Human Herpes viruses


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Human Herpes viruses

  1. 1. Medicine clinic Dr. MajdAhlam Taweel 20911199 Ala’ Rabea 20911677 -
  2. 2. Alpha-group :Herpes simplex virus type 1 (HSV-1)Herpes simplex virus type 2 (HSV-2)Varicella-zoster virus (VZV)Beta-group :Cytomegalovirus (CMV)Human herpesvirus type 6 (HHV-6)Human herpesvirus type 7 (HHV-7)Gamm-groupEpstein-Barr virus (EBV)
  3. 3.  The Herpes simplex viruses (HSV) are DNA virus of which 2 main group are known . Herpes simplex type 1 :Affects the oral mucosa, Pharynx ,skin. Primary Herpetic Gengivostomatitis Herpes Labialis Herpes simplex type 2 involves the genitalia ( cervical carcinoma)
  4. 4.  The most common viral infection affecting the mouth. Age group : young children and young adult. The incubation period : about 5 days. Serological studies of populations indicate that some 50% of 20-years-old patients have been exposed to HSV. This condition may be severe in immuno compromised patients (HIV) which may lead to herpetic hepatitis or encephalitis, which may be fatal in the absence of treatment.
  5. 5.  Clinical presentation : Grey blisters, which rapidly break down to form small ulcers. Ulcers are circular and shallow with yellowish floor and red margins. The ulcers often becomes super infected and painful. This virus causes fever, malaise and lympohoadenopathy. Site : may be present anywhere on the oral mucosa and most frequently involve the gingivae. transmitted by droplet spread or contact with the lesions.
  6. 6.  Resolution occurs within 2 to 3 weeks. Management: Rest, maintaining fluid intake, chlorhexidine mouthwash to prevent secondary infection of the oral lesions and advice about cross-infection risks should be given. acyclovir is only of benefit in the early stages of the infection.
  7. 7.  Risks : Infants under 6 months are at special risk of developing central nervous system infection and contact with infected siblings should be avoided. Diagnosis : is usually made on clinical grounds, where doubt exists, serology performed on samples of acute and convalescent (2–3 weeks after onset of symptoms) blood should reveal a significant rise (of the order of fourfold or greater) in IgG antibodies against HSV in the later sample. Swabs, for culture
  8. 8.  HSV is a neurogenic virus and the virus may become latent within the trigeminal ganglia of the brain and may be reactivated to cause a secondary infection in 20-30% of individuals. Reasons : exposure of the lip to intense sunlight. systemic factors, such as depressed general immunity. Local irritation (Trauma, chemicals). Menstruation. Common cold.
  9. 9.  Clinical appearance: Prodromal stage : parasthesia or burning sensation and erythema. Vesicles form after hours, along the mucocutanous junction of the lips, and sometimes onto the adjacent skin. The vesicles rupture and form crusted ulcers after 2-3 days. They finally heal without scaring. In a small number of individuals, recurrent intra-oral HSV infection may occur, lesions most commonly affect the hard palate and attached gingivae.
  10. 10. Management : treatment must start as soon as burning sensations are felt. Acyclovir or pencyclovir cream could be effective if applied at prodromal phase (before tissue damage has started). In a small number of individuals, recurrent intra-oral HSV infection may occur, lesions most commonly affect the hard palate and attached gingivae. Severe recurrent HSV infection may occur in the immunocompromised.
  11. 11.  Zoster is the manifestation of recurrent infection following a primary attack of chicken pox. Both chicken pox and herpes zoster (shingles) are caused by varicella. Unlike herpes labialis, repeated recurrences of zoster are very rare. Infection typically affect adult of middle age or over.
  12. 12.  Pain precedes the rash (vesicles). Shingles causes severe pain, and commonly occurs on the trunk on one side. The trigeminal nerve is affected in about 15% of cases of shingles. Lesions localized to one side, within the distribution of any of the divisions of the trigeminal nerve and in the mouth up to the midline. Malaise can be severe. Regional lymph node are enlarged and can be life-threatening in HIV disease.
  13. 13.  in severe case : oral acyclovir 800 mg five times daily for 7-10 days should be given at the earliest possible moment, together with analgesic.
  14. 14.  Shingles usually heals with some scaring after 2-3 weeks. Shingles is a significant painful condition, and the pain may persist after resolution leading to a condition called post herpetic neuralgia. This pain arises more commonly with advancing age.
  15. 15.  Difficult to relieve completely. Carbamazepine and antidepressent therapy tends to provide partial relief. There is evidence that acyclovir reduces the prevalence of post herpetic neuralgia.
  16. 16.  Involvement of facial nerve with VZV Facial nerve palsy Vesicles in external auditory meatus Vesicles on palate Symptoms :dizziness, loss of taste. In most cases, this is self limiting condition but rarely in some patients there may be permanent facial weakness.
  17. 17.  Belong to the gammaherpesvirus subfamily of herpes viruses Nucleocapsid 100 nm in diameter, with 162 capsomers Membrane is derived by budding of immature particles through cell membrane and is required for infectivity. Genome is a linear double stranded DNA molecule with 172 kbp The viral genome does not normally integrate into the cellular DNA but forms circular episomes which reside in the nucleus. The genome is large enough to code for 100 - 200 proteins but only a few have been identified.
  18. 18.  Once infected, a lifelong carrier state develops whereby a low grade infection is kept in check by the immune defenses. Low grade virus replication and shedding can be demonstrated in the epithelial cells of the pharynx of all seropositive individuals. EBV is able to immortalize B-lymphocytes in vitro and in vivo Furthermore a few EBV-immortalized B-cells can be demonstrated in the circulation which are continually cleared by immune surveillance mechanisms. EBV is associated with several very different diseases where it may act directly or one of several co-factors.
  19. 19.  Epstein-Barr virus (EBV) is a human γ-herpesvirus that is able to establish a long-term, latent infection in human B cells for the life of the host. EBV infection is associated with a range of human cancers, including Burkitt’s lymphoma (BL) and Hodgkin’s disease, as well as several AIDS-associated cancers of which the most prevalent is diffuse large B-cell lymphoma (DLBCL). EBV has ability for infecting B lymphocytes. B lymphocytes become activated and produce their own antibody (non-specific antibody), and not necessarily antibody against EBV. The body then produces activated suppressor cells to damper down this process.
  20. 20.  EBV in B Cell Infectious mononucleosis X-Linked Lymphoproliferative Disease Chronic active EBV Hodgkin Disease Burkitt Lymphoma Lymphoproliferative disease EBV in Other Cells Nasopharyngeal carcinoma Gastric carcinoma Nasal T/NK cell lymphomas Peripheral T cell lymphomas Oral hairy leukoplakia Smooth muscle tumors in transplant patients
  21. 21.  Infectious mononucleosis Chronic Active EBV X-linked lymphoproliferative disease Lymphoproliferative disease Oral hairy leukoplakia Hodgkin disease EBV EBV- Driven Nasopharyngeal carcinoma Gene Cell T cell lymphoma Expression Proliferation Burkitt lymphoma
  22. 22.  EBV is the usual cause of infectious monucleosis and these large activated suppressor cells are the mononuclear cells which give mononucleosis its name and are the basis of monospot test.
  23. 23.  Fever. Malaise. Lymphoadenopathy. Petechial rash in the palate. Oral ulceration. The condition occurs mainly in childhood or early adolescence and is believed to be transmitted via saliva.
  24. 24. Cervical Hepatosplenomegalylymphadenopathy
  25. 25. Treatment:Treatment of glandular fever issymptomatic so, no real specific treatmentpencilline is avoided since it is likely to produceerythromatous skin rash.
  26. 26.  EBV+: 60-70% of cases in developing countries 35-50% cases in US EBV in Reed-Sternberg cells Therapy: Chemotherapy, radiation Anti-EBV CTLs effective in some cases
  27. 27.  Belong to the betaherpesvirus subfamily of herpesviruses double stranded DNA enveloped virus Nucleocapsid 105nm in diameter, 162 capsomers The structure of the genome of CMV is similar to other herpesviruses, consisting of long and short segments which may be orientated in either direction, giving a total of 4 isomers. A large no. of proteins are encoded for, the precise number is unknown.
  28. 28.  Virus Structure Enveloped, slightly pleomorphic Spherical 120 – 200 nm in diameter Capsid Envelope Tegument Genome double stranded DNA per virion
  29. 29. Human Cytomegalovirus Virion Structure envelope glycoproteins tegument capsid200 nm DNA core Dr.T.V.Rao MD 38
  30. 30.  A complex -herpesvirus Large genome (230kb) Slow replicating Restricted host range Infects 60-90% of the population worldwide, typically asymptomatic infection Infection in immunocompromised individuals life threatening Stem cell and solid organ transplant recipients HIV infected individuals Cancer patients receiving intensive chemotherapy regimens Infection in utero: Leading cause of infectious disease related birth defects 1 in 100 infected; 1 in 1000 present symptoms/pathology Mild to severe hearing loss Cognitive deficits Physical abnormalities
  31. 31. • Person to person contact (kissing, sexual contact, getting saliva or urine on hands and then touching eyes, or the inside of nose or mouth)• Through the breast milk of an infected woman• Infected pregnant women can pass the virus to their unborn babies• Blood transfusions and organ transplantations Dr.T.V.Rao MD 40
  32. 32.  Once infected, the virus remains in the person for life and my be reactivated from time to time, especially in immunocompromised individuals. The virus may be transmitted in utero, perinatally, or postnatally. Perinatal transmission occurs. 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. Dr.T.V.Rao MD 41
  33. 33.  Congenital infection - may result in cytomegalic inclusion disease 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, lymphadenopathy, and splenomegaly. The heterophil antibody test is negative although atypical lymphocytes may be found in the blood. Immunocompromised patients such as transplant recipients and AIDS patients are prone to severe CMV disease such as pneumonitis, retinitis, colitis, and encephalopathy. Reactivation or reinfection with CMV is usually asymptomatic except in immunocompromised patients. Dr.T.V.Rao MD 42
  34. 34. DIFFICULT Diagnosis  presence of virus or antibody to CMV does not indicate that current disease is due to CMV  Different strategies used in different clinical situationsCongenital CMV isolation of virus from urine within 30 days of birth immunocompromised * antigen detection in patient buffy coat - indicates viraemia * CMV specific Ig G positive indicates past infection Dr.T.V.Rao MD 43
  35. 35.  Congenital infections - it is not usually possible to detect congenital infection unless the mother has symptoms of primary infection. If so, then the mother should be told of the chances of her baby having cytomegalic inclusion disease and perhaps offered the choice of an abortion. Perinatal and postnatal infection - it is usually not necessary to treat such patients. Immunocompromised patients - it is necessary to make a diagnosis of CMV infection early and give prompt antiviral therapy. Anti-CMV agents in current use are ganciclovir, forscarnet, and cidofovir. Dr.T.V.Rao MD 44
  36. 36.  No licensed vaccine is available. There is a candidate live attenuated vaccine known as the Towne strain but there are concerns about administering a live vaccine which could become latent and reactivates. Prevention of CMV disease in transplant recipients is a very complicated subject and varies from center to center. It may include the following measures.  Screening and matching the CMV status of the donor and recipient  Use of CMV negative blood for transfusions  Administration of CMV immunoglobulin to seronegative recipients prior to transplant  Give antiviral agents such as acyclovir and Ganciclovir prophylactically. Dr.T.V.Rao MD 45
  37. 37. Simple hand washing with soap and water iseffective in removing the virus from the hands. 46
  38. 38.  Text books : Pediatric Infectious Diseases5th ed;2004 Oral Patology 4th edition, 2005. Master dentistry 2nd edition,2008. Tyldestry’s Oral Medicine, 5th edition.
  39. 39.  Websites: 10/herpes-zoster.html Simplex-(Oral).htm herpes-simplex-type-1/symptoms