Micro 6. Flashcards

1
Q

What is HIV?

A

a zoonotic disease - introduced to humans by chimpanzees in central Africa

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2
Q

What is treatment for HIV?

A

HAART - highly active antiretroviral therapy

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3
Q

What is PEP?

A

post exposure prophylaxis - the use of antiretroviral drugs after a single high-risk event to stop HIV from making copies of itself and spreading through your body - must be used within 3 days

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4
Q

Who has the highest risk of HIV in the US?

A

gay/bisexual African American Men - especially younger

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5
Q

Upon exposure, who is most likely to become infected with HIV?

A

women

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6
Q

What do HIV virions infect?

A

lymphoid cells that are embedded in the vaginal and rectal epithelium - tissue macrophages, dendritic cells, etc

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7
Q

Where do visions migrate after initial infection?

A

to lymph nodes

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8
Q

What are the main symptoms of acute HIV infection?

A

fever, weight loss, sores and thrush of mouth, myalgia, hepatomegaly, nausea, vomiting, rash, lymphadenopathy, headache, neuropathy, malaise

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9
Q

Bacteriology HIV

A

ssRNA, (+) strand, slow to cause disease (lentivirus), two copies in each vision (diploid - for more variability)

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10
Q

What receptors must be present on a cell in order to induce HIV attachment and fusion? (early in infection)

A

CD4 and CCR5 coreceptor

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11
Q

Mutations in what change the coreceptor HIV binds to on CD4 cells? What is the advantage of this for the virus?

A

mutations in Env change binding to CXCR4 instead of CCR5 - this helps cells fuse together

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12
Q

What is mRNA synthesis completed by?

A

host RNAPII

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13
Q

What is replication phase I?

A

genomes are reverse-transcribed in the cytoplasm (by RT) and then integrate (IN) of HIV into host chromosome

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14
Q

What is replication phase II?

A

mRNA by host RNAPII and genome synthesis - protease cleave for final step of maturation

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15
Q

When can syncytia be formed?

A

after virion maturation - a multinucleate cell - multiple fusions of cells

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16
Q

What is Env?

A

HIV - composed of TM (transmembrane, gp41) and SU (surface gp120 domains) and cleaved by host proteases - SU binds CD4 and chemokine receptors which causes conformation change in TM - TM inserts in target cell membrane and induces virus entry

17
Q

CCR5

A

for macrophages

18
Q

CXCR4

A

for T cells (mutations in Env in order to infect these cells)

19
Q

What is the primer in reverse transcription of HIV?

A

tRNA bound to ssRNA

20
Q

What is the primary obstacle to eradicating HIV from a person?

A

viral genome becomes part of the cell for the life of the cell creating a reservoir of latent virus

21
Q

What does discontinuation of HAART allow?

A

viral relapse from latent reservoir

22
Q

Do patients successfully treated with HAART after 10 years exhibit an appreciable decrease in the size of the latent reservoir?

A

NO

23
Q

Mature virion

A

infectious - HIV protease cleaves Gag into subunits resulting in capsid assuming its trapezoidal shape

24
Q

Immature virion

A

not infectious - formed when they bud from plasma membrane

25
Q

What is significant about the HIV protease?

A

essential because takes immature virion and makes it mature - target for antiretroviral drug therapy

26
Q

3 domains for Gag polyprotein

A

MA - binds cytoplasmic tail of TM+SU, CA structural, NC bind to the RNA genome

27
Q

Functions of Env

A

mediates HIV virion attachment and entry into T cells and macrophages; fuse infected T cells with unaffected T cells

28
Q

Which version of HIV is most virulent?

A

syncytium-inducing strains

29
Q

How does HIV infect macrophages and T helper cells/

A

through Env binding to CD4 receptor and CCR5 and CXCR4 co-receptors

30
Q

What are the stages of HIV disease?

A
  1. exposure to virus (transmission) 2. primary HIV infection (acute phase) 3. seroconversion 4. clinical latent period 5. early symptomatic HIV infection 6. AIDS 7. advanced HIV infection (CD4 below 50)
31
Q

What are the main symptoms of AIDS?

A

encephalitis, meningitis, retinitis, pneumonia, TB, tumors, esophagitis, chronic diarrhea

32
Q

How does HIV escape immune control?

A

accumulation of virulence mutations

33
Q

How are CD8 cells affected by HIV?

A

as CD4 cells are depleted, less IL-2 is produced causing poor cytotoxic T cell functions

34
Q

How are B cells affected by HIV?

A

hyper-activation but lacking T cell help prevents mature Ig responses

35
Q

What is the main means of HIV transmission worldwide?

A

unprotected heterosexual sex

36
Q

What is the HIV structure?

A

enveloped, trapezoidal capsid, ssRNA genome

37
Q

What are the co-receptors used by the HIV virus for entry?

A

chemokine receptors

38
Q

Following entry, what are the next steps in the HIV lifecycle?

A

conversion to DNA, circularization, migration to the nucleus, integration into the chromosome