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Najran University College of Applied Medical Sciences

Najran University College of Applied Medical Sciences. Retroviruses BY Dr. Ahmed Morad Asaad Associate Professor of Microbiology Coordinator of Applied Medical Sciences College. Retroviruses RNA viruses that contain reverse transcriptase enzyme and replicate in an unique manner

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Najran University College of Applied Medical Sciences

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  1. Najran UniversityCollege of Applied Medical Sciences Retroviruses BY Dr. Ahmed MoradAsaad Associate Professor of Microbiology Coordinator of Applied Medical Sciences College

  2. Retroviruses • RNA viruses that contain reverse transcriptase enzyme and replicate in an unique manner • Human retroviruses are found in 2 sub-families: • Oncovirinae: RNA tumour viruses including • Human T-cell lymphotropicvirus I (HTLV-I) and other 2 viruses of unknown importance HTLV-II and HTLV-IV • Lentivirinae: RNA viruses causing chronic infections including: • Human immunodifficiencyvirus (HIV) previously called HTLV-III. It is cytolytic and non-transforming

  3. Human immunodifficiency virus (HIV) • A non-oncogenic retrovirus and a member of of the lentivirinae subfamily • The aetiological agent of acquired immunodefficiencysyndrome (AIDS) • First described in 1981. Originated in central Africa. Monkeys may originally harbored the virus • Infected individuals may remain asymptomatic for several years • The carriers develop fatal illness after several years

  4. Structure of HIV particle • The virion is a spherical particle 100 – 140 nm with a cylindrical core containing diploid ss RNA genome and reverse transcriptase enzyme

  5. There is an outer glycoprotein envelope, which undergoes antigenic variations: • Viral core proteins: p15, p17, p24 and p55 • Envelope glycoproteins:gp41, gp120 and gp160 • Reverse transcriptase proteins: p3 and p66 • Two types of the virus are known: HIV-1 and HIV-2 (more in west Africa and less virulent) • They differ in the envelope

  6. Disinfection and inactivation • HIV is inactivated by treatment for 10 minutes with 10% household bleach, 50% ethanol, 0.5% lysol or 0.3 H2O2 • Also inactivated by extremes of pH • The virus is protected in lypholized blood products and heating at 68ºC for 72 hours is needed for complete inactivation

  7. Pathogenesis • HIV attacks T4helper cells • CD4 molecules are the receptors for viral glycoproteins (attachment site) • Infected T4 cells express high levels of HIV envelop glycoproteins leading to fusion with neighboring uninfected T4 cells • This leads to lysis of large numbers of fused T4 cells and marked supression of the immune response • The virus remains latent in lymphocytes and monocytes • Clinical diseases may appear 7 years after infection due to virus activation from: • Concomitant virus infection by EBV, HSV, HBV or CMV

  8. Death of T helper cells is attributed to: 1- Cytocidal effects of HIV 2- Fusion of infected and non-infected cells 3- The immunologic attack by T cytotoxic cells 4- HIV acts as a superantigen with release of cytokines

  9. Mode of transmission • Sexual contact • *- Homo and hetero sexual are at high risk • *- HIV is prsent in serum • Parenteral • *- Transfusion of infected blood or blood products • *- Drug abusers and haemodialysis patients are at high risk • Vertical (mother to fetus) • *- Transplacental • *- To newborn during labour • - Saliva – insect bites are non-infectious

  10. Clinical manifestations • IP varies from 6 months to 7 years • Infected neonates develop symptoms after 2 years • AIDS related complex (ARC) may proceed AIDS, characterized by fatigue, wasting, fever, chronic diarrhea, oral candidiasis and persistent lymphadenopathy • In full-blown picture, AIDS manifestations are: • 1- Infection with opportunistic organisms: • *- Protozoa (Toxoplasmagondii) • *- Fungi (Candida albicans, Pneumocystitiscarinii • *- Bacteria (M. tuberculosis, M. avium, L. monocytogenes)

  11. 2- Malignancies: Kaposi’s sarcoma and malignant lymphoma 3- Neuralgic manifestations: subacute encephalitis, encephalopathy, dementia and peripheral neuropathy

  12. Laboratory diagnosis • Detection of anti HIV Abs by ELISA: • Positive results should be confirmed by Western blot to detect Abs to viral core proteins (P24) and envelop glycoproteins (gp41, gp120 or gp160). • Detection of HIV antigens by ELISA: • Circulating HIV-1 p24 antigen soon after infection. Reappear in late stage of infection (poor prognosis) • Detection of viral nucleic acids • RT-PCR to detect viral RNA in clinical specimens • Plasma viral load determination by quantitative RT-PCR • Important predictive marker for disease progression and efficiency of antiviral therapies

  13. Laboratory diagnosis • Detection of viral RT activity • Virus isolation: • By viral culture from clinical specimens. Available only in few medical centers • Early diagnosis of HIV infection in infants • By using HIV-1 RNA tests

  14. Treatment • Using 2 nucleoside inhibitors • *- Zidovudine and Lamivudine • *- This combination is known as HAART (Highly active antiretroviral therapy) • *- Effective in reducing viral load but not curative • Prevention and control • HIV vaccines (Under trial) • *- Envelop glycoproteins by recombinant techniques • *- Soluble CD4 by recombinant techniques

  15. Control measures • *- Screening of donors for HIV Abs • *- Sex education • *- Use of disposable syringes • *- Care in handling blood and tissue specimens

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