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Microbiology Exam IV > AIDS/HIV > Flashcards

AIDS/HIV Flashcards

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1
Q

AIDS (Hallmark Features)

A

Pneumocystis carninii
Kaposi’s Sarcoma
Marked reduction in CD4+ T-Lymphocytes (less than 200/uL or HIV infected individual with “indicator infections” to be considered AIDS)
Increased susceptibility to opportunistic infections

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2
Q

HIV (Characteristics)

A

Retroviridae family
+ssRNA
Enveloped
Two types: HIV-1 and HIV-2

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3
Q

HIV-2 (Characteristics)

A

Primarily found in Western Africa
SLOWER declined in CD4+ T-cells
LONGER asymptomatic period
LOWER mortality

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4
Q

gp120

A

Attachment Protein

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5
Q

gp41

A

Fusion Protein

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6
Q

pol

A

Reverse Transcriptase

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7
Q

p17

A

Matrix protein

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8
Q

p24

A

Capsid protein

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9
Q

Retrovirus Life Cycle (General Overview)

A

Attachment –> Fusion –> Reverse Transcription –> Integration (of dsDNA)forming a Provirus –> Genome replication/Transcription –> Budding –> Protein Cleavage (Activates) –> Mature Virion

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10
Q

HIV Life Cycle (Attachment)

A

gp120 binds to CD4 on T-lymphocyte, monocyte, or macrophage

Conformational change in gp120 allows binding to a co-receptor (CCR5 or CXR4)

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11
Q

R5-tropic HIV

A

CCR5 is used as coreceptor
Transmitted from PERSON-TO-PERSON
Predominant EARLY IN DISEASE
Efficiently infects monocytes/macrophages and microglia

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12
Q

X4-tropic HIV

A

CXCR4 is used as a coreceptor
Approximately 40% of patients TRANSITION from R5 to X4 viruses during course of disease
This is associated with Rapid progression to AIDS

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13
Q

CCR5 gene (delta 32) Deletion (Hetero- vs. Homozygous)

A

Deletion affects binding to gp120

Heterozygous Deletion = LONGER ASYMPTOMATIC PERIOD before onset of AIDS

Homozygous Deletio = NO INFECTION with R5-tropic viruses
***X4-tropic can still infect

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14
Q

HIV Life Cycle (Fusion)

A

gp41 mediates fusion between the viral envelope and plasma membrane

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15
Q

HIV Life Cycle (Reverse Transcription)

A

Virally-encoded enzyme (pol gene)
Found within the virion
Produces a linear dsDNA copy of the RNA HIV genome
MOST ERROR PRONE of all retroviruses (1/2000 nucleotides)
High error rate –> Rapid evolution during course of disease

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16
Q

HIV Life Cycle (Integration)

A

dsDNA copy of the genome moves into the nucleus of the cell
VIRAL INTEGRASE incorporates DNA copy of genome into host DNA
Now called a PROVIRUS, which is replicated with the regular cellular genes

PROVIRUS will remain in the cell for AS LONG AS IT SURVIVES (i.e. it is PERMANENT)

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17
Q

HIV Life Cycle (Egress)

A

Progeny HIV virions exit the infected cell by BUDDING through the plasma membrane at LIPID RAFTS

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18
Q

HIV Life Cycle (Maturation)

A

VIRAL PROTEASE cleaves the gag and gag-pol viral polyproteins in a process called VIRION MATURATION

Cleavage is essential for INFECTIVITY of the virion

Mature –> Dark, dense nuclear capsid

19
Q

HIV (Transmission: 3 types)

A

Sexual
Perinatal
Blood or body fluid exposure

NO casual contact or insect vector transfer

20
Q

HIV (Sexual Transmission)

A
  • More efficient from MALE-TO-FEMALE than female-to-male
  • MOST COMMON ROUTE worldwide is HETEROSEXUAL transmission
  • Presence of other STDs, especially those that generate lesions (e.g. Herpes Simplex Virus or Syphilis), INCREASE the risk for transmission
21
Q

HIV (Mother-to-Child Transmission)

A

Overall Risk = 1/4

20-30% before birth
50-65% at birth
12-20% after birth (nursing)

22
Q

HIV (Accidental Exposure of Healthcare Workers)

A

Skin puncture from needle contaminated with blood from HIV patient = ~0.3%

Due to mucous membrane exposure = ~0.09%

Risks are reduced with prophylactic antiviral regimens

23
Q

HIV (Acute HIV Syndrome)

A

Approximately 3-6 weeks following infection
Symptoms (similar to MONONUCLEOSIS)
-Fever, malaise, arthralgia, lymphadenopathy, sore throat
Rash (usually faint)
Burst of viremia
May NOT have detectable levels of anti-HIV antibodies at this time

24
Q

HIV (Immune Response)

A

Following initial burst of viremia, an immune response is mounted that curtails the levels of virus in the blood

25
Q

HIV (Chronic Phase)

A

Chronic Infection:

  • A low level of viremia (NOT LATENT) is present during this time due to viral replication
  • HIV escape from immune system includes:
    1) Antigenic Drift of gp120
    2) Inactivation of key elements of the immune response
    3) Cell-to-cell fusion

Patients often ASYMPTOMATIC
Median time of clinical latency in untreated patients is 10 years

26
Q

HIV (Set Point)

A

Predicts PROGRESSION RATE in untreated patients

Amount of virus in the system one year following initial infection

27
Q

HIV (Progression to AIDS)

A

Reduction in CD4+ T-cell numbers

  • Copius BUDDING of virions budding off T-cells
  • Interference with cellular processes
  • Other mechanisms

Reduced ability to fight other microbial infections

28
Q

HIV (Associated Infections: Oral Hairy Leukoplakia and Pneumonia)

A

1) Oral Hairy Leukoplakia (Epstein Barr Virus)
- White, plaques (wart-like) found on the LATERAL SURFACE of the tongue; concerning because indicative of immune suppression

2) Pneumonia
- Pneumocystitis carinii
- Mycobacterium tuberculosis
* More severe in HIV infection*

29
Q

HIV (Associated Infections: Thrush and CMV Retinitis)

A

3) Thrush
-Candida albicans
Slightly reduced immune capacity –> oral thrush
Severely reduced immune capacity –> spread to lungs or other parts

4) CMV Retinitis
- Cytomegalovirus (Herpes Virus)
* **Seen when the CD4 counts are VERY LOW (~50/uL)

30
Q

HIV (Associated Infections: Neoplasms and Diarrhea)

A

5) Neoplasms
Kaposi’s Sarcoma (HHV-8)
B-ell lymphomas

6) Diarrhea
- Cryptosporidium
- Isospora belli

31
Q

HIV-1 Infection Laboratory Marker Detection Order

A

1) Nucleic acid test (Viral RNA)

2) p24 antigen (3rd generation immunoassay > 2nd generation > 1st generation)

32
Q

Recommended Laboratory HIV Testing for Serum or Plasma Specimens

A

HIV-1/2 antigen/antibody combination immunoassay —> If POSITIVE, then undergose HIV-1/HIV-2 antibody differentiation immunoassay —> if NEGATIVE for both, then undergoes HIV-1 NAT (nucleic acid test) —> if this is NEGATIVE, then probably had a FALSE positive in the first place

33
Q

What does the HIV-1/2 antigen/antibody combination immunoassay look for and what is its purpose?

A

HIV p24 antigens (viral protein)
HIV-1 antibodies
HIV-2 antibodies

Purpose: SCREENING TEST for HIV diagnosis

34
Q

What does the HIV-1/2 antibody differentiation immunoassay look for and what is its purpose?

A

HIV-1 antibodies
HIV-2 antibodies

Purpose: DIFFERENTIATES between HIV-1 and HIV-2 infections

35
Q

What does the HIV nucleic acid test look for and what is its purpose?

A

HIV RNA genomes

Purpose: Detects RNA GENOMES. These genomes are detectable at EARLIER times of the infection than antibodies

36
Q

HIV (Other Detection Tests)

A

HIV NAT
PCR
Rapid tests for in-office (~20 mins; requires subsequent confirmatory testing)

37
Q

HIV Treatment (Entry Inhibitors)

A

NOT recommended for initiation of treatment to newly-diagnosed patients

1) Chemokine coreceptor antagonists
- Bind to CO-RECEPTOR and prevent its interaction with gp120
- MARAVIROC is a CCR5 antagonist and is limited to use in patients that possess ONLY R5-tropic HIV R5

2) Fusion inhibitors (FI)
- Binds to gp41 and prevents conformation change needed for fusion of the viral envelope with the cellular plasma membrane
e. g. ENFUVIRTIDE

38
Q

HIV Treatment (Reverse Transcriptase Inhibitors)

A

1) Nucleoside Inhibitors (NRTIs)
- Incorporated into growing DNA chain during provirus synthesis and cause chain termination
e. g. AZIDOTHYMIDINE (AZT)

2) Nonnucleoside Inhibitors (NNRTIs)
- Bind to reverse transcriptase and inhibit its activity
e. g. NEVIRAPINE

39
Q

HIV Treatment (Integrase Inhibitor)

A

Blocks the integration of the DNA copy of the viral genome into the cellular genome
e.g. RALTEGRAVIR

40
Q

HIV Treatment (Protease Inhibitors (PIs))

A
  • Peptidomimetic inhibitors of the viral protease
  • Protease inhibition leads to the production of immature, defective HIV particles
    e. g. SAQUINAVIR
41
Q

General Features of ARV Therapy (Goal and Recommendation)

A

Goal: Reduce viral load as low as possible for as long as possible

Current recommendation for starting ARV therapy:
>500 cells/uL CD4 count (BIII)
350-500 cells/uL CD4 count (AII)
<350 cells/uL CD4 count (AI) Strongest Recommendation

42
Q

HIV (General Features)

A
  • Rapid resistance to monotherapy; ineffective
  • Highly Active Antiretroviral Therapy (HAART):
    1) Combination therapies
    2) Greatly increased the lifespan of HIV infected patients
    3) Issues: toxicity, compliance, resistance
  • Prophylactic treatments for opportunistic infections (depends on the CD4 count)
    e. g. Gangciclovir for CMV, Pentamidine for Pneumocystis carinii and toxoplasmosis
43
Q

ARV Therapy (Treatment)

A

Standard of Care uses combination of AT LEAST THREE ARV DRUGS. Usually from two different classes:

1 NNRTI + 2 NRTIs
1 PI + 2 NRTIs
1 II + 2 NRTIs

Testing for resistance to ARV is commonplace

44
Q

HIV (Prevention)

A

1) Public education
2) Accidental health risk exposure risk reduce –> Prophylactic antivirals
3) Mother-to-infant spread reduced –> Antiviral treatment of mother and child, refrain from breastfeeding, caesarian section delivery
4) NO VACCINE AVAILABLE

Microbiology Exam IV (6 decks)

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