HIV Microbiology

  1. Which strain of HIV is found worldwide and which is found in West Africa?
    • HIV-1 worldwide (the one that we care more about)
    • HIV-2 West Africa
  2. Family and genus of HIV? Genome?
    • Retroviridae
    • Lentivirus genus
    • Single stranded RNA+ (positive polarity)
  3. T/F: HIV causes rapid infection and short incubation time
    False; HIV causes slow infections (Start with very mild symptoms) and has a long latent period, aka long incubation time before (if) it progresses to AIDS
  4. What are the receptor(s) that HIV bind to enter human cells?
    • CD4 T cell receptor
    • CCR5 receptor= to infect monocytes, macrophages and dendritic cells
    • CXCR 4 receptor = probably the same thing as above
  5. T/F: CD8 T cell is infected by HIV
    False; CD 4 T is
  6. Which enzyme does HIV utilize to convert its genome once inside human cell?
    Reverse transcriptase which makes double stranded DNA from RNA
  7. What is p24?
    • It is a nucleocapsid protein (gag protein), that protects viral RNA
    • It is also a marker for early infection detection (we have anti- p24 antibodies to look for them early on)
  8. What is the enzyme used to incorporate viral DNA into our genome?
    Viral integrase
  9. How does HIV enter human cells?
    Gp120 and gp41, both envelope glycoproteins, work together to get the virus to bind the host cell specific receptors (Gp120), and gp41 helps with fusion of HIV into human host cell.
  10. T/F: retrovirus envelope comes from host nuclear membrane
    False; these viral envelopes come from our cell membrane; envelope from host nuclear membrane is a unique property of herpeviridae family, i.e. EBV
  11. What are the three typical retrovirus genes?
    • Gag
    • Pol
    • Env
  12. What are proteins encoded by gag gene:
    P24 nucleocapsid and p17 matrix protein
  13. What are proteins encoded by pol gene?
    Protease, integrase, reverse transcriptase polymerase
  14. What are proteins encoded by env gene?
    Glycoprotein 120 and 41
  15. Which is the protein that gives stability to the virus?
    P17 matrix
  16. Which is the protein that is used as an early marker for HIV detection?
    P24 nucleocapsid
  17. Which protein cleaves viral polyproteins into their functional units after translation
    Protease
  18. Which genes are required for HIV replication?
    • Tat
    • Rev
  19. What is the tat gene?
    A required HIV replication gene for TRANSACTIVATING factor- aka production of virus
  20. What is the rev gene?
    A required HIV replication gene that regulates expression of Virion protein
  21. What is nef?
    • A notable accessory gene that is important in reducing host CD 8 cytotoxic T cell ability to attack the virus
    • Can also cause CD 8 death
  22. Which protein can induce CTL death and decrease CD4 proteins and class I MHC proteins on surface of the infected cells?
    Nef, a protein product of the accessory gene nef
  23. Which glycoprotein mutates rapidly causing antigenic variation so making it hard for our immune system to target and eradicate?
    Gp 120
  24. T/F: both gp 120 and P24 are proteins that mutate rapidly inducing antigenic shifts, thereby evading our immune attacks
    False; only true for gp120, p24 does not vary, and we use it as a diagnostic marker in early infection
  25. T/F: antibodies made against p24 nucleocapsid is important for our immune system to attack the virus
    False; these antibodies are not protective, they just serve as a serological marker
  26. Where does viral DNA replication occur in host cell?
    Nucleus
  27. T/F: people with mutations on the gene encoding CCR5 can be protected from HIV
    True
  28. How is HIV transmitted?
    • Sexual transmission is #1. Physical breach of epithelial barrier
    • They bind to dendritic cells/ macrophages and gets brought to the lymphoid tissue where they feast on all the CD4 T cells tehre
  29. What is a pro-virus?
    Virus where their RNA genome has been incorporated into our genome
  30. What role does our acting and tubulin play in RNA infection?
    These act like shuttle, basically helping viral genome to get incorporated into our nucleus
  31. What is the function of host cell RNA polymerase in viral infection?
    • Viral mRNA transcribed from the proviral DNA via host RNA polymerase
    • This process is augmented by virus Tat protein
  32. Gag and pol polyproteins are cleaved by _____, while env polyprotein is cleaved by ____.
    • Viral protease
    • Cellular protease
  33. T/F: like EBV, HIV can be transmitted via saliva and kissing
    False; HIV is only transmitted primarily through sexual contact, transfer of infected blood or perinatally
  34. T/F: the most common transmission of HIV worldwide is homosexual contact
    False; it is actually heterosexual worldwide, however, in the US, it is through homosexual contact
  35. T/F: HIV infection immediately presents with flu like symptoms upon transmission
    False; acute infection does not present until 2-4 weeks post-infections
  36. What are symptoms of acute HIV infection?
    • Flu like symptoms, fevers, headache, fatigue, lymphadenopathy in neck and groin
    • Some with maculopapular rash on trunk, arms and legs (no palms or soles)
  37. T/F: Acute HIV infections do not present with any hallmark symptoms, however in Chronic HIV infection, patient presents with hepatosplenomegaly and drenching night sweats
    False; there is little or no symptoms again in chronic HIV infections – latent period
  38. What is the CD 4 cell count that defines AIDS?
    CD 4 cells less than 200 is AIDS-defining
  39. AIDS patients are susceptible to which diseases?
    • pneumocytosis
    • Candidiasis
    • Mycobacteriosis
    • CMV retinitis
  40. T/F: HIV can infect brain monocytes and macrophages which can lead to multinucleated giant cell encephalitis
    True
  41. T/F: much like antibiotics use, only give one HIV drug at a time to treat so to prevent resistance
    False; because of HIV’s fast mutations, always give a cocktail treatment – the HAART (highly active antiretroviral therapy) or ART (antiretroviral therapy)
  42. How can HIV evade our immune system?
    • Antigenic variation
    • Hide in microglial cells and T cells
    • Removing MHC to avoid CD8 killing
    • Decrease NK cell ligands so NK can’t kill them either
    • Destroy CD 8, CD4, monocytes and macrophages
  43. What is confirmatory diagnosis of HIV?
    • HIV-1 nucleic acid test (RT-PCR)
    • Western Blot for HIV proteins
  44. At initial infection, what is the CD 4 level vs viral load
    • Initially, CD 4 is low and viral load is high
    • This is at around 4-8 week mark
  45. During latent period (could last 7-10 years or lifetime if on treatment), what is CD 4 vs viral load?
    • CD 4 remains high/ acceptable level
    • Viral load lower
  46. What is the acute HIV infection window period?
    Lag time between exposure to HIV and presence of detectable antibodies or viral RNA
  47. T/F: a newly infected HIV patient may have negative antibody test for p24 antigen and HIV antibody but could be positive for Viral RNA detection
    True; this HIV RNA can be detected the earliest at 10 days post infection
  48. What is the viral set point?
    • It predicts the progression of AIDS progression based on cytotoxic T cell response to virus months post infection and measuring HIV RNA level
    • The lower the set point, meaning CTL responds well to virus and been killing them, the slower the progression to AIDS and better prognosis
  49. What are some factors that can cause HIV to never progress into AIDS?
    • Mutated HIV-1 strains
    • Having genetic mutation that does not allow the virus to even bind to cells
    • Robust CD4 and CD 8 responses
  50. T/F: in chronic/latent HIV infection, p24 antibody level remains at relatively high in order to protect the virus capsid
    False; p24 goes away after the initial acute infection, will not be present at all in latent stage
  51. Levels of virus and viral load (RNA) are ____ in early infection, _____ for several years, and _____ during AIDS
    • High
    • Low
    • Rise
  52. As HIV slowly progresses into AIDS (in latent stage), CD4 counts starts to _____ and risk for opportunistic infections or malignancies ______
    • Decrease
    • Increase
  53. What is TH17?
    A subset of CD4+ T cell in the mucosa, HIV infection also targets these cells resulting in bacterial infection in mucous-lined area such as the colon
  54. When does our body start to make antibodies for HIV? When does a patient become seroconverted and show positive HIV antibodies
    • 2 weeks after infection (10-14 days)
    • 3 to 4 weeks to have seroconverted
  55. What to do if antibody test is negative but still suspect HIV in a patient who may have recently contracted the virus?
    PCR based assay for viral RNA in the plasma
  56. T/F: higher the set point at the end of the initial infection, the less likely the individual is to progress to symptomatic AIDS because this means the CD 8 T cells respond well
    False; if high set point, this means CD 8 T is not doing shit, and patient will have a fast progression and not good prognosis. You want low set point if you want the patient to live
  57. T/F: large amount of HIV is being produced by lymph node cells but remain within the lymph node during latent period, so the viral load remains low during this time
    True
  58. What is AIDS-related complex? When does it occur?
    • ARC can occur during the latent period with symptoms of persistent fevers, fatigue, weight loss and lymphadenopathy
    • Often progress to AIDS
  59. Common AIDS opportunistic infections:
    • Pneumocystic jiroveci (a fugnal infection)
    • Toxoplasma
    • Mycobacterium avium
    • Cytomegalovirus
  60. PCP can be prominent when CD4 is ______. Toxoplasma when CD 4 is ____. Mycobacterium avium and Cytomegalovirus when CD 4 is ______
    • Less than 200 (PCP)
    • < 100 (toxoplasma)- which is cat poop fungus
    • < 50 (Mycobacterium avium and CMV)
  61. Prophylaxis for common AIDS opportunistic infections: PCP, toxoplasma, mycobacterium avium and CMV?
    • PCP- TMP-SMX
    • Toxoplasma- TMP-SMX
    • M. avium- Azithromycin (macrolide) + ethanmbutol
    • CMV- ganciclovir
  62. What is Kaposi’s sarcoma?
    • Cancer from the lymph vessels
    • Caused by human herpesvirus 8 oncogene transmitted through saliva
  63. Clinical presentation of Kaposi sarcoma:
    Red, raised bumpy rash on legs, feet or face. Can also be in genital area, mouth or LN
  64. T/F: Over 35% of people with AIDS may get Kaposi sarcoma
    True. One of the AIDS defining illnesses
  65. T/F: Kaposi sarcoma is caused by a virus of the retroviridae family that is why it is so commonly seen in AIDS patients
    False; Kaposi is caused by Human Herpesvirus 8. This just happens simply because of AIDS patient being immunocompromised and susceptible to opportunistic infections
  66. How can PCP be diagnosed?
    A fungal infection via aerosol transmission seen often in AIDS patients (CD4 < 200). Dx’d: Sputum/lavage sample – PCR
  67. In very late stage of AIDS (CD4 < 50!), what infection may occur that otherwise never occurs with immunocompetent patients?
    Mycobacterium avium and M. intracellulare; through inhalation/ ingestion, most commonly affect lungs
  68. T/F: CD 4 is present on macrophage, monocytes, helper T cells and dendritic cells
    Yes
  69. What is the strongest indication of disease progression in AIDS?
    CD 4 T cells count
  70. What test is used to screen for HIV?
    ELISA to look for antibodies against viral proteins
  71. What are 3 mechanisms by which HIV-infected CD 4 T cells are lost?
    • HIV cytopathic effect
    • Apoptosis
    • HIV-specific CD 8 T cell killing
Author
lykthrnn
ID
348629
Card Set
HIV Microbiology
Description
HemeOnc Final
Updated