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Epstein Barr Virus Herpes virus group Cytomegalovirus Herpes virus group Mumps VirusParamyxovirus group.

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Presentation on theme: "Epstein Barr Virus Herpes virus group Cytomegalovirus Herpes virus group Mumps VirusParamyxovirus group."— Presentation transcript:

1 Epstein Barr Virus Herpes virus group Cytomegalovirus Herpes virus group Mumps VirusParamyxovirus group

2 Herpes Virus Structure  Icosahedral virus  Lipoprotein envelope, derived from the nuclear membrane  Genome: linear, ds DNA  Replicate in the nucleus

3 Herpes Virus Group  Includes: HSV-1, HSV-2, VZV CMVEBV CMV, EBV HHV-6 and others  Lytic and latent infections  Immortalizing effect (EBV)

4 EPSTEIN-BARR VIRUS

5 CD21)  EBV has a very limited host range and tissue tropism defined by the limited cellular expression of its receptor (CD21).  This receptor is expressed on B lymphocytes Epithelial cells of the oro – and nasopharynx

6 Diseases  Infectious Mononucleosis  African Burkitt’s Lymphoma  Nasopharyngeal Carcinoma  EBV-induced lymphoproliferative disease

7 EPIDEMIOLOGY  EBV is transmitted in saliva.  The immunosuppressive potential of malaria has been suggested as a cofactor in progression of latent EBV infection to African Burkitt’s lymphoma.  The restriction of nasopharyngeal carcinoma to certain regions of China has suggested a genetic predisposition.  Transplant patients, AIDS patients are at high risk for Lymphoproliferative disorders initiated by EBV.  B-lymphocytes transformation, by EBV does not need viral genome integration. (Episomal genome)

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9 EBV in saliva Epithelial cells of oropharynx B cells proliferation T cells activation Liver Lymph node Spleen Shedding in saliva Pharyngitis Heterophile antibodies Atypical lymphocytes swelling

10 THE LATENT CYCLE EB nuclear antigen 1 ((EBNA-1 Viral promoter (ori P) EBNA-2 B cell immortalization Monoclonal antibodies (Heterophile antibodies) Antibodies to EBNA persist for life. Antibodies to viral capsid antigen (VCA)appear during active disease. CD8+ T cells are activated against EBNA proteins Destroy infected B cells Atypical lymphocytes T cell immunodeficiencies B cell lymphoma

11 Infectious Mononucleosis CLINICAL FEATURES Infectious Mononucleosis (IM)  Fever, malaise, pharyngitis, lymphadenopathy, hepatosplenomegaly.  The disease is rarely fatal.  Heterophile antibody positive.  The classical lymphocytosis associated with IM is due to activation and proliferation of suppressor (CD8+) T cells. These cells appear as atypical lymphocytes (Downey cells).

12 EBV-induced lymphoproliferative disease  Individuals lacking T-cell immunity are likely to suffer polyclonal leukemia-like B-cell proliferative disease and lymphoma upon EBV infection.  Transplant patients are at high risk for post-transplant lymphoproliferative disorder (PTLD).

13 African (endemic) Burkitt’s lymphoma  Poorly differentiated monoclonal B- cell lymphoma  jaw and face  endemic to children of malarial regions of Africa.  The tumor cells contain chromosomal translocations that moves the C-myc oncogene to a very active promoter. (Immunoglobulin gene promoter)

14  Nasopharyngeal carcinoma The tumor is endemic to China The tumor is of epithelial origin.  Oral hairy leukeplakia Mouth lesions An opportunistic presentation in AIDS patients.

15 LABORATORY DIAGNOSIS  Atypical lymphocytes, lymphocytosis

16  Heterophile Antibody (Paul-Bunnell or Monospot Test) (Paul-Bunnell or Monospot Test) IgM antibody that recognizes the Paul-Bunnell antigen on sheep and bovine erythrocytes but not guinea pig kidney cells. It is an excellent indication of EBV infection in adults, not children.  Other Serological Tests IgM antibody to VCA, most specific test.  Treatment No vaccine available. Acyclovir is used in treating oral hairy leukoplakia.

17 CYTOMEGALOVIRUS

18 DISEASES  Cytomegalic inclusion disease  Heterophile negative mononucleosis  Diseases in the immunocompromised patients

19 PROPERTIES  Icosahedral virus  Lipoprotein envelope, derived from the nuclear membrane  Genome: linear, ds DNA  Replicate in the nucleus  Latent infections  Single serotype  Humans are the natural hosts  Giant cell formation (Cytomegalo)

20 TRANSMISSION  Oral (saliva) and respiratory routes  Transplacental, within the birth canal and in breast milk  Sexual (semen, cervical secretions)  Blood transfusion and organ transplantation  More the 80% of adults have antibody against this virus.

21 CLINICAL FORMS  Normal host Asymptomatic latent infection Infectious mononucleosis-like syndrome (Heterophile antibodies- negative).  Immunocompromized host (AIDS patients, those receiving organ transplants or chemotherapy) Pneumonia, hepatitis Severe diarrhea and retinitis in AIDS patients  Congenital infection in utero: Infection of the fetus occurs when a primary infection happens in a pregnant woman (no virus neutralizing antibodies) Abortion Stillbirth

22 Cytomegalic inclusion disease  Congenital abnormalities are more common when the fetus is infected during the first trimester of pregnancy.  Includes microcephaly, mental retardation, blindness or deafness.  Hepatosplenomegaly is very common.

23 LABORATORY DIAGNOSIS  Cell culture with the use of immunofluorescent antibody.  PCR-based assays. intranuclear and an oval “owl’s-eye” shape  Histological staining of inclusion bodies in giant cells: intranuclear and an oval “owl’s-eye” shape.  Rising IgG antibody titre or single IgM antibody test

24 TREATMENT  Ganciclovir is effective in the treatment of CMV retinitis and pneumonia in AIDS patients.  Fomiversin is antisense DNA approved for the intraocular treatment of CMV retinitis. It is the first antisense molecule to be approved for the treatment of human disease.

25 MUMPS VIRUS

26  VIRUS Paramyxovirus ssRNA, non- segmented genome Single serotype  TRANSMISSION Humans are the natural host Respiratory droplets Peak incidence in winter

27 PATHOGENESIS  URT Blood Parotid glands, testes, pancreas and meninges  Lifelong immunity occurs

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29 CLINICAL PICTURE  Incubation period: 18-21 days  Prodrome: fever, malaise and anorexia  Parotid gland swelling  Resolve spontaneously within 1 week  Complications  Orchitis bilateral sterility  Meningitis

30  LABORATORY DIAGNOSIS  Virus isolation from saliva, spinal fluid  Rising antibody titre  PREVENTION  Live attenuated vaccine  MMR (Measles, Mumps, Rubella)


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