Lecture 21 HIV and AIDS Flashcards

1
Q

Define and Types HIV

A

human immunodeficiency virus 1)HIV-1 in U.S. and most other areas 2) HIV-2 in W. Africa; India

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2
Q
  1. HIV disease
A

when HIV causes signs/symptoms to the body

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3
Q
  1. AIDS
A

acquired immunodeficiency syndrome (end-stage HIV disease) When CD4 helper T cells < 200)

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4
Q

HIV Disease Structure 4

A

1) retro Virus 2) proteins (enzymes(REVERSE TRANSCRIPTASE); capsid; matrix; surface and transmembrane proteins) 3) Lipid envelope

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5
Q

RetroVirues 3 parts

A

1)RNA viruses 2) Reverse transcriptase (uses viral SS RNA to make DD DNA 3) Inserts DNA into the genome of the host cell

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6
Q

HIV Genome

A

Genes flanked by long terminal repeats (LTR)

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7
Q

HIV Pathogenesis

A

Target various cells with CD4 receptors(Th cells; Macrophages; intestinal epithelium; brain cells) 2) Attaches to receptor via viral surface protein (host CD4 and CCR5 CXCR4 co receptors)(fusion receptors)

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8
Q

HIV replication 8 Steps

A

1) Virus gets into cell and uncoated release of viral genome 2) cDNA copy synthesized by reverse transcriptase 3) RNA degraded second DNA strand synthseized4) DNA circularizes or INTEGRASE function to incorporate DNA into host cell genome(integrated provirus) 5) With hose activation; viral DNA is transcribed yielding messenger RNA and viral genome RNA 6) Viral Rna are translated yielding viral enzymes including PROTEASE 7) viral membrane proteins are transported to host cell membrane 8) final viral assembly and budding take place

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9
Q

Why is the mutation rate of HIV so high?

A

Because reverse transcriptase is very error prone (highly variable regions easily change)

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10
Q

How is a latent infection different from an active infection?

A

Latent is when viral DNA is integrated into cellular DNA and forms provirus 2) Active infection: the provirus is activated allowing it to control the synthesis of new viruses which bud from host

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11
Q

Acute retroviral syndrome

A

Flu like symptoms HIV spread through body (couple weeks)

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12
Q

Asymptomatic interval

A

Clinical well being (can last years) CD4 begins to drop RNA rises

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13
Q

AIDS

A

Lymph node enlargement; fever ; weight loss

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14
Q

Typical v. atypical pathogenesis

A

Typical: 80 slowly decrease CD4 over 9-10 years Atypical: 10% rapid progression few years 5-10% show no fall in CD4 over 20 years

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15
Q

What are the main categories of AIDS-defining conditions? Why do these occur?

A

Any opportunist infection or cancers. 1)Infection Pneumoystosis(Tiroveci -used to be leading cause of death) 2)Cancer :Kaposi Sacome 3) TB

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16
Q

Infection: Pneumocystosis

A

Lung infection from a fungus that used to be the leading cause of deaths cause from tiruvici is now treated w/ medications

17
Q

Cancer: Kaposi’s sarcoma

A

Associated with human herpes virus -8 Causes tumor in skin mucous membranes; Incidences rose 2000x in 1984 in unmarried gay men in SF tipped off doctors

18
Q

HIV Modes of transmission:

A

1) contact w/ semen or vaginal fluid(sex artificial insemination) 2) contaminated drug tattoo piercing needles 3) contamination w/ HIV infected blood Mother to baby

19
Q

HIV Antibody tests Benefits/Drawbacks?

A

Indirect Elisa(antibodies from patient) Most common. Cheap but can produce false negative because of 3 month period

20
Q

HIV Treatment Options Categories 4

A

1) Reverse transcriptase inhibitors( Nucleoside and Non nucleoside RT inhibitors)2) protease inhibitors 3) intagrase (DNA cant get into human genome) inhibitors 4) Fusion inhibitors(stop from binding cell wall

21
Q

HAART What is it? Effective? Drawbacks?

A

High active antiretroviral therapy: a cocktail of drugs cause is more effective because less mutation immunity Though it can have toxic side effects and is costly

22
Q
  1. PEP (Post-exposure prophylaxis) What? Who? When?
A

For healthcare providers that had contact with contaminated HIV blood. Treatment stars within 2 hours of exposures and last for 4 weeks (very effective)