HERPESVIRUSES
Dr. Pendru Raghunath Reddy
Introduction

• Herpes viruses are a leading cause of human viral
diseases, second only to influenza and cold viruses

• A...
Morphology
 100 – 200 nm in diameter, contains an icosahedral capsid containing
linear double stranded DNA genome
 Surro...
Classification of Human Herpesviruses
Subfamily

Scientific name

Common name

Alphaherpesvirinae

Human herpesvirus 1
Hum...
Herpes Simplex Virus (HSV)
 These are very large viruses and their genome (150 kb)
encodes at least 80 proteins

 Almost...
Pathogenesis
Source of infection
Saliva, skin lesions or respiratory secretions
from patients or carriers

Mode of transmi...
 HSV is shed in saliva, tears, genital and other secretions
 The primary infection occurs through the skin, oral mucous
...
Diseases caused by HSV-1
1. Acute gingivostomatitis

2. Herpes labialis

3. Keratoconjunctivitis

4. Eczema herpeticum

5....
 Acute gingivostomatitis is the
commonest manifestation of primary
herpetic infection
 The patient experiences pain and
...
 Following primary infection, 45% of
orally infected individuals will
experience reactivation
 Herpes labialis (cold sor...
 This is found in children with
active eczema

 The virus can spread to other
organs such as the liver
and adrenals

Ecz...
Diseases caused by HSV-2
1. Genital herpes (penis, urethra, cervix, vulva, vagina)

2. Neonatal herpes

3. Aseptic meningi...
Herpes Simplex Viruses (HSV)
Characteristic
Urogenital infections
Nongenital infections:
Labialis
Keratitis
Whitlow (hand)...
HSV-1 and HSV-2 cross react serologically. They can be differentiated
by the following features

 By using specific monoc...
Laboratory diagnosis
Specimens
Vesicle fluid, skin swab, saliva, corneal scrapings, brain biopsy and CSF
according to the ...
Cowdry type A intranuclear inclusion bodies may be seen in
Giemsa stained smears
Herpes virions may be demonstrated in spe...
2. Cell culture
 Virus can be isolated on human fibroblasts, HEp-2 cells, Vero cells
and CAM of embryonated egg

 Swolle...
3. Serology
Primary infection can be diagnosed by detection of virus specific
IgM antibody or by a rising titre of antibod...
Varicella-Zoster
 Varicella (chickenpox) and herpes zoster (shingles) are caused
by a single virus

 Chickenpox follows ...
Epidemiology

• Primary varicella is an endemic disease. Varicella is one of the
classic diseases of childhood, with the h...
Varicella
Pathogenesis
Source of infection
Patient with varicella or zoster

Mode of transmission
Inhalation of respirator...
Pathogenesis
• The virus is thought to gain entry via the respiratory tract and
spreads shortly after to the lymphoid syst...
• Primary infection results in varicella (chickenpox)
• Incubation period of 7-23 days
• Presents fever, a widespread vesi...
Rash of Chickenpox
Congenital Varicella Infection
• 90% of pregnant women already immune, therefore
primary infection is rare during pregnanc...
Herpes Zoster (Shingles)
 Herpes Zoster mainly affect a single dermatome of the skin

 It may occur at any age but the v...
 Herpes

zoster affecting the eye (ophthalmic zoster) and face
(Ramsay Hunt syndrome affecting the facial nerve) may pose...
Laboratory diagnosis
The clinical presentations of varicella or zoster are so characteristic
that laboratory confirmation ...
2. Virus isolation
 VZV isolated in human fibroblast cells, human amnion, HeLa or
Vero cells
 Cytopathic effect is focal...
3. PCR
4. Serology
specific IgM antibody in patient’s serum can be
detected by ELISA

 Varicella-zoster

 Other methods ...
Cytomegalovirus
• Belong to the betaherpesvirus subfamily of herpesviruses

• Double stranded DNA enveloped virus and 150-...
Pathogenesis
Mode of transmission
• The virus may be transmitted from person to person in several
ways (in utero, perinata...
• Initial replication of the virus occurs in the epithelial cells of
the respiratory and GI tracts which is followed by vi...
Clinical Manifestations
• Congenital infection - may remain inapparent at birth or may lead to
cytomegalic inclusion disea...
• Immunocompromised patients such as transplant recipients and
AIDS patients are prone to severe cytomegalic inclusion dis...
Laboratory diagnosis
Specimens
CMV can be isolated from urine, saliva, breast milk, semen,
cervical secretions and blood l...
Isolation of virus
 Virus can be grown in human fibroblast cultures
 The virus replicates very slowly, therefore, cytopa...
Antigen detection
CMV antigen can be detected from blood leucocytes using
monoclonal antibodies

PCR
Serology
CMV-specific...
Treatment
For treatment of severe CMV infections, ganciclovir is the drug of
choice

Prophylaxis
 Indicated only in high ...
Epstein-Barr virus
 Belong to the gammaherpesvirus subfamily of herpesviruses

 EBV has affinity for lymphoid tissue. Th...
Pathogenesis

Source of infection
Saliva of infected persons

Mode of transmission
Intimate oral contact, as in kissing ap...
 The virus enters the pharyngeal epithelial cell through CD21
(or CR2) receptors
 It multiplies locally, enters the bloo...
 EB virus antigens are expressed on the surface of infected
B lymphocytes. T lymphocytes will be activated in response
to...
Clinical manifestations
 Most EBV infections are inapparent

 Once infected, the virus is present in the individual for ...
Infectious Mononucleosis
(Glandular fever)
It is an acute self-limiting disease of children and young adults
characterised...
In some patients, chronic IM may occur where eventually
the patient dies of lymphoproliferative disease or lymphoma
EBV ac...
3. EBV-associated malignancies
a) Burkitt’s lymphoma
 It is a malignant neoplasm of B-lymphocytes (tumour of jaw)
which o...
Burkitt’s lymphoma
affecting jaw

Burkitt's lymphoma showing
disruption of teeth and partial
obstruction of airway
Laboratory diagnosis
1. White blood cell count
 During the initial phase, patient develops leucopenia
 Later there is le...
Procedure
 Inactivated serum in doubling dilutions is mixed with equal
volumes of 1% sheep erythrocytes suspension

 The...
Confirmation
Absorption test for Paul – Bunnell antibody
Absorption with
Guinea pig kidney

Ox red cells

Normal serum

Ab...
3. EBV – specific antibodies
 The IgM antibody to EBV viral capsid antigen (VCA) appears
soon after primary infection and...
4. Antigen detection
 EBV antigen can be detected by immunofluorescence using
monoclonal antibodies
 EBNA1 is very impor...
Human Herpesvirus 6
 HHV – 6 infects dividing CD4+ T lymphocytes
 Saliva is the main route of transmission
 Most HHV – ...
 Primary HHV-6 or HHV-7 infection is associated with
Roseola Infantum, which is a classical disease of childhood
 Most c...
 Human Herpesvirus 8 is associated with Kaposi’s sarcoma,
which is the commonest tumour in HIV infected individuals

Kapo...
Herpesviruses
Herpesviruses
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Herpesviruses

  1. 1. HERPESVIRUSES Dr. Pendru Raghunath Reddy
  2. 2. Introduction • Herpes viruses are a leading cause of human viral diseases, second only to influenza and cold viruses • Are capable of causing overt disease or remaining silent for many years only to be reactivated • Name Herpes comes from the Latin herpes which, in turn, comes from the Greek word herpein which means to creep
  3. 3. Morphology  100 – 200 nm in diameter, contains an icosahedral capsid containing linear double stranded DNA genome  Surrounded by a lipid envelope containing peplomers  Between capsid and envelope is tegument
  4. 4. Classification of Human Herpesviruses Subfamily Scientific name Common name Alphaherpesvirinae Human herpesvirus 1 Human herpesvirus 2 Human herpesvirus 3 Herpes simplex virus type 1 Herpes simplex virus type 2 Varicella-zoster virus Betaherpesvirinae Human Human Human Human Gammaherpesvirinae Human herpesvirus 4 Human herpesvirus 8 herpesvirus herpesvirus herpesvirus herpesvirus 5 6 6a 7 Cytomegalovirus Epstein-Barr (EB) virus Kaposi’s sarcoma associated virus
  5. 5. Herpes Simplex Virus (HSV)  These are very large viruses and their genome (150 kb) encodes at least 80 proteins  Almost any human cell type can be affected by HSV  The genome of HSV-1 and HSV-2 share 50 - 70% homology  Man is the only natural host  HSV-1 is usually associated with oral and occular lesions  HSV-2 is responsible for the majority of genital infections
  6. 6. Pathogenesis Source of infection Saliva, skin lesions or respiratory secretions from patients or carriers Mode of transmission Direct contact with virus containing secretions or with lesions HSV 1: Kissing or saliva contaminated fingers HSV 2 : Sexual intercourse, congenital infection
  7. 7.  HSV is shed in saliva, tears, genital and other secretions  The primary infection occurs through the skin, oral mucous membranes, or eyes resulting in a vesicle formation  The virus spreads to draining lymphnodes producing lymphadenitis  After primary infection the virus travels by retrograde intra-axonal flow to sensory root ganglia  They settle within the neurons in the ganglia (trigeminal-HSV-1; sacral-HSV-2)  The Herpesvirus DNA gets integrated into the host cell genome  These get reactivated when provoked by various stimuli (common cold, fever, pneumonia, stress, exposure to sunlight etc)
  8. 8. Diseases caused by HSV-1 1. Acute gingivostomatitis 2. Herpes labialis 3. Keratoconjunctivitis 4. Eczema herpeticum 5. Encephalitis 6. Dendritic keratitis
  9. 9.  Acute gingivostomatitis is the commonest manifestation of primary herpetic infection  The patient experiences pain and bleeding of the gums  1 - 8 mm ulcers with necrotic bases are present  Neck glands are commonly enlarged accompanied by fever  Usually a self limiting disease which lasts around 13 days Gingivostomatitis
  10. 10.  Following primary infection, 45% of orally infected individuals will experience reactivation  Herpes labialis (cold sore) is a recurrence of oral HSV  A prodrome of tingling, warmth or itching at the site usually heralds the recurrence  About 12 hours later, red-ness appears followed by papules and then vesicles Herpes labialis (cold sore)
  11. 11.  This is found in children with active eczema  The virus can spread to other organs such as the liver and adrenals Eczema herpeticum
  12. 12. Diseases caused by HSV-2 1. Genital herpes (penis, urethra, cervix, vulva, vagina) 2. Neonatal herpes 3. Aseptic meningitis Note: Besides above mentioned primary infections, herpesviruses may present as latent infection, reactivation and recrudescence
  13. 13. Herpes Simplex Viruses (HSV) Characteristic Urogenital infections Nongenital infections: Labialis Keratitis Whitlow (hand) Encephalitis (adult) Neonatal infection Transmission HSV-1 10 - 30% HSV-2 70 - 80% 80 - 90 % + + + 30 % primarily non-genital 10 - 20 % + 70 % primarily genital
  14. 14. HSV-1 and HSV-2 cross react serologically. They can be differentiated by the following features  By using specific monoclonal antibodies  HSV-2 forms larger pocks on chick embryo CAM  HSV-2 replicates well in chick embryo fibroblast cells  HSV-2 is more neurovirulent in laboratory animals  The infectivity of HSV-2 is more temparature sensitive than that of HSV-1  HSV-2 is more resistant to antiviral agents  Restriction endonuclease analysis of viral DNA
  15. 15. Laboratory diagnosis Specimens Vesicle fluid, skin swab, saliva, corneal scrapings, brain biopsy and CSF according to the site of invovlement 1. Direct examination Smears prepared from base of vesicles are stained with toludine blue. multinucleated giant cells with faceted nuclei and homogeneously stained chromatin (Tzanck cells) are present in a positive smear
  16. 16. Cowdry type A intranuclear inclusion bodies may be seen in Giemsa stained smears Herpes virions may be demonstrated in specimens by electron microscopy Viral antigens can also be demonstrated in the scrapings from the base of the lesions and tissue preparation by immunofluorescence
  17. 17. 2. Cell culture  Virus can be isolated on human fibroblasts, HEp-2 cells, Vero cells and CAM of embryonated egg  Swollen, rounded cells may appear within 1-5 days  Diagnosis can be confirmed by immunofluorescent staining of infected cell culture Cytopathic effect of HSV in cell culture: Note the ballooning of cells
  18. 18. 3. Serology Primary infection can be diagnosed by detection of virus specific IgM antibody or by a rising titre of antibody Various tests like CFT, neutralisation, immunofluorescence, ELISA and RIA have been employed for antibody detection 4. PCR Chemotherapy  HSV infection can be treated with acyclovir (acycloguanosine)  Valaciclovir and famciclovir are more effective oral agents  When resistance to these drugs develop, drugs like trisodium -phosphonoformate (Foscarnet) may be useful
  19. 19. Varicella-Zoster  Varicella (chickenpox) and herpes zoster (shingles) are caused by a single virus  Chickenpox follows primary infection in a non-immune individual, whereas herpes zoster is a reactivation of the latent virus  VZV is similar to the HSV in its morphology  Only one antigenic type of VZV is known
  20. 20. Epidemiology • Primary varicella is an endemic disease. Varicella is one of the classic diseases of childhood, with the highest prevalence occurring in the 4 - 10 years old age group • Varicella is highly communicable, with an attack rate of 90% in close contacts • Most people become infected before adulthood but 10% of young adults remain susceptible • Herpes zoster, in contrast, occurs sporadically and evenly throughout the year
  21. 21. Varicella Pathogenesis Source of infection Patient with varicella or zoster Mode of transmission Inhalation of respiratory droplets Sometimes through conjunctiva
  22. 22. Pathogenesis • The virus is thought to gain entry via the respiratory tract and spreads shortly after to the lymphoid system • After an incubation period of 14 days, the virus arrives at its main target organ, the skin • Following the primary infection, the virus remains latent in the cerebral or posterior root ganglia. In 10 - 20% of individuals, a single recurrent infection occurs after several decades • The virus reactivates in the ganglion and tracks down the sensory nerve to the area of the skin innervated by the nerve, producing a varicellaform rash in the distribution of a dermatome
  23. 23. • Primary infection results in varicella (chickenpox) • Incubation period of 7-23 days • Presents fever, a widespread vesicular rash mostly on the trunk • The features are so characteristic that a diagnosis can usually be made on clinical grounds alone • Complications are rare but occurs more frequently and with greater severity in adults and immunocompromised patients • Most common complication is secondary bacterial infection of the vesicles • Severe complications which may be life threatening include viral pneumonia, encephalititis, and haemorrhagic chickenpox
  24. 24. Rash of Chickenpox
  25. 25. Congenital Varicella Infection • 90% of pregnant women already immune, therefore primary infection is rare during pregnancy • Primary infection during pregnancy carries a greater risk of severe disease, in particular pneumonia First 20 weeks of Pregnancy • Up to 3% chance of transmission to the fetus, recognised congenital varicella syndrome; • Scarring of skin • Hypoplasia of limbs • CNS and eye defects • Death in infancy normal
  26. 26. Herpes Zoster (Shingles)  Herpes Zoster mainly affect a single dermatome of the skin  It may occur at any age but the vast majority of patients are more than 50 years of age  The latent virus reactivates in a sensory ganglion and tracks down the sensory nerve to the appropriate segment  The reactivation is associated with the inflammation of the nerve which leads to neuritic pain that often precedes the skin lesions  There is a characteristic eruption of vesicles in the dermatome which is often accompanied by intensive pain which may last for months (postherpetic neuralgia)
  27. 27.  Herpes zoster affecting the eye (ophthalmic zoster) and face (Ramsay Hunt syndrome affecting the facial nerve) may pose great problems  As with varicella, herpes zoster in a far greater problem in immunocompromised patients in whom the reactivation occurs earlier in life and multiple attacks occur as well as complications  Complications are rare and include encephalitis and disseminated herpes zoster Shingles
  28. 28. Laboratory diagnosis The clinical presentations of varicella or zoster are so characteristic that laboratory confirmation is rarely required. Laboratory diagnosis is required only for atypical presentations, particularly in the immunocompromised 1. Direct Microscopy  Toludine blue or Giemsa stained smears from the base of early vesicles show multinucleated giant cells and type A intranuclear inclusion bodies under light microscope  Eelectron microscopy may be used but cannot distinguish between HSV and VZV  Immunofluorescense using monoclonal antibody on skin scrappings can distinguish between the two
  29. 29. 2. Virus isolation  VZV isolated in human fibroblast cells, human amnion, HeLa or Vero cells  Cytopathic effect is focal with refractile ballooned cells  Virus antigen can be demonstrated in nuclear inclusions by immunofluorescence using monoclonal antibody Cytopathic effect of VZV
  30. 30. 3. PCR 4. Serology specific IgM antibody in patient’s serum can be detected by ELISA  Varicella-zoster  Other methods such as CFT, neutralisation test and immunofluorescence can be used for detection of VZV-specific antibodies Treatment Acyclovir and vidarabine are effective in the treatment of severe varicella and zoster
  31. 31. Cytomegalovirus • Belong to the betaherpesvirus subfamily of herpesviruses • Double stranded DNA enveloped virus and 150-200 nm in size • The virus exhibits strict host-specificity • Cytomegalovirus infections are almost always inapparent, leading to prolonged latency, with occasional reactivation • Cytomegalovirus disease is rare but infection with the virus is extremely common
  32. 32. Pathogenesis Mode of transmission • The virus may be transmitted from person to person in several ways (in utero, perinatally, or postnatally) • Perinatal infection is acquired mainly through infected genital secretions, or breast milk. Overall, 2 - 10% of infants are infected by the age of 6 months worldwide. Perinatal infection is thought to be 10 times more common than congenital infection • Postnatal infection mainly occurs through saliva. Sexual transmission may occur as well as through blood and blood products and transplanted organ
  33. 33. • Initial replication of the virus occurs in the epithelial cells of the respiratory and GI tracts which is followed by viraemia resulting in infections of all organs of the body • In symptomatic cases, renal tubular epithelium, liver and CNS are also affected • The virus establishes lifelong latent infection in monocytes, B lymphocytes, epithelial cells and stromal cells of bone marrow and in some organs like kidneys and heart • Once infected, the virus remains in the person for life and may be reactivated from time to time, especially in immunocompromised individuals
  34. 34. Clinical Manifestations • Congenital infection - may remain inapparent at birth or may lead to cytomegalic inclusion disease which is often fatal • The disease is characterised by hepatosplenomegaly, jaundice, thrombocytopenic purpura, microcephaly and chorioretinitis • Perinatal infection - usually asymptomatic • Postnatal infection - usually asymptomatic. However, in a minority of cases, the syndrome of infectious mononucleosis may develop which consists of fever, malaise, fatigue, and splenomegaly. The heterophil antibody test is negative although atypical lymphocytes may be found in the blood
  35. 35. • Immunocompromised patients such as transplant recipients and AIDS patients are prone to severe cytomegalic inclusion disease characterised by hepatosplenomegaly, jaundice, thrombocytopenic purpura, pneumonia and micro cephaly • Reactivation or reinfection with CMV is usually asymptomatic except in immunocompromised patients
  36. 36. Laboratory diagnosis Specimens CMV can be isolated from urine, saliva, breast milk, semen, cervical secretions and blood leucocytes Demonstration of Cytomegalic cells Enlarged cells with large intranuclear “owl’s eye” appearance inclusions (cytomegalic cells) can be demonstrated in the centrifuged deposits from urine or saliva
  37. 37. Isolation of virus  Virus can be grown in human fibroblast cultures  The virus replicates very slowly, therefore, cytopathic effects (swollen refractile cells with cytoplasmic granules) may take 2-3 weeks to appear  For precise identification, these cultures may be stained by immunofluorescence using monoclonal antibody Cytopathic effect of CMV
  38. 38. Antigen detection CMV antigen can be detected from blood leucocytes using monoclonal antibodies PCR Serology CMV-specific IgM can be detected in the serum by ELISA
  39. 39. Treatment For treatment of severe CMV infections, ganciclovir is the drug of choice Prophylaxis  Indicated only in high risk cases such as organ transplants, premature infants, immunodeficient persons  Screening of blood and organ donors  Administration of CMV immunoglobulins and Acyclovir  No vaccine is available
  40. 40. Epstein-Barr virus  Belong to the gammaherpesvirus subfamily of herpesviruses  EBV has affinity for lymphoid tissue. The B lymphocytes of human beings have receptors (CD21 molecules) for EBV  EBV infected B lymphocytes are transformed in such a way that they multiply continuously
  41. 41. Pathogenesis Source of infection Saliva of infected persons Mode of transmission Intimate oral contact, as in kissing appears to be main mode of transmission
  42. 42.  The virus enters the pharyngeal epithelial cell through CD21 (or CR2) receptors  It multiplies locally, enters the blood stream and infects B lymphocytes  In most cases, the virus remains latent inside the lymphocytes, which become transformed  The activated B lymphoblast, along with the antigen of EBV, matures into a long-lived memory lymphocyte in the germinal centre of the lymph node This leads to polyclonal activation of the infected B lymphocytes resulting in production of many kinds of antibodies to many antigens -accompanied by nonspecific increase in total IgM, IgG and IgA
  43. 43.  EB virus antigens are expressed on the surface of infected B lymphocytes. T lymphocytes will be activated in response to such neoantigens  In immunocompetent persons, proliferation of transformed B lymphocytes is kept in check by activated T lymphocytes  In the immunodeficient persons, lymphomas may occur because of unchecked replication of B lymphocyte clones
  44. 44. Clinical manifestations  Most EBV infections are inapparent  Once infected, the virus is present in the individual for life  The following clinical manifestations may result from EBV infection 1. Infectious mononucleosis 2. Infections in immunocompromised hosts 3. EBV-associated malignancies
  45. 45. Infectious Mononucleosis (Glandular fever) It is an acute self-limiting disease of children and young adults characterised by fever, sore throat, lymphadenopathy and splenomegaly In some patients jaundice may be seen which is due to hepatitis Abnormal lymphocytes are present in the blood The incubation period is 4-7 weeks and infection is believed to occur through respiratory route by close contact with patients Complications occur rarely but may be serious e.g. splenic rupture, meningoencephalitis, and pharyngeal obstruction
  46. 46. In some patients, chronic IM may occur where eventually the patient dies of lymphoproliferative disease or lymphoma EBV activates B lymphocytes and leads to secretion of immunoglobulins (IgM antibodies) 2. Infections in immunocompromised hosts EBV may cause progressive lymphoproliferative disease in immunodeficient children, transplant recipients and AIDS patients
  47. 47. 3. EBV-associated malignancies a) Burkitt’s lymphoma  It is a malignant neoplasm of B-lymphocytes (tumour of jaw) which occurs in regions of Africa and New Guinea  The disease occurs in endemic or sporadic type  Cells of Burkitt’s lymphoma carry multiple copies of EBV genome b) Nasopharyngeal carcinoma c) B-cell lymphoma
  48. 48. Burkitt’s lymphoma affecting jaw Burkitt's lymphoma showing disruption of teeth and partial obstruction of airway
  49. 49. Laboratory diagnosis 1. White blood cell count  During the initial phase, patient develops leucopenia  Later there is leucocytosis with a predominance of abnormal or atypical lymphocytes 2. Paul-Bunnell test  During infectious mononucleosis, heterophile antibodies (IgM) appear in the serum of the patient  These antibodies agglutinate sheep erythrocytes  These antibodies appear in 85-90% of patients sera during the acute phase of illness
  50. 50. Procedure  Inactivated serum in doubling dilutions is mixed with equal volumes of 1% sheep erythrocytes suspension  These tubes incubated at 370C for 4 h and examined for agglutination  A titre of 100 or above is suggestive of infectious mononucleosis
  51. 51. Confirmation Absorption test for Paul – Bunnell antibody Absorption with Guinea pig kidney Ox red cells Normal serum Absorbed Not absorbed Antibody after serum injections Absorbed Absorbed Infectious mononucleosis Not absorbed Absorbed
  52. 52. 3. EBV – specific antibodies  The IgM antibody to EBV viral capsid antigen (VCA) appears soon after primary infection and disappears in 1 – 2 weeks  The IgG antibody to VCA persists throughout life and is an indication of past or recent infection  These can be demonstrated by indirect immunofluorescence or ELISA  Antibody to the EBV nuclear antigen (EBNA) is also a reliable marker for primary infection  Antibodies to early antigens (EA) can be demonstrated in EB – associated lymphomas
  53. 53. 4. Antigen detection  EBV antigen can be detected by immunofluorescence using monoclonal antibodies  EBNA1 is very important antigen 5. Virus isolation  Saliva or throat washings and peripheral blood cells can be inoculated onto lymphocytes  If specimen contains EBV, it produces a lymphoblastoid cell line 6. Nucleic acid hybridisation 7. PCR
  54. 54. Human Herpesvirus 6  HHV – 6 infects dividing CD4+ T lymphocytes  Saliva is the main route of transmission  Most HHV – 6 infections appear to be asymptomatic  They may, however cause exanthem subitum or roseola infantum and infectious mononucleosis – like disease with cervical lymphadenopathy  HHV – 6 can be isolated from peripheral blood mononuclear cells in early febrile stage of the illness by co – cultivation with lymphocytes
  55. 55.  Primary HHV-6 or HHV-7 infection is associated with Roseola Infantum, which is a classical disease of childhood  Most cases occur in infants between the ages of 4 months and two years  A spiking fever develops over a period of 2 days followed by a mild rash  The fever is high enough to cause febrile convulsions  There are reports that the disease may be complicated by encephalitis Roseola infantum
  56. 56.  Human Herpesvirus 8 is associated with Kaposi’s sarcoma, which is the commonest tumour in HIV infected individuals Kaposi’s sarcoma

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