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viral infection of blood cells Flashcards

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Biology 101 flashcards
1
Q

list Viruses infecting white blood cells

A
  1. Human Immune deficiency virus (HIV)
  2. Human Lymphotropic virus (HTLV)
  3. Cytomegalovirus (CMV)
  4. Epstein Barr virus (EBV)
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2
Q

what’s Human Immune Deficiency Virus (HIV )?

A
  • Non oncogenic retrovirus that causes AIDS
  • Kills cells with CD4 protein on their surface (T-helper lymphocytes, MQ & monocytes):
    1. Loss CMI
    2. Develop opportunistic infection
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3
Q

illustrate structure of HIV

A
  1. capsid : cone shape
  2. genome : 2 identical RNA copies
  3. internal protein
  4. surface (envelope) glycoproteins:
    GP120 : major Ag on surface
    GP41
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4
Q

illustrate internal protein of HIV

A
  1. three enzyme :
    integration & replication
    - reverse transcriptase
    - protease
    -integrase
  2. core proteins :
    P24
    -most abundant core protein
    - detect during early infection
    - indicate viral replication
  3. other proteins :
    - enhance gene transcription
    - dec MHC class I expression
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5
Q

list steps of pathogenesis

A
  1. cell tropism
  2. attachment & entry into CD4
  3. transcription & translation
  4. assembly
  5. release
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6
Q

illustrate cell tropism in HIV pathogenesis

A
  • CD4 Th cells are the 1ry target of HIV
  • certain subsets of monocytes & MQ express CD4 molecules
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7
Q

illustrate attachment & entry into CD4 in HIV pathogenesis

A
  1. GP120 binds to CD4 molecules on target cell
  2. exposuer for binding site to coreceptor (chemokine) receptor CXCR4 on Th or CCR5 on MQ
  3. exposure of fusogenic GP41 = fusion of viral envelope with target cell membrane lead to entry of virus content & infection
  4. Abs against GP120 neutralize the virus cause rapid mutation in env gene lead to GP120 antigenic variant =
    - escape from immunity
    - difficulty in vaccine development
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8
Q

illustrate transcription & translation in HIV pathogenesis

A
  • reverse transcriptase converts RNA into Ds DNA which is transported to nucleus
  • integrase inserts Ds DNA into host chromosome
    (HIV DNA integrated into DNA of the cell is called provirus)
  • host cell polymerase transcribes viral genes into viral mRNA than translation into viral proteins & replication of viral genome
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9
Q
  • assembly take place at the ……….. = immature version
  • illustrate how the maturation happen
A
  • membrane of the host cell
  • HIV protease processes capsid polyproteins leading to maturation & production to the infectious virus
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10
Q
  • release by ………..through the cell membrane leading to …………..
A
  • budding
  • infection of new target cells
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11
Q

illustrate Fate of infected cells

A
  • HIV destroys CD4+ TH cells in an HIV infected individual. These include 3 mechanisms :
    1. Direct cell killing
    2.Apoptosis
    3.lysis of Innocent bystanders
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12
Q

illustrate Fate of infected cells by
Direct cell killing

A
  1. budding of large amounts of viruses from cell surface
  2. accumulation of viral proteins& nucleic acids
  3. cytotoxic T lymphocytes
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13
Q

illustrate Fate of infected cells by Apoptosis

A

distortion of cell regulations by HIV proteins.

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14
Q

illustrate Fate of infected cells by
lysis of Innocent bystanders

A

CTLs destroy uninfected cells bound by HIV (have the appearance of the infected cells)

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15
Q

illustrate mechanisms of immune system evasion by HIV

A
  1. Integration of viral DNA into host cell DNA, resulting in a persistent infection
  2. A high rate of mutation of the genes encoding surface glycoproteins.
  3. Down regulation of class I MHC proteins required for cytotoxic T cells
    to recognize and kill HIV-infected cells.
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16
Q

illustrate ttt oh HIV

A
  1. immunotherapy :
    - monoclonal antibodies aganist GP120
    - soluble CD4 molecules
  2. antibiotic :
    for opportunistic infections
  3. antiretroviral drugs:
    *aim : suppress HIV replication not eradication (no cure) + protection of immune system
    *Mode of action :
    - fusion inhibitor = fuzeon
    - reverse transcriptase inhibitor =
    nucleoside analog = AZT , DDI
    non-nucleoside analog = navirapine
    - integrase inhibitor = Raltigravir
    - protease inhibitor = inhibit budding &assembly (indinavir)
    * combination HAART regimen
    (highly active antiretroviral ttt)= 2 nucleoside analog + protease inhibitor
    to avoid development of resistance due to high mutation rate of HIV
    * monitoring of ttt =
    measurement of virus load
    CD4+cell count
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17
Q

clinical picture of HIV appear in ………….

A

3 stages:
1. early acute stage
(2-4 weeks after infection)
2. middle latent stage
3. late (AIDS) stage

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18
Q

virological feature of early acute stage of HIV differ from early than late one . discuss

A
  1. early : high viremia
    a- spread to many regions as lymphoid tissue & brain
    b- most infectious stage
  2. later on : low level viremia , dec viral load
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19
Q

what’s clinical feature of early acute stage ?

A
  • infectious mononucleosis-like symptoms (90%): fever, sore throat , LN enlargement & maculopapular rash
  • asymptomatic in 10%
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20
Q

what’s immunological feature of acute early stage?

A
  1. CD4+count:
    a- early: low significantly
    b-late: rebound to original level due to high CD8+cells &Ab against HIV
  2. seroconversion: detection of Abs in serum usually 1-4 weeks after infection

** may be delayed up to 6 months :
(window period) NO Abs are detected although the viral load is high & the patient is symptomatic

21
Q

illustrate virological feature of middle latent stage

A

HIV continuous to replicate in lymphoid organs = large amount of virus is produced by LN cells, but remains sequestered in LNs

22
Q

clinical feature of middle latent stage…………….& lasts for ……..

A
  • asymptomatic
  • (7-11) years
23
Q

discuss immunological feature of middle latent stage

A
  • early : immune competence
  • generation of new CD4+T cells by bone marrow compensate the destroyed one
  • immune surveillance prevents most of infection
24
Q

discuss the three ways for HIV Transmission

A
  1. sexual route (main route)
    virus present in semen or vaginal secretion
    - male homosexual (commonest)
    - heterosexual
  2. blood or blood products route
    - blood transfusion
    - sharing needle or syringes
  3. perinatal route
    - transplacental
    - time of delivery
    - breast feeding
25
Q

describe the virological feature of late (AIDS) stage

A
  • collapse of LNs architecture
  • inability of immune system to trap HIV or other pathogens
  • viral load inc in peripheral circulation
26
Q

discuss immunological feature of late (AIDS) stage

A

CD4+ count dec to < 200 cells / mm3
lead to loss of immune competence

27
Q

clinical feature of late (AIDS) stage……………after infection (faster in absence of ttt)

A

10 years

28
Q

illustrate clinical feature of late (AIDS) stage

A

a. long lasting fever (>1 month) & weight loss
b. inc susceptibility to cancers & opportunistic infections characteristic of AIDS:
- Kaposi sarcoma
-pneumocystis jiroveci pneumonia
- bacterial : listeria, mycobacterium TB
- viral : CMV, HSV&VZV
- fungal : candida, cryptococcus

29
Q

list steps of laboratory diagnosis of HIV

A
  1. initial HIV screening test
  2. follow up testing
  3. CD4 cell count
30
Q

illustrate initial HIV screening test

A
  1. Ab test
    ( detect Ab for both HIV1/HIV2 Ags )
  2. Ag /Ab test
    (detect Ab & P24 Ag )
31
Q

illustrate follow up testing

A
  1. Ab differentiation test:
    distinguishes HIV1 from HIV2
  2. qualitative & quantitative detection of HIV nucleic acid :
    initial baseline viral load for :
    -predictor of the time for disease appearance
    - prognostic marker after initiation of treatment
32
Q

illustrate CD4 cell count

A
  • lower limit of normal cell count is 500 cells / mm3
  • patient needs chemoprophylaxis against opportunistic infection
  • When CD4 count falls < 200cells / mm³
    opportunistic infections increases
33
Q

what about vaccination of HIV ?

A
  • no available vaccine
  • vaccine is under trial & hindered by :
    1. rapid mutation in env region
    2. spread from cell to cell by fusion, no contact with Abs
    3.no animal models for AIDS
34
Q

humanT- Cell Lymphotropic Viru( HTLV )
a- it is an ………
b-causes:
1. ……..
2. …………

A

a- Oncogenic retrovirus

b-
1. T- cell leukemia
2. Tropical spastic paraparesis

35
Q

list Mode Of Transmission of HTLV

A
  1. Breast feeding
  2. sexual
  3. blood transfusion
  4. sharing contaminated needles
    (IV drug users)
36
Q

illustrate Pathogenesis of HTLV

A
  1. on mature T cell:
    - oncogenic non-cidal
    - viral RNA turned to Ds DNA by reverse transcriptase
  2. on nervous system :
    degeneration lead to spastic paraparesis
37
Q

diagnosis of HTLV :
1……
2……

A

. Diagnosis :
- Detection of viral RNA by RT- PCR
- Detection of Abs to HTLV by ELISA

38
Q

ttt of HTLV

A

No treatment or cure for latent infection

39
Q

how to prevent HTLV ?

A

-Screening of blood for Abs
-infected mother refrain breast feeding
-condom to prevent sexual transmission

40
Q
  • EBV infects ……….
  • lead to latent infection in……….
A
  • B lymphocytes & RES (liver, spleen)
  • B lymphocytes & pharyngeal epithelial cell
41
Q
  • CMV infect & become latent in ………..
  • reactivated in ……..
A
  • mononuclear cells
  • immunocompromised pts
42
Q

EBV cause ………

A
  1. infectious mononucleosis
  2. Burkitt’s lymphoma
43
Q

CMV cause…………

A
  1. infectious mononucleosis
  2. serious disease e.g. pneumonia in IC pts
44
Q

list structure of parvovirus B19

A
  • ss DNA
  • non enveloped
45
Q

MOT of parvovirus B19

A
  1. droplet
  2. transplacental (vertical)
  3. blood transfusion
46
Q

illustrate pathogen of parvovirus B19

A

infects 2 types of cells
- RBCs precursors(erythroblasts) =Aplastic anemia
- endothelial cells = rash with erythema infectiosum

47
Q

discuss Clinical manifestations in parvovirus B19.

A
  1. transiant aplastic crisis(TAC):
    - temporary arrest of RBCs production
    apparent only in patients with chronic hemolytic anemia
  2. Pure Red Cell Aplasia :
    A persistent infection in IC pts =
    chronic aplastic anemia ,
    need blood transfusion
48
Q

illustrate Laboratory diagnosis of parvovirus B19.

A
  • specimen: serum / blood cell
  1. Direct detection:
    - ELISA for viral antigen
    - PCR for viral DNA (most sensitive)
  2. Serology; ELISA
    to detect B19 IgM (recent infection)
49
Q

discuss treatment & prevention of parvovirus B19.

A
  • Treatment : symptomatic
  • Prevention and control
    1. Screening of blood donors
    2. Infection control to health workers from :
  • the patient with TAC
  • immunodeficient pts with chronic infection (PRCA)
    3. NO Vaccine against human parvovirus B19

microbiology (3 decks)

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