Beta & gamma herpesvirinae


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Beta & gamma herpesvirinae

  1. 1. Betaherpesvirinae (Cytomegalovirus) GIANE CARLA BUMAGAT
  2. 2. Betaherpesvirinae Virus classification Group: GroupI (dsDNA) Order: Herpesvirales Family: Herpesviridae Subfamily: Betaherpesvirinae Genera: Cytomegalovirus Muromegalovirus Proboscivirus Roseolovirus
  3. 3. Betaherpesvirinae GENOME STRUCTURE Enveloped Spherical to Pleomorphic 150-200 nm in diameter, Icosahedral symmetry Capsid consists of 162 capsomers and is surrounded by an amorphous tegument. o Glycoproteins complexes are embeded in the lipid envelope. o o o o o o Monopartite o Linear o dsDNA genome of 140-240 kb. (The genome contains terminal and internal reiterated sequences.)
  4. 4. Cytomegalovirus (CMV) - From - - - the Greek cyto-"cell" & megalo-"large“ Human cytomegalovirus alternatively known as Human herpesvirus 5 (HHV-5) Largest genetic content of Herpesvirus. “Oldest” type of herpesvirus in evolutionary terms. Very specific species & Cell-type specific. CMV is detected in histopathological sections by visualization of owl's eye inclusion bodies.
  5. 5. Cytomegalovirus (CMV) SPECIES o Type: - Human cytomegalovirus (HHV5) o Main: - Cercopithecine herpesvirus 5 (CeHV-5) - Cercopithecine herpesvirus 8 (CeHV-8) - Pongine herpesvirus 4 (PoHV-4)
  6. 6. Cytomegalovirus (CMV) CELL TROPISM HHV-5 - Mucosal epithelium of the genitourinary tract - Upper alimentary tract, or respiratory tract is the primary site of infection. - Followed by a leukocyteassociated viremia - Wide range of infected tissues Latency: remains latent in lineage-committed myeloid cells IN VITRO: - Human fibroblast cells are required for isolation of the virus in vitro. IN VIVO: - Salivary Glands - Kidneys - Respiratory tract - Other epithelial (endothelial) sites
  7. 7. Transmission - Humans are the only reservoir for human CMV and transmission occurs by person to person contact. - CMV is very labile and close or intimate contact is necessary for spread of infection - Sources of infection include oropharyngeal secretions, urine, cervical and vaginal secretions, breast milk, tears, feces and blood.
  8. 8. Epidemiology - Acquire by 40-60% of persons by mid-adult life - >90% Multiple intimate exposure - <5% Whole blood seropositive donors - 80% Kidneys transplant
  9. 9. Pathogenesis INFECTION  Virus shed in: - - Body secretion Urine Semen Breast milk Cervical fluid  Mononuclear cells carry the latent virus genome & viral RNA transcript.  Bone Marrow- Prime sit of the latency  Macrophage can enter the replication cycle.  Reactivation- Endogenous  Re-infection- Exogenous  Endothelial cells (Multinucleate cells) found in the circulation during disseminate CMV infection. These cells are fully permissive for CMV replication
  10. 10. Intra-uterine infection  Maternal viraemia may result fetal infection.  Acquired in utero when mother suffers in CMV reactivation (rare).  Transplacental infection carried by infected cells & transmission associated with a high viraemic load.  Cause damage to target cells.
  11. 11. Perinatal & Postnatal Infection Perinatal infection  Acquired from infected maternal genital tract secretion or breastfeeding. Postnatal infection  Acquired by: - Saliva - Semen - Whole blood transfusion - Organ transplant  All CMV IgG antibody positive (“Seropositive”) cells
  12. 12. Clinical features CMV CONGENITAL CMV INFECTION o Asymptomatic at birth o May show sensorineural deafness or intellectural impairment. o Cyromegalic inclusion disease: - - Intrauterine growth retardation Hepatosplenomegaly Jaundice Thrombocytopenia CNS-CMV: Microcephaly - Encephalitis - Choriorentinitis Myocarditis Peunomonitis MONONUCLEOSIS o Respiratory tract infect is common in o o o o infancy. Mononucleosis syndromereminiscent of symptomatic primary EBV infection. Hepatitis Fever Atypical lymphocytosis
  13. 13. Clinical features CMV IMMUNOCOMPROMISED PATIENT o Dissemination of the virus in blood indicate: Hectic fever & bad prognostic sign o Cellular immunodeficiency: - Pneumonitis Encephalitis Retinitis Oseophagitis/ Colitis Pancreatitis/ Adrenalitis o AIDS: - Retinitis o Transplant recipient:  Direct- caused by virus  Indirectcause by interaction w/ immune system o Transplant protocol: - Prophylaxis - Pre-emptive treatment
  14. 14. Laboratory Diagnosis  Specimen of choice: - Urine - Saliva - Broncho-alveolar lavage fluid - Biopsy tissue - Blood (EDTA)  PCR Assay
  15. 15. Treatment & Control TREATMENT CONTROL  Ganciclovir  Screening of organ  Foscarnent donors & recipients  Blood donor screening  NO VACCINE
  16. 16. Gammaherpesvirinae (Epstein – Barr Virus) SIDOCON, ERISIA SHOROUK A. BMLS-3A
  17. 17. Epstein – Barr Virus (EBV)  Family: Herpesviridae  Subfamily: Gammaherpesvirinae  ds DNA; enveloped; icosahedral  First isolated from malignant Burkitt’s lyphoma cell
  18. 18. Epidemiology  Developing countries  Early adulthood  Incubation period: 1-2mos.  MOT:  oral route  sexual transmission  blood transfusion  organ transplantation
  19. 19. Infectious Mononucleosis          Kissing disease 15-24 years of age Diagnosis: hematology and serological test Accompanied by the production of heterophile agglutinins that can be detected by a rapid slide agglutination test (Paul Bunnell test). Differential WBC count: >50% atypical lymphocytes Presence of heterophile antibodies-Ha test Monospot test Culture from saliva or throat washings PCR
  20. 20. Infectious Mononucleosis  Symptoms    Sore throat with pus Marked fatigue Enlarged spleen & lymph nodes  Prevention & Treatment    Avoiding the saliva of another person No vaccine acyclovir
  21. 21. Burkitt’s Lymphoma  Children in East Africa and New Guinea  Cancer starts in B cells  Fastest growing human tumor  Patients: elevated titers of EBV antibodies
  22. 22. EBV TREATMENT  Adoptive humoral immunotherapy  EFFECTIVE AGAINST EBV-ASSTD B CELL TUMORS(PTLD)  Adoptive cellular immunotherapy  Effective to individuals does not respond to any Tx for PTLD CONTROL  Subunit vaccines  Screening for IgA Ab to EBV VCA