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Virology > Chapter 18: HIV > Flashcards

Chapter 18: HIV Flashcards

1
Q

HIV

A

Human Immunodeficiency Virus

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2
Q

AIDS

A

Acquired Immunodeficiency Syndrome

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3
Q

1983

A

HIV discovered

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4
Q

AIDS

A 
emerging infectious disease, now pandemic
78 million infected
5 million new infections/year
3 million deaths/year
4th leading cause of mortality
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5
Q

Transmission

A

fresh body fluid-“man-made” disease
Horizontal: sex, blood, needles…
Vertical: mother to fetus and infant

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6
Q

2 types

A

HIV-1: most prevalent

HIV-2: in West Africa

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7
Q

Group M: Major

A

A, B, C, D, F, G, H, J, K; 16 CRFs

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8
Q

Group N: non major

A

A few cases

Group outliers: unclassified

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9
Q

Predominants

A

Subtype B: USA, N. America, Europe

Subtype C: the world

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10
Q

Virion

A

Spherical enveloped particle
Conical capsid
~100nm in diameter
transmembrane protein: gp41(glycoprotein, 41 kD); C terminus bind MA protein
SU(surface protein): gp120 has 5 variable loops
Spike: a gp41-gp120 trimer

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11
Q

Genome

A 
•	“diploid”: 2 ss RNAs, each
o	9.3 kb, “fake” (+) sense
•	9 genes: 3 major structural
o	6 Regulatory
•	Use all 3 reading frames
•	Extensive overlapping
•	2 are split genes
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12
Q

Attachment

A

Interaction of gp120, CD4 and co-receptor-> conformational change in gp41-> membrane fusion

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13
Q

Anti-receptor

A

gp120

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14
Q

Receptor

A

CD4 on helper T, macrophage, dendritic cell-> cell tropic
A surface glycoprotein
Has Ab-like domains
Outer domain for viral binding

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15
Q

Co-receptor

A

CCR5 (used by most HIV-1 strains) or CCR4
Chemokine receptor: bind chemokines in immune system
leukocytes to infected area and control T cell differentiation

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16
Q

RNA processing

A
  • 5’ cap; 3’ poly A
  • Genome length mRNA contains overlapping genes  differential splicing
  • 3 size classes of viral mRNAs
  • Unspliced (genome-length: 9.3 kb)
  • Singly spliced (about 4.5 kb)
  • Multiply spliced (about 2kb)
17
Q

Maturation

A

• During and after budding
• Gag-Pol  auto-proteolytic cleavage in nucleocapsid
o PolPR, T=RT, RNase H, IN
o Gag  other structural proteins (MA, CA, NC)
• Capsid: spherical

18
Q

High Mutation rate

A

10^-4 to 10^-5
Rt has inherently high error rate and no proof-reading activity
Maturation can be at any position in HIV genome
Each new HIV genome can contain one point mutation

19
Q

High Recombination rate

A

During coinfection by 2 different but related strains by 3 mechanisms
Reassortment: “diploid” genome-> can be “heterozygous”
Cleavage/ligation: homologous,…
Template switching

20
Q

Consequences of HIV genetic diversity: Rapid Evolution

A 
o	 rabid antigen changes
	Evade host immune system
	Difficult for development of vaccines and diagnostic tests
o	 rapid adaptation
	Drug resistance
21
Q

Acquired Immunodeficiency Syndrome

A

Slow but deadly caused by HIV

Immunodeficiency: unable to respond effectively to pathogens

22
Q

Initial Infection

A

viremia and flu-like symptoms (immune response)

23
Q

Clinical “latent” phase

A

asymptomatic
HIV relocates to lymph nodes
CD4 T cell number in blood decreses progressively
8-10 years(rapid: 2-3 years)

24
Q

AIDS

A

CD4 cells< 200/microliter
full blown immune deficiency
Susceptible to any infections

25
Q

Immune Response

A
  • Ab against HIV
  • T cell responses to HIV
  • Host immune responses can not clear HIV
26
Q

Host immune Responses cannot clear HIV because

A

o Daily net loss of CD4 T cells  immunodeficiency
o New variants  hide from immune response and anti-HIV drugs
o Latency  hide from immune response and anti-HIV drugs
o Syncytium  rapid spread to other cells; also  cell lysis

27
Q

Clinical Diagnostic

A 
•	Test Ab against HIV by ELISA
o	If (+), confirmed by Western Blot
o	If (-), test again after 1-3 month “window”
28
Q

Drugs

A

Cannot clear HIV
Only delay progress
Drug-resistant Variants
Cost, many pills/day, complex schedule

29
Q

Vaccine

A

Some, but not so effective

No animal model except humans- big challenge to research

Virology (17 decks)

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