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    RNA Viruses

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    JaveriaZafar
    This document discusses RNA viruses. It begins by describing the diverse group of RNA viruses and their classification into 12 families. It then focuses on influenza viruses, describing the three types (A, B, C), with type A causing most infections. Key aspects of influenza viruses discussed include their ability to bind and enter host cells, replicate their segmented RNA genome, and bud off new virus particles. The document also describes antigenic drift and shift that allows influenza to evade host immunity. It provides details on influenza A, B, and C, and discusses diagnosis, treatment and prevention of influenza. The document concludes by briefly discussing other important RNA viruses such as paramyxoviruses, hepatitis C virus, rabies virus and HIV.

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    © All Rights Reserved
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    RNA Viruses

    Uploaded by

    JaveriaZafar
    131 views56 pages
    This document discusses RNA viruses. It begins by describing the diverse group of RNA viruses and their classification into 12 families. It then focuses on influenza viruses, describing the three types (A, B, C), with type A causing most infections. Key aspects of influenza viruses discussed include their ability to bind and enter host cells, replicate their segmented RNA genome, and bud off new virus particles. The document also describes antigenic drift and shift that allows influenza to evade host immunity. It provides details on influenza A, B, and C, and discusses diagnosis, treatment and prevention of influenza. The document concludes by briefly discussing other important RNA viruses such as paramyxoviruses, hepatitis C virus, rabies virus and HIV.

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    RNA viruses

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    This document discusses RNA viruses. It begins by describing the diverse group of RNA viruses and their classification into 12 families. It then focuses on influenza viruses, describing the three types (A, B, C), with type A causing most infections. Key aspects of influenza viruses discussed include their ability to bind and enter host cells, replicate their segmented RNA genome, and bud off new virus particles. The document also describes antigenic drift and shift that allows influenza to evade host immunity. It provides details on influenza A, B, and C, and discusses diagnosis, treatment and prevention of influenza. The document concludes by briefly discussing other important RNA viruses such as paramyxoviruses, hepatitis C virus, rabies virus and HIV.

    Copyright:

    © All Rights Reserved
    Download as PPT, PDF, TXT or read online from Scribd
    Download as ppt, pdf, or txt
    131 views56 pages

    RNA Viruses

    Uploaded by

    JaveriaZafar
    This document discusses RNA viruses. It begins by describing the diverse group of RNA viruses and their classification into 12 families. It then focuses on influenza viruses, describing the three types (A, B, C), with type A causing most infections. Key aspects of influenza viruses discussed include their ability to bind and enter host cells, replicate their segmented RNA genome, and bud off new virus particles. The document also describes antigenic drift and shift that allows influenza to evade host immunity. It provides details on influenza A, B, and C, and discusses diagnosis, treatment and prevention of influenza. The document concludes by briefly discussing other important RNA viruses such as paramyxoviruses, hepatitis C virus, rabies virus and HIV.

    Copyright:

    © All Rights Reserved
    Download as PPT, PDF, TXT or read online from Scribd
    Download as ppt, pdf, or txt
    of 56
    At a glance
    Powered by AI
    The key takeaways are that RNA viruses are a diverse group that infect humans and include influenza, HIV, hepatitis C, and SARS-CoV-2. They have enveloped or non-enveloped structures and can have segmented or non-segmented genomes.

    Influenza viruses cause infection by attaching to and multiplying in the cells of the respiratory tract. The viral RNA enters the nucleus where it is transcribed and translated. New viruses are then assembled and bud off the cell with an envelope.

    The main types of influenza viruses are A, B, and C. Type A causes most infections and can undergo antigenic shift. Type B only undergoes antigenic drift. Type C usually causes minor respiratory disease. Influenza A is also associated with seasonal epidemics and pandemics.

    RNA Viruses

    Diverse group of microbes


    Assigned to one of 12 families based on
    envelope, capsid, and nature of RNA
    genome

    Insert Table 25.1


    RNA viruses

    Enveloped Segmented
    Single-Stranded RNA Viruses

    The Biology of Orthomyxoviruses:


    Influenza
    3 distinct influenza virus types: A, B, C; Type
    A causes most infections
    Viral infection
    Virus attaches to, and multiplies in, the cells of the
    respiratory tract
    Segments of RNA genome enter the nucleus
    (transcribed/translated)
    Finished viruses are assembled and budded off the
    cell with an envelope
    4

    Influenza virus cycle

    Key to influenza are glycoprotein spikes


    Hemagglutinin (H) 15 different subtypes; most
    important virulence factor; binds to host cells
    Neuraminidase (N) 9 subtypes hydrolyzes
    mucus and assists viral budding and release

    Both glycoproteins frequently undergo genetic


    changes decreasing the effectiveness of the host
    immune response
    Constant mutation is called antigenic drift gradually
    change their amino acid composition
    Antigenic shift one of the genes or RNA strands is
    substituted with a gene or strand from another
    influenza virus from a different animal host
    Genome of virus consists of 10 genes encoded on 8 separate
    RNA strands

    Hemagglutinin (HA)

    Antigenic
    shift event

    10

    Influenza B
    Only undergo antigenic drift
    Not known to undergo antigenic shift
    Influenza C
    Known to cause only minor respiratory
    disease; probably not involved in epidemics

    11

    Influenza A
    Acute, highly contagious respiratory illness
    Seasonal, pandemics; among top 10 causes of death in
    U.S. most commonly among elderly and small
    children
    Binds to ciliated cells of respiratory mucosa
    Causes rapid shedding of cells, stripping the
    respiratory epithelium; severe inflammation
    Fever, headache, myalgia, pharyngeal pain, shortness
    of breath, coughing
    Weakened host defenses predispose patients to
    secondary bacterial infections, especially pneumonia
    12

    Diagnosis, Treatment, Prevention


    Rapid immunofluorescence tests to detect
    antigens in a pharyngeal specimen; serological
    testing to screen for antibody titer
    Treatment: control symptoms; amantadine,
    rimantadine, zanamivir (Relenza), and
    oseltamivir (Tamiflu)
    Flu virus has developed high rate of resistance
    to amantadine and rimantadine
    Annual trivalent vaccine recommended
    13

    Enveloped Nonsegmented ssRNA Viruses

    14

    Paramyxoviruses
    Paramyxoviruses (parainfluenza, mumps virus)
    Morbillivirus (measles virus)
    Pneumovirus (respiratory syncytia virus)
    Respiratory transmission
    Envelope has glycoprotein and F spikes that
    initiate cell-to-cell fusion
    Fusion with neighboring cells syncytium or
    multinucleate giant cells form
    15

    The effects of paramyxoviruses


    Insert figure 25.5
    Effects of paramyxoviruses

    16

    Parainfluenza

    Widespread as influenza but more benign


    Respiratory transmission
    Seen mostly in children
    Minor cold, bronchitis, bronchopneumonia,
    croup
    No specific treatment available; supportive
    therapy

    17

    Mumps
    Epidemic parotitis; self-limited, associated with painful
    swelling of parotid salivary glands
    Humans are the only reservoir
    40% of infections are subclinical; long-term immunity
    300 cases in U.S./year
    Incubation 2-3 weeks fever, muscle pain and malaise,
    classic swelling of one or both cheeks
    Usually uncomplicated invasion of other organs; in 2030% of infected adult males, epididymis and testes
    become infected; sterility is rare
    Symptomatic treatment
    Live attenuated vaccine MMR
    18

    Mumps

    19

    Measles

    Caused by Morbillivirus
    Also known as red measles and rubeola
    Different from German measles
    Very contagious; transmitted by respiratory aerosols
    Humans are the only reservoir
    Less than 100 cases/yr in U.S.; frequent cause of death
    worldwide
    Virus invades respiratory tract
    Sore throat, dry cough, headache, conjunctivitis,
    lymphadenitis, fever, Koplik spots oral lesions
    Exanthem
    20

    Signs and symptoms of measles

    21

    Measles
    Most serious complication is subacute sclerosing
    panencephalitis (SSPE), a progressive
    neurological degeneration of the cerebral cortex,
    white matter, and brain stem
    1 case in a million infections
    Involves a defective virus spreading through the brain
    by cell fusion and destroys cells
    Leads to coma and death in months or years

    Attenuated viral vaccine MMR

    22

    Rabies

    Rhabdovirus family; genus Lyssavirus


    Enveloped, bullet-shaped virions
    Slow, progressive zoonotic disease
    Primary reservoirs are wild mammals; it can be
    spread by both wild and domestic mammals by bites,
    scratches, and inhalation of droplets

    23

    Structure of the rabies virus


    Insert figure 25.8
    Structure of rabies virus

    24

    Rabies in the United States

    25

    Rabies
    Virus enters through bite, grows at trauma site for a
    week and multiplies, then enters nerve endings and
    advances toward the ganglia, spinal cord and brain
    Infection cycle completed when virus replicates in the
    salivary glands
    Clinical phases of rabies:
    Prodromal phase fever, nausea, vomiting, headache,
    fatigue; some experience pain, burning, tingling
    sensations at site of wound
    Furious phase agitation, disorientation, seizures,
    twitching, hydrophobia
    Dumb phase paralyzed, disoriented, stuporous
    Progress to coma phase, resulting in death
    26

    Pathologic pictures of rabies

    27

    Often diagnosed at autopsy intracellular inclusions


    (Negri bodies) in nervous tissue
    Bite from wild or stray animals demands assessment
    of the animal, meticulous wound care, and specific
    treatment
    Preventive therapy initiated if signs of rabies appear
    Treatment passive and active postexposure
    immunization
    Infuse the wound with human rabies immune globulin
    (HRIG) and globulin; vaccination with human diploid cell
    vaccine (HDCV), an inactivated vaccine given in 6 doses
    with 2 boosters

    Control vaccination of domestic animals,


    elimination of strays, and strict quarantine practices
    Live oral vaccine incorporated into bait for wild animals
    28

    Hepatitis C Virus (HCV)


    Flavivirus
    Acquired through blood contact blood transfusions,
    needle sharing by drug abusers
    Infections with varying characteristics 75-85% will
    remain infected indefinitely; possible to have severe
    symptoms without permanent liver damage; more
    common to have chronic liver disease, without overt
    symptoms
    Cancer may also result from chronic HCV infection
    Treatment with interferon and ribavirin to lessen liver
    damage; no cure
    No vaccine
    29

    Hemorrhagic Fevers
    Yellow fever eliminated in U.S.
    Two patterns of transmission:
    Urban cycle humans and mosquitoes, Aedes aegypti
    Sylvan cycle forest monkeys and mosquitoes; South
    America

    Acute fever, headache, muscle pain; may progress to


    oral hemorrhage, nosebleed, vomiting, jaundice, and
    liver and kidney damage; significant mortality rate
    Dengue fever flavivirus carried by Aedes mosquito; not
    in U.S.; usually mild infection
    Dengue hemorrhagic shock syndrome, breakbone fever
    extreme muscle and joint pain; can be fatal
    30

    HIV Infections and AIDS

    Human immunodeficiency virus


    Acquired immunodeficiency syndrome
    First emerged in early 1980s
    HIV-1 may have originated from a
    chimpanzee virus
    1959 first documented case of AIDS

    31

    Causative Agent
    Retrovirus, genus Lentivirus
    Encode reverse transcriptase enzyme which makes a
    double stranded DNA from the single-stranded RNA
    genome
    Viral genes permanently integrated into host DNA
    Human Immunodeficiency Virus (HIV) the cause of
    Acquired Immunodeficiency Syndrome (AIDS)
    HIV-1 and HIV-2
    T-cell lymphotropic viruses I and II leukemia and
    lymphoma
    HIV can only infect host cells that have the required CD4
    marker plus a coreceptor
    32

    The general
    structure of
    HIV

    Insert figure 25.13


    HIV general structure

    33

    Epidemiology of HIV Infections


    Transmission occurs by direct and specific
    routes: mainly through sexual intercourse and
    transfer of blood or blood products; babies
    can be infected before or during birth, and
    from breast feeding
    HIV does not survive long outside of the
    body

    34

    Infection by HIV

    35

    First nationally notifiable in 1984


    6th most common cause of death among people aged
    25-44 years in the U.S.
    Men account for 70% of new infections
    Anal sex provides an entrance for the virus
    IV drug abusers can be HIV carriers; significant
    factor in spread to heterosexual population
    In 2006, the number of infected individuals
    worldwide is estimated to be 33 million with ~1
    million in the U.S.
    36

    Patterns of
    HIV infection

    Insert figure 25.15


    Patterns of HIV infections

    37

    Pathogenesis and
    Virulence Factors of HIV

    HIV enters through mucous membrane or skin and


    travels to dendritic phagocytes beneath the
    epithelium, multiplies, and is shed
    Virus is taken up and amplified by macrophages in
    the skin, lymph organs, bone marrow, and blood
    HIV attaches to CD4 and coreceptor; HIV fuses
    with cell membrane
    Reverse transcriptase makes a DNA copy of RNA
    Viral DNA is integrated into host chromosome
    Can produce a lytic infection or remain latent
    38

    Multiplication cycle of HIV

    39

    Primary effects of HIV infection:


    Extreme leukopenia lymphocytes in particular
    Formation of giant T cells and other syncytia
    allowing the virus to spread directly from cell to
    cell
    Infected macrophages release the virus in central
    nervous system, with toxic effect, inflammation

    Secondary effects of HIV:


    Destruction on CD4 lymphocytes allows for
    opportunistic infections and malignancies
    40

    Signs and Symptoms of


    HIV Infections and AIDS
    Symptoms of HIV are directly related to viral blood
    level and level of T cells
    Initial infection mononucleosis-like symptoms that
    soon disappear
    Asymptomatic phase 2-15 years (avg. 10)
    HIV destroys the immune system
    When T4 cell levels fall below 200/L, AIDS
    symptoms appear including fever, swollen lymph
    nodes, diarrhea, weight loss, neurological symptoms,
    opportunistic infections, and cancers
    41

    Timeline in HIV infection

    42

    Changes in virus, antibody levels, and T cells

    43

    Diagnosis of HIV Infection


    Testing based on detection of antibodies specific to
    the virus in serum or other fluids; done at 2 levels
    Initial screening
    ELISA, latex agglutination, and rapid antibody tests
    Rapid results but may result in false positives

    Follow up with Western blot analysis to rule out false


    positives
    False negatives can also occur; persons who may have
    been exposed should be tested a second time 3-6
    months later
    44

    Diagnosis of AIDS is made when a person meets the


    criteria:
    1. Positive for the virus, and
    2. They fulfill one of the additional criteria:

    They have a CD4 count of fewer than 200 cells/ml of


    blood
    Their CD4 cells account for fewer than 14% of all
    lymphocytes
    They experience one or more of a CDC-provided list
    of AIDS-defining illnesses

    45

    Insert Table 25.A page 776


    AIDS-defining illnesses

    46

    Preventing and Treating HIV


    No vaccine available
    Monogamous sexual relationships
    Condoms
    Universal precautions

    No cure; therapies slow down the progress of the


    disease or diminish the symptoms
    Inhibit viral enzymes: reverse transcriptase, protease,
    integrase
    Inhibit fusion
    Inhibit viral integration
    Highly active anti-retroviral therapy
    47

    Mechanisms of action of anti-HIV drugs

    48

    Nonenveloped Nonsegmented ssRNA


    Viruses: Picornaviruses and Caliciviruses
    Picornaviruses
    Enterovirus poliovirus, HAV
    Rhinovirus rhinovirus
    Cardiovirus infects heart and brain

    49

    Hepatitis A Virus and Infectious Hepatitis


    Cubical picornavirus relatively resistant to heat
    and acid
    Not carried chronically, principal reservoirs are
    asymptomatic, short-term carriers or people
    with clinical disease
    Fecal-oral transmission; multiplies in small
    intestine and enters the blood and is carried to
    the liver
    Most infections subclinical or vague, flu-like
    symptoms occur; jaundice is seldom present
    50

    No specific treatment once the symptoms


    begin
    Inactivated viral vaccine
    Attenuated viral vaccine
    Pooled immune serum globulin for those
    entering into endemic areas

    51

    Nonenveloped Segmented
    dsRNA Viruses: Reoviruses
    Unusual double-stranded RNA genome
    Two best known:
    Rotavirus oral-fecal transmission; primary
    viral cause of mortality and morbidity resulting
    from diarrhea in infants and children
    Treatment with rehydration and electrolyte
    replacement

    Reovirus cold-like upper respiratory infection,


    enteritis
    52

    Prions and Spongiform Encephalopathies


    Prions proteinaceous infectious particles; highly
    resistant to chemicals, radiation, and heat
    Cause transmissible spongiform
    encephalopathies (TSEs) in humans and
    animals
    Neurodegenerative diseases with long incubation
    periods

    53

    Human TSE:
    Creutzfeldt-Jakob Disease (CJD)
    alteration in the structure of normal PrP
    protein found in the brain
    Abnormal PrP converts normal PrP into
    abnormal form

    Abnormal PrP results in nerve cell death,


    spongiform damage, and severe loss of
    brain function
    Transmission is through direct or indirect
    contact with infected brain tissue or CSF
    54

    Variant CJD became apparent in the late


    1990s after eating meat from cattle afflicted
    with bovine spongiform encephalopathy
    Difficult to diagnose; requires examination of
    biopsied brain or nervous tissue
    Prevention relies on avoidance of
    contaminated tissue
    Treatment focuses on easing symptoms

    55

    The microscopic effects of


    spongiform encephalopathy

    56

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