Microbio FINAL: Herpes & HIV/AIDS

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  1. HERPES Virus Info:
    --> features
    --> Latency in sensory nerve ganglia
    • -->Virion features
    • • Linear dsDNA genome: different from previous viruses
    • • Very large genome
    • • Icosahedral capsid 20 small triangles
    • • Envelope with glycoproteins (sugars + protein)

    -->Who gets infected?  Humans, Primates, Reptiles, Elephants, etc.

    --> Common feature of herpes viruses: Ability to establish latency as closed circular DNA; dna can sit in infected cell and wait

    • -->Latency in sensory nerve ganglia
    • • HSV-1
    • • HSV-2
    • • Varicella zoster virus (VZV)
  2. Herpes simplex viruses: HSV-1 and HSV-2
    • • HSV-1 causes cold sores
    • • HSV-2 causes genital herpes
    • • These can infect other sites•
    • Transmission by contact with sores or intact skin
    • • Blisters break open; Painful; initial outbreak  will subside but then virus will come back and cause another outbreak(latency);Herpes virus never completely leaves
    • •12 Treatments (not cures): Acyclovir, valacyclovir
  3. Varicella zoster virus (VZV) (Herpes Family)
    -initial and then reactivated disease?
    • -->Chickenpox rash (initial infection) and then shingles-reactivated
    • 1. chickenpox: Transmitted by respiratory secretions; Contagious; Rash; Vaccines availabe
    • 2. shingles: Reactivated VZV; Painful; Rash typically on one side of trunk

    -12 Treatments (not cures): Acyclovir, valacyclovir-shorten healing time & used for all 3 viruses (HSV-1, HSV-2, VZV)
  4. Epstein-Barr virus (EBV) (Herpes Family)
    -Mono treatment
    -"Burkitt's lymphoma"
    • -Infects B cells & Causes mononucleosis (kissing disease)
    • a) transmisson: Saliva transmission ( also fomites)
    • b) symptoms: persistent fatigue, swollen lymph nodes, enlarged spleen,fever, sore throat
    • C) Treatment for mononucleosis: Rest, Recovery in weeks or months
    • --> Epstein Barr virus in Africa: causes different disease--Burkitt’s lymphoma is a B cell cancer (deadly)
  5. Human Herpes Virus 8 (HHV8):
    Associated with Kaposi’s sarcoma ( a oppurtunistic cancer) in HIV+ patients
  6. CMV (Cytomegalovirus) (Herpes Family)
    -common age
    -complication with babies and HIV?
    • - Majority of adults in U.S. have virus by age 40
    • -Most people have no symptoms; establishes latency
    • -->• Possible signs and symptoms: fever, sore throat, fatigue, swollen glands

    • -->CMV transmission
    • Most bodily fluids including: saliva, urine, tears, breastmilk and blood & Also sexually transmitted

    -->CMV disease in babies: CMV passed to fetus from mother;  1 out of 5 children with CMV have severe developmental disabilities

    --> HIV patients can become blind
  7. AIDS  & HIV Discovery
    • Discovery of AIDS: First noticed by doctors (strange group of disease) in Los Angeles, San Francisco, and New York City in late 1970’s and early 1980’s; Young adult gay men had:
    • • Kaposi’s sarcoma, a rare cancer (HHV8)
    • • Pneumocytsis pneumonia, a rare fungal pneumonia
    • • Thrush: in the mouth (Candida albicans yeast infection)
    • • Other opportunistic infections...CMV blindness, HPV2 break outs, weightloss...

    --> Discovery of HIV (Human Immunodeficiency Virus):Virus was isolated in 1983; 2 separate discoveries: one in france (nobel prize) and another in San Francisco
  8. HIV Virus Family & subgroups
    • -->Part of Retrovirus family; has two subgroups
    • 1) Lentiviruses: includes Semi Immunodeficiency Virus (SIV)-affects some primates, FIV, HIV

    • 2) Oncoviruses: includes viruses that can cause cancer
    • ex: Rous sarcoma virus (cancer in chickens)
  9. HIV Structure & Mode of Infection:
    -infects what two cells
    -two glycoproteins
    -What part of the cell is used for attachment and entry?
    • HIV structure:  
    • -enveloped with gp 120 & gp 41-
    • -core with 2 copies of ssRNA (diploid) & Reverse Transcriptase enzyme

    -HIV infects CD4+ T cells/T Helper Cells ("boss" wbc's) and Macrophage ("scavenger" wbc's); both cells are infected by HIV

    • -Two glycoproteins: gp 120 (attachment onto host cell) and gp41 (Fusion & entry into host cell)
    • -What part of the cell is used for attachment and entry?
    • • Macrophage - has CD4 and CCR5 (chemokine receptor)
    • • T helper cell - has CD4 and CXCR4 (chemokine receptor)
  10. HIV Virus Life Cycle:
    -3 enzymes
    1. Attachment: HIV binds using gp120 that attaches CD4 & CCR5 on the T Helper cell. 

    2. Fusion: Uses gp41 and entry into Host cell

    3. Viral RNA is now sitting is host cytoplasm, gets copied by Reverse Transcription enzyme and makes DNA copy from the RNA (opposite of transcription) to eventually make dsDNA (ProViral DNA)

    4. Integration: Proviral dna ends up in nucleus; Integrase enzyme intergrates proviral dna into chromosome (explains why virus is hard to remove)

    5. Biosynthesis: making more RNA/viral proteins, RT enzymes to make more virions

    6. Protease: enzyme that cuts polyproteins (three proteins in a row)

    7. Assembly

    8. Release of virions
  11. HIV Transmission
    --> Modes of Transmisson
    -> Prevent Transmission
    • MODES:
    • 1.Sexual transmission, including:men who have sex with men, heterosexual sex
    • 2. Contact with infected blood: intravenous drug use of any kind. blood transfusion of infected, untested blood, and health care worker risk
    • 3. Mother-to-child transmission: before or during birth, breastmilk
    • **note: NOT transmitted by mosquitoes, casual contact, air, water. (One case of transmission from professional dentist to 6 patients)

    • -->Preventing Transmission
    • • Abstinence
    • • Screening partners before sexual activity
    • • “Safer” sex - use condoms
    • • Monogamy or fewer sex partners
    • • Getting tested - get prompt treatment, don’t spread disease
    • • Health care workers - gloves, proper protocol
    • • Clean needles: not available in third world countries
    • • HIV infected mothers- getting treatment
  12. Testing: What does it mean to be HIV positive?
    • • Blood or sometimes oral fluid is tested for antibodies against HIV proteins; response against the virus
    • • Someone who has antibodies against HIV is considered HIV positive.
    • • It can take up to 3months for antibodies to be detectable; vary by person and diagnostic test.
  13. Detecting HIV infection
    • ELISA to detect anti-HIV antibodies; can also test for antigens;
    • • Western Blot to detect anti-HIV antibodies; tells you about WHICH antibodies are there; backs up the Elisa if positive
    • • Less common: detect viral antigens or nucleic acid/viral RNA; detecting for the virus itself.
    • • New test: Oraquick test on oral fluid- takes; 20 minutes to get results
  14. HIV infection and AIDS
    • 1. Acute illness - flulike symptoms
    • 2. Asymptomatic
    • 3. Development of symptoms and Progression to AIDS (opportunistic infections, CD4 T cell count below 200 per μl, TB, etc.)
    • • May take up to about 10 years for development of severe AIDS disease if person is not treated.
  15. seroconversion:
    change in antibody status; so you had antibodies against something and now you don't, or vice versa; going from HIV- to HIV+; RH
  16. Antiretroviral drugs:
    1. Nucleoside analog RT inhibitor:
    2. Non-Nucleoside RT inhibitors:
    3. other drugs...
    • how do they work:
    • • Block action of viral proteins; like enzyme inhibitors (enzymees are proteins)
    • • Reverse transcriptase inhibitors
    • DRUGS:

    1. Nucleoside analog RT inhibitor: nucleotide before the phosphate is added to it; "fake nucleotide", looks like a normal nucelotide but it's not, it's a terminator rather than ATGC, stop RT from making viral RNA when the RT runs into this fake nucleotide terminator    ex: zidovudine (AZT) first drug used in 1980’s; strict regimen

    2. Non-Nucleoside RT inhibitors: act like allosteric inhibitors; Ex: Nevirapine: shown to stop transmission of HIV from preggie mom to child

    3. More antiretroviral drugs:(targets) Protease Inhibitors, Fusion inhibitors-gp41, Integrase inhibitors: inhibits proviral dna integrated into chromosome, CCR5 inhibitor: unusual b/c it blocks OUR proteins that HIV uses to get into host cells- new in 2007
  17. HAART
    • • Highly active anti-retroviral therapy; triple drug threrapy to avoid resistance
    • • Use a combination of several antiretrovirals at the same time ( e.g. 2 RT inhibitors and a protease inhibitor)
Card Set:
Microbio FINAL: Herpes & HIV/AIDS
2013-05-27 06:00:48

05.14: Herpes (ppt) --(✔)-- 05.14: HIV & AIDs (ppt) --(✔)--
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