Epstein-barr virus 6.HSV-6 7.HSV-7 8.Kaposi’s sarcoma herpesvirus
STRUCTURE AND GENOME OF
HERPESVIRUS
HSV is large enveloped icosahedral virus.
HSV are of two types:- hsv-1 and hsv-2.
Two viruses are structurally and morphologically similar.
Size :- 12-200nm in diameter
Genome :- linear ds DNA
ANTIGENIC CHARACTERS
 Antigenic differences can be made out using type specific monoclonal antibodies.
Type 2 strains replicate well in chick embryo fibroblast cells , while type 1 strains do so poorly.
The infectivity of type 2 is more temperature sensitive than type 1.
Type 2 strains are more neurovirulent in laboratory animals than type 1.
Type 2 strains are more resistant to antiviral agents like IUDR and cytarabine in culture.
Restriction endonuclease analysis of viral DNA enables differentiation between the 2 types as
well as between strains within same type.
PATHOGENESIS
Pathogenesis of herpes virus mainly involves three stages :-
1. Primary infection :-
 HSV 1 infections are usually limited to oropharynx and transmitted by respiratoy droplets or
saliva whereas HSV 2 infection transmittes by genital route.
 Primary infection of Herpes results in vesicle formation under the layer of keratinized squamous
epithelium cell.
 The vesicle is filled with fluid which contains multinucleated gaint cells and eosinophilic
intracellular inclusion bodies along with inflammatory cell and cellular debris.
2.Latent infection :-
 During latency no virus particles are produced.
 Also the latent infection does not causes any demonstrable damage in neuron.
 This latency phase may be reactivated periodically in some individuals causing recurrent oral
and genital lesion.
3. Recurrence herpes :
 In recurrence the virus travels back from neuron and multiply in mucosal epithelial cell producing
lesion at the same spot each time.
 The recurrent infection can also occurs in presence of specific antibodies. However, recurrent
infections are less severe, more localized and of shorter duration than primary infection.
CLINICAL FEATURES
Clinical patterns depends upon site of infection, age and immune status of host as well as
antigenic type of Herpes virus.
1. Cutaneous infections :-
 The most common site is face –on cheecks,chin,around the mouth or on the forehead.
 Lesions may also appear on the buttocks in infants as napkin rash.
 The typical lesion is ‘fever blister’ or herpes febrilis, caused by viral reactivation in febrile
pateints.
Cutaneous infections Ophthalmic infection
2. Mucosal infection :-
 The buccal mucosa is commonly affected site.
 Gingivostomatitis and pharyngitis are the most frequent conditions in primary and recuurent
herpes infections.
3. Ophthalmic infection :-
 These infections are mainly related to eye infections. HSV infection is the most common cause of
corneal blindness .
 Acute keratoconjuctuvitis may occur by itself or by extension from facial herpes.
 Chorioretinitis and acute necrotizing retinitis are uncommon but serious manifestations.
4. Nervous system infection :-
 Herpes encephalitis; caused by HSV-1
 Herpes meningitis; caused by HSV-2
 Autonomic dysfunction of nervous system
 Guillain-barre syndrome
5. Visceral herpes:-
 Herpes esophagitis
 Tracheobronchitis
 Pneumonitis
6. Genital Herpes :-
 Primary genital herpes is asymptomatic caused by both HSV-1 and HSV-2 but mostly by HSV-2
 In male lesions appears in glans or shaft and occasionally on urethra.
 In female lesions appears on vulva, vagina, cervix, perianal area
 In both sexes, genital herpes is characterized by fever, pain, dysuria, mucoid urethral discharge
with enlarged in lymph node.
7. Congenital Herpes :-
 Transplacental transmission leads to congenital infection but it is rare.
 Neonatal herpes is caused by HSV-2, and it is manifested as infection of eye, mouth, skin and
more commonly a disseminated infection with multiple organ involvement.
 Mortality rate is high and survivors may have neurological disabilities.
TRANSMISSION
Transmission of both HSV types is by direct contact with virus containing secretions or with
lesions on mucosal or cutaneous surfaces.
Hsv-1 is spread by contact , usually by infected saliva.
Hsv-1 primarily infects the skin above the waist.
Hsv-2 is transmitted sexually or from the maternal genital infection to a newborn.
Hsv-2 primarily infects the skin below the waist.
LABORATORY DIAGNOSIS
1.Specimens :-
 Vesicle fluid,skin swabs, saliva, corneal scrapings or brain biopsy on autopsy.
 The diagnosis of herpes virus infection may be made by microscopy,antigen or DNA detection ,
virus isolation or serology.
2.Microscopy :-
 The Tzanck smear is a rapid, fairly sensitive and inexpensive diagnostic method.
 Intranuclear type A inclusion bodies may be seen in Giemsa-stained smears.
 The herpes virus antigen may be demonstrated in smears or sections from lesions by fluorescent
antibody technique.
3. Virus isolation :-
 Inocultion in mice and on chick embryo CAM is not sensitive and has been replaced by tissue
culture for virus isolation.
 Drug susceptibility is also tested in cell cultures.
4. Seology :-
 Differentiation between HSV types 1 and 2 made by a variety of serological techniques, by
nucleic acid hybridization or by restriction endonuclease cleavage and electrophoretic analysis of
viral DNA or viral proteins.
 Serological methods are useful in diagnosis of primary infections.
 Antibodies develop within a few days of infection and rise in titre of antibodies may be
demonstrated by ELISA, neutralization or complement fixation tests.
5.PCR :-
 PCR based detection methods are now being used more often for diagnosis.
Herpesvirus in Tzanck smear
PREVENTION AND CONTROL
Transmission can be reduced by :-
 Avoidance of contact with potential virus-shedding lesions.
 Safe sexual practice.
 Antiviral therapy.
Chemptherapy :-
 Idoxyuridine used in eye and skin infections was one of the first successful antiviral agents.
 Aciclovir,Valaciclovir and famiciclovir are more effective oral agents.
THANK
YOU

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Herpes Simplex Virus

  • 2. INTRODUCTION The herpes viruses derived their name from the greek word ‘herpein’, meaning to creep(sneak). Herpes viruses have been isolated from a various range of hosts that include mammals, birds, reptiles,fish,amphibians and molluscs. A notable characteristic of herpesviruses is that, once they have infected the host, they often remain as persistant infection for the lifetime of the host.
  • 3. CLASSIFICATION OF HSV There are 3 groups of herpes viruses isolated routinely from humans:- 1. Alpha herpesviruses 2. Beta herpesviruses 3. Gamma herpesviruses Out of 100 only 8 herpesviruses have been isolated from humans:- 1.HSV-1 2.HSV-2 3.Varisella-zoster virus 4.Cytomegalovirus 5.Epstein-barr virus 6.HSV-6 7.HSV-7 8.Kaposi’s sarcoma herpesvirus
  • 4. STRUCTURE AND GENOME OF HERPESVIRUS HSV is large enveloped icosahedral virus. HSV are of two types:- hsv-1 and hsv-2. Two viruses are structurally and morphologically similar. Size :- 12-200nm in diameter Genome :- linear ds DNA
  • 5.
  • 6. ANTIGENIC CHARACTERS  Antigenic differences can be made out using type specific monoclonal antibodies. Type 2 strains replicate well in chick embryo fibroblast cells , while type 1 strains do so poorly. The infectivity of type 2 is more temperature sensitive than type 1. Type 2 strains are more neurovirulent in laboratory animals than type 1. Type 2 strains are more resistant to antiviral agents like IUDR and cytarabine in culture. Restriction endonuclease analysis of viral DNA enables differentiation between the 2 types as well as between strains within same type.
  • 7. PATHOGENESIS Pathogenesis of herpes virus mainly involves three stages :- 1. Primary infection :-  HSV 1 infections are usually limited to oropharynx and transmitted by respiratoy droplets or saliva whereas HSV 2 infection transmittes by genital route.  Primary infection of Herpes results in vesicle formation under the layer of keratinized squamous epithelium cell.  The vesicle is filled with fluid which contains multinucleated gaint cells and eosinophilic intracellular inclusion bodies along with inflammatory cell and cellular debris.
  • 8. 2.Latent infection :-  During latency no virus particles are produced.  Also the latent infection does not causes any demonstrable damage in neuron.  This latency phase may be reactivated periodically in some individuals causing recurrent oral and genital lesion. 3. Recurrence herpes :  In recurrence the virus travels back from neuron and multiply in mucosal epithelial cell producing lesion at the same spot each time.  The recurrent infection can also occurs in presence of specific antibodies. However, recurrent infections are less severe, more localized and of shorter duration than primary infection.
  • 9. CLINICAL FEATURES Clinical patterns depends upon site of infection, age and immune status of host as well as antigenic type of Herpes virus. 1. Cutaneous infections :-  The most common site is face –on cheecks,chin,around the mouth or on the forehead.  Lesions may also appear on the buttocks in infants as napkin rash.  The typical lesion is ‘fever blister’ or herpes febrilis, caused by viral reactivation in febrile pateints.
  • 11. 2. Mucosal infection :-  The buccal mucosa is commonly affected site.  Gingivostomatitis and pharyngitis are the most frequent conditions in primary and recuurent herpes infections. 3. Ophthalmic infection :-  These infections are mainly related to eye infections. HSV infection is the most common cause of corneal blindness .  Acute keratoconjuctuvitis may occur by itself or by extension from facial herpes.  Chorioretinitis and acute necrotizing retinitis are uncommon but serious manifestations.
  • 12. 4. Nervous system infection :-  Herpes encephalitis; caused by HSV-1  Herpes meningitis; caused by HSV-2  Autonomic dysfunction of nervous system  Guillain-barre syndrome 5. Visceral herpes:-  Herpes esophagitis  Tracheobronchitis  Pneumonitis
  • 13. 6. Genital Herpes :-  Primary genital herpes is asymptomatic caused by both HSV-1 and HSV-2 but mostly by HSV-2  In male lesions appears in glans or shaft and occasionally on urethra.  In female lesions appears on vulva, vagina, cervix, perianal area  In both sexes, genital herpes is characterized by fever, pain, dysuria, mucoid urethral discharge with enlarged in lymph node. 7. Congenital Herpes :-  Transplacental transmission leads to congenital infection but it is rare.  Neonatal herpes is caused by HSV-2, and it is manifested as infection of eye, mouth, skin and more commonly a disseminated infection with multiple organ involvement.  Mortality rate is high and survivors may have neurological disabilities.
  • 14. TRANSMISSION Transmission of both HSV types is by direct contact with virus containing secretions or with lesions on mucosal or cutaneous surfaces. Hsv-1 is spread by contact , usually by infected saliva. Hsv-1 primarily infects the skin above the waist. Hsv-2 is transmitted sexually or from the maternal genital infection to a newborn. Hsv-2 primarily infects the skin below the waist.
  • 15. LABORATORY DIAGNOSIS 1.Specimens :-  Vesicle fluid,skin swabs, saliva, corneal scrapings or brain biopsy on autopsy.  The diagnosis of herpes virus infection may be made by microscopy,antigen or DNA detection , virus isolation or serology. 2.Microscopy :-  The Tzanck smear is a rapid, fairly sensitive and inexpensive diagnostic method.  Intranuclear type A inclusion bodies may be seen in Giemsa-stained smears.  The herpes virus antigen may be demonstrated in smears or sections from lesions by fluorescent antibody technique.
  • 16. 3. Virus isolation :-  Inocultion in mice and on chick embryo CAM is not sensitive and has been replaced by tissue culture for virus isolation.  Drug susceptibility is also tested in cell cultures. 4. Seology :-  Differentiation between HSV types 1 and 2 made by a variety of serological techniques, by nucleic acid hybridization or by restriction endonuclease cleavage and electrophoretic analysis of viral DNA or viral proteins.  Serological methods are useful in diagnosis of primary infections.  Antibodies develop within a few days of infection and rise in titre of antibodies may be demonstrated by ELISA, neutralization or complement fixation tests.
  • 17. 5.PCR :-  PCR based detection methods are now being used more often for diagnosis. Herpesvirus in Tzanck smear
  • 18. PREVENTION AND CONTROL Transmission can be reduced by :-  Avoidance of contact with potential virus-shedding lesions.  Safe sexual practice.  Antiviral therapy. Chemptherapy :-  Idoxyuridine used in eye and skin infections was one of the first successful antiviral agents.  Aciclovir,Valaciclovir and famiciclovir are more effective oral agents.