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Microbiology > Exam #6: Viral STIs > Flashcards

Exam #6: Viral STIs Flashcards

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Biology 101 flashcards
1
Q

List the characteristics of HIV. What is the difference between HIV-1 & HIV-2?

A 
Retroviridae 
\+ssRNA
Enveloped
2 Types= HIV-1 & HIV-2 (HIV-1 is more common worldwide & HIV-2 is more endemic to West Africa
- Slower decline in CD4 T-cells
- Longer asymptomatic period
- Lower mortality

Note that the genome consists of a homodimer of two identical sequences; thus, it is functionally diploid.

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2
Q

Describe the structure of HIV. What proteins are associated with each part of the HIV structure?

A

+ssRNA (2x copies)

Enveloped= gp120 (attachment) & gp41 (fusion)

Matrix protein= p17

Nucelocapsid= p24

Genome= pol gene that encodes reverse transcriptase

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3
Q

List the stages retrovirus lifecycle.

A 
Attachment (gp120)
Fusion (gp41)
Reverse transcription (pol gene)
Integration (integrase)
Transcription of provirus 
New genome & mRNA 
Budding
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4
Q

How does HIV attach? What cells does HIV attach to?

A
  • gp120 binds CD4
  • CD4 is found on T-lymphocytes, monocytes, & macrophages
  • Conformational change in gp120 to allow binding to co-receptor (CCR5 or CXCR4)
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5
Q

What is the difference between R5-tropic HIV & X4-trophic HIV?

A

After attachment, gp120 undergoes a conformational change that allows binding to a co-receptor

  • CCR5= person to person transmission
  • CXCR4= more rapid progression to AIDS
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6
Q

What is the significance of CCR5 deletions in HIV?

A

Deletion in the CCR5 gene augments disease pathogeniticity

  • Heterozygous= longer asymptomatic to R5
  • Homozygous= no infection with R5 (1% of the Caucasian population)

However, can be infected with CXCR4

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7
Q

How does HIV fuse with the plasma membrane?

A

Gp41 mediates fusion between the viral envelope & plasma membrane by bringing the two close together

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8
Q

What codes for Reverse Transcription? What is the function of Reverse Transcriptase?

A
  • pol gene
  • Produces dsDNA linear copy of RNA HIV

*Note that this is associated with a high error rate because this is what allows for rapid evolution during the time course of disease e.g. resistance to antivirals

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9
Q

How does HIV integrate into the host genome?

A
  • dsDNA moves into the nucleus
  • viral integrase causes DNA copy to be incorporated into the host DNA

Viral DNA integrated into the host genome is called “provirus”

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10
Q

How does HIV egress?

A
  • Viral envelope proteins are incorporated into the plasma membrane to form lipid rafts
  • Virions acquire envelope as they bud from the cell, giving the the appearance of spheres with an electron dense ring surrounding
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11
Q

What is maturation?

A

Virion maturation= viral protease cleaves gag & gag-pol that is essential for infectivity

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12
Q

How is HIV transmitted? What is the risk associated with each mode of transmission?

A

Sexually

  • Male-to-female is most effective
  • Most common route
  • Presence of other STIs increases risk

Perinatal= 1/4

  • 25-30% before birth
  • 50-65% at birth i.e. HIGHEST at birth
  • 12-20% during nursing

Exposure to blood or body fluids

  • Needle stick= 0.3%
  • Mucous membrane= 0.09%

Note that the exposure risk to healthcare workers is less than that of Hepatitis B & C

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13
Q

What are the difference stages of HIV infection?

A
  • Acute Infection= mononucleosis-like symptoms
  • Chronic Phase= host immune response curtails plasma viremia; asymptomatic but chronic lymphadenopathy
  • AIDS= opportunistic infections
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14
Q

Draw the graph of viral load, CD4 T-cell, & anti-HIV antibody through the course of the disease.

A

N/A

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15
Q

What symptoms are seen in acute HIV syndrome?

A

3-6 weeks post infection

Fever
Malaise
Arthralgia 
Lymphadenopathy 
Sore throat 
Rash

*May not have detectable levels of anti-HIV antibodies at this time.

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16
Q

What are the characteristics of chronic HIV infection?

A
  • Low viermia
  • HIV escape from immune response
  • Patient asymptomatic

10 years in the absence of antivirals

17
Q

What is the HIV-set point? Why is it important?

A

Level of the virus in the blood 1 year following infection

  • Lowest= fewest individuals progressing to AIDS in 10 years following infection
  • Highest load= most individuals progressing to AIDS in 10 years
18
Q

How does HIV kill T-cells?

A
  • Copious budding
  • Interference with cellular processes
  • Other mechanisms
19
Q

How is AIDS defined?

A

CD4 T-cell count less than 200

20
Q

List some common HIV associated infections.

A
  • Oral Hairy Leukoplakia
  • Peumonia
  • Thrush
  • CMV retinitis
  • Neoplasms
  • Diarrhea
21
Q

What causes Oral Hairy Leukoplakia?

A

EBV

22
Q

What causes HIV associated Pneumonia?

A

Pneumocystis carinii

Mycobacterium tuberculosis

23
Q

What causes HIV associated Thursh?

A

Candida albicans

24
Q

What causes HIV associated CMV retinitis?

A

Cytomegalovirus

25
Q

What causes HIV associated Neoplasms?

A

Kaposi’s sarcoma

B-cell lymphomas

26
Q

What causes HIV associated diarrhea?

A

Cryptosporidium

Isopsora belli

27
Q

Draw the sequence & appearance of laboratory markers for HIV-1 infection.

A

1) HIV-RNA
2) HIV-1 p24 antigen
3) HIV antibody

28
Q

Draw the algorithm for HIV testing.

A

1) Screen (HIV 1/2 antigen/antibody immunoassay for HIV p24 antigen & HIV1-2 antibodies)
2) Confirmatory test to differentiate HIV-1 & HIV-2
3) If negative or indeterminate, then nuclei acid testing to detect RNA genome

29
Q

How is HIV NAAT used?

A

To follow the course of antiretroviral treatment

30
Q

What are the different classes of anti-retrovirals?

A 
Entry inhibitors or chemokine coreceptor antagonists
Fusion inhibitors 
Reverse Trascriptase Inhibitors 
Integrase Inhibitors 
Protease Inhibitors
31
Q

Describe the mechanism of action of the Entry inhibitors.

A

Chemokine receptor antagonists

- Bind to the co-receptor (CCR5 or CXCR4) & prevent interaction with gp120

32
Q

Describe the mechanism of action of the Fusion inhibitors.

A
  • Bind gp41 & prevent conformational change needed for fusion of the viral envelope with cellular plasma membrane
33
Q

Describe the mechanism of action of the Reverse Transcriptase Inhibitors.

A

NRTIs i.e. “Nuceloside reverse transcriptase inhibitors”
- Nucloside analogs incorporated into the growing DNA chain during synthesis of provirus & cause early termination

NNRTIs i.e. “Nonnucleoside reverse transcriptase inhibitors”
- Reverse transcriptase antagonists

34
Q

Describe the mechanism of action of the Integrase Inhibitors

A

Inhibit viral integrase to prevent DNA incorporation/ formation of the provirus

35
Q

Describe the mechanism of action of the Protease inhibitors.

A

Act on the enzyme needed to cleave gag & gag-pol during virion maturation

36
Q

What is the standard of care for ARV therapy?

A

Combination of drugs from three classes
- 2x NRTIs +

1) NNRTI
2) PI
3) II

Microbiology (49 decks)

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