viral infection

viral infection

1. human immunodeficiency virus (HIV)

   • Where did HIV come from
     • They believe that the chimpanzee version of the immunodeficiency virus (called simian immunodeficiency virus, or SIV) most likely was transmitted to humans and mutated into HIV when humans hunted these chimpanzees for meat and came into contact with their infected blood
   • Structure of HIV
   • RNA Virus with 2 identical strands of RNA (+) sense
     • Reverse transcriptase [RT]
   • Types of HIV Virus
     • HIV-1 and HIV-2
       • Morphologically they are similar but genetically they are different
       • The most common type is HIV-1 and cause worldwide AIDS epidemic
   • mechanism
     • Attachment of the virus to the host cells
       • HIV uses the CD4 molecule to attach to T cells
         • CD4 molecule is expressed at the cell surface of a subset of T cells (T-helper cells) but also on monocytes, macrophages, dendritic cells, and microglia
         • virus's gp120 molecules bind tightly to CD4 molecule(s) on the cell's surface
           • the fusion takes place under the influence of the viral gp41 molecule
       • Two Co-receptors
         • M-tropics virus binds to CD4 and CCR5 receptors
           • from M-tropic to T-tropic (X4) virus
             • the gp120 of T-tropic virus binds to CD4 and the CXCR4 chemokine receptor
   • When does HIV become AIDS?
     • CD4 count is 200 or less
       • HIV and the CD4 Count
         • As the amount of HIV in the body increases the amount of CD4 cells in the body decreases
     • the patients usually have multiple opportunistic infection and malignancies
   • The typical course of HIV infection can be described in three phases
     • Primary infection (1 to 3 months):
       • first peak in HIV RNA copies and a steep decline in CD4 cells in the blood
       • HIV can replicate without being controlled by the immune system. When the body's anti-HIV immune response begins (antibody responses begin to develop 4 to 8 weeks after infection), symptoms of seroconversion may develop and viral load falls
     • Clinical latency (on average 8-10 years, without antiretroviral treatment
       • After the acute infection phase, CD4 cell concentration in the peripheral blood increases again, although not as high as before infection. HIV RNA copy number in the plasma declines.
     • AIDS (on average 2-3 years, without antiretroviral treatment):
       • The third phase is characterized by a rapid increase in HIV RNA copies and a decline in CD4 cell counts in peripheral blood.
   • Laboratory Tests for HIV Infection
     • Testing for Viral Infection and Immune Response
       • Viral infection Viral Load p24 Antigen
       • Immune response Antibody (IgG, IgM) Cellular response (CD4)
     • ELISA - enzyme linked immunosorbent assay test (most common)
       • will fail to detect the infection in the initial 3-8 wks. of infection
       • detect antibodies to HIV in the blood, urine, or oral fluid
     • Confirmatory Tests for HIV Infection
       • Western Blot test
         • Immunofluorescent tests
         • Like ELISA it may not be positive in the initial 3-4 wks. of infection
       • RNA tests
         • PCR
         • Usually positive after 10 days of exposure Detect viral load – quantitation
   • Treatment
     • Recommendation: Combination therapy with 3 (or more) antiretroviral drugs
       • Entry/Fusion Inhibitors
         • Enfuvirtide: binds to gp 41, prevents its conformational change, and inhibits fusion of HIV-1 to CD4+ cells
         • Maraviroc blocks CCR5 co-receptor on T-cell surface to prevent viral entry
       • Reverse Transcriptase Inhibitors
         • Nucleoside and Nucleotide Reverse Transcriptase Inhibitors (NRTIs)
           • Zidovudine Lamivudine Abacavir Stavudine
         • Non-Nucleotide Reverse Transcriptase Inhibitors
           • Nevirapine Efavirenz Etavirine
       • Integrase Inhibitors
         • Raltegravir: It inhibits the final step in integration of strand transfer of the viral DNA into the host cell DNA.
       • Protease inhibitors
         • Saquinavir Indinavir Nelfinavir Ritonavir most effective drugs available
     • Highly Active Antiretroviral Therapy (HAART) prolongs life and improves quality of life
   • Transmission
     • ONLY through certain body fluids: Blood Semen Rectal Vaginal fluids Breast milk
     • HIV cannot survive outside of the body
   • Epidemiology
     • In 2017 an estimated 36.9 million people were living with HIV (including 1.8 million children) . Estimated 77.3 million people have become infected with HIV
   • preventions
     • Health education Safe sex “practices” - condom Clean needles – for IVDU Screening of blood & organ donors ARV prophylactic treatment of HIV-infected pregnant women
   • Psychological Aspect
     • Social Impact Increased dependence on unaffected individuals Increasing HIV-related stigma
     • Economic Economic decline Increased governmental expenditures
   • Signs and symptoms in all the stages of HIV
     • The early stage
       • Fever ,Chills, Rash, Night sweats, Muscle aches, Sore throa,t Fatigue ,Swollen lymph nodes, Mouth ulcers
     • late stage
       • Rapid weight loss. fever or night sweats. Tiredness. Prolonged swelling of the lymph glands. Diarrhea. Sores of the mouth. Pneumonia. blotches on or under the skin or inside the mouth, nose, or eyelids. neurologic disorders.
   • HIV/AIDS-related cancer
     • Kaposi sarcoma Non-Hodgkin lymphoma Cervical cancer
   • Opportunistic Infections
     • Many of these microbes don’t cause disease in a healthy host
     • Tuberculosis (TB). Hepatitis B and hepatitis C . Esophageal candidiasis. PCP. Toxoplasmosis .Cryptococcal meningitis
   • UAE laws and confidentiality
     • The list requires the authorities to isolate the infected person and to notify the health authorities immediately within 24 hours, when those specific authorities have suspected that any person or death has been infected with any of the communicable diseases listed in section (a) of Table 1 of the law. Complete all casualty data, injury and illness data, according to the reporting format.

2. structure of a virus

   • a viral particle is called a virion
   • each one is made up of
     • • Genetic material – either DNA or RNA • CAPSID – protective protein coat
     • some viruses have an additional coat ( envelope)
       • from host cell membrane [lipids+proteins and glycoproteins]

3. Enveloped viruses

   • properties - environmentally labile • Detergents • Drying • Heat
   • must stay wet – require body fluids cannot survive the gastrointestinal tract
   • spreads in secretions, organ transplants, and blood transfusions

4. Non enveloped viruses

   • outer layer of the virion is the capsid
     • CAPSID – protective protein coat
   • properties - environmentally stable
     • Temperature Detergents Drying
   • spread easily by dust, water, feco-oral routes
   • resistant to detergents and poor sewage treatment

5. Classification and Naming of Viruses

   • Various approaches, (do not obey the binomial nomenclature) derived from
     • Named after the diseases eg. Measles virus, smallpox virus
     • Name after the places where the disease first reported eg. Newcastle disease virus, Ebola virus, Norwalk virus, Bunyaviridae
     • Host and signs of disease eg. Tobacco mosaic virus, cauliflower mosaic virus brome mosaic virus
   • Baltimore Classification of viruses
     • The division of the viruses into classes based on genome type and mode of replication and transcription
   • DNA viruses associated with human disease are divided into seven families
   • The RNA viruses may be divided into at least 13 families

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