FINAL REVIEW part 2 - Infectious diseases/aging/nutrition

Question 1

When cell infected it present antigens by?

Answer 1

MHC class1

Question 2

Ig inactivate microbes by?

Answer 2

Neutralizing
Agglutination
Precipitation of soluble antigens

Question 3

Smallpox eradicated due to vaccins?

Answer 3

TRUE

Question 4

Difference between influenza and cold?

Answer 4

Influ: resp and systemic Sx, with sudden onset (Otitis Media complication in child)
Cold only throat and nose Sx, gradual onset

Question 5

What allows flu virus to recognize epithelial cells?

Answer 5

Hemagglutinin

Question 6

Influenza type A and B difference with type c?

Answer 6

A/B: 8 RNA, neurominidase and hemagglutinin. B only antigenic shift, A shift and drift.
C: 7 RNA and no neurominidase. Once you get infected you retain immunity, which is not true of A/B

Question 7

1. Antigenic drift?

2. Antigenic shift?

Answer 7

1. Small mutation in RNA of virus overtime as virus replicates, happens all the time. This can make Ig less effective with time
2. Different RNA strains inside a cell recombine resulting in abrupt major change resulting in new hemagglutinin or neuraminidase or both, rare.

Question 8

Influenza life cycle? + complete time?

Answer 8

1) Absorption: H binds to alpha 2-6 lnikage in sialic acid on epithelial cells
2) Endocytosis
3) Fusion: M2 p+ proton ion channel acidify interior, weakening bond between cell and virus
4) Replication/transcription of RNA
5) Assembly
6) Release: Neuraminidase frees the new virus by breaking bond with sialic acid on cell membrane
- > 4-6 hours

Question 9

Specificity of virus is due to?

Answer 9

sialic acid uniqueness in the epi. cell of upper airways

Question 10

1. Herpes Virus targeting neurons?

2. Herpes Virus targeting leukocytes?

Answer 10

1. Neurotropic: HSV-1 (mouth), HSV-2 (genitals) and varicella-zoster
2. Blood-born: CMV (usually ASx), Epstein-Barr Virus (mononucleosis), human herpes virus 6/7 (Roseola)-8 (Kaposis Sarcoma cancer in HIV)

Question 11

Herpes cause?

special property?

Answer 11

1. Cell lysis

2. Latency + ractivation

Question 12

Gene/p+ involved in apoptosis?

Answer 12

Bcl-2: block apoptosis
MYC: nucleaus, stimulate apoptosis
FAS: stimulate apoptosis
p53: triggers apoptosis

Question 13

Cellular factors of aging (9)?

Answer 13

1. Altered intracellular comm. (inflamm)
2. Stem cell exhaustion
3. Cellular senescence
4. Mitochondrial dysfunction (ROS, atp dysfunction)
5. Deregulated nutrient sensing (calorie restriction)
6. Loss of proteostasis (=protein homeostasis)
7. Epigenetic alterations
8. telomere attribution : the end part of chromosomes. The enz. that fill the gap when DNA replication occurs. Only present in some cells.
9. genomic instability (accumulation of mutation)

Question 14

2 proteolytic (break p+ into AA) systems are?

Answer 14

1-Ubiquitin Proteosome system: Misfolded p+ are ubiquinidated (marked) and then broken down by proteosme
2-Lysosome Autophagy system: p+ encapsulated and destroyed by lysosomal Enz.

Question 15

Bone turnover by? Homeostasis?

Answer 15

Osteoclast: breakdown with HCL pump (Clast = hCl)
Osteoblast: Building (blast = build)

RANK ligand ->RANK receptor on osteoclast ->more osteoclast
Osteoprotegerin (estrogen) ->binds to RANK ligand blocking its binding to RANK receptor ->lower number of osteoclast

Question 16

Adaptive change to starvation?

Answer 16

Decrease in:
Na/K pump
temperature homeostasis
Infertility
inflam./immune responses decreased

Question 17

Kid deficiency in vit. d=?

Answer 17

Rickets

Question 18

Adipocytes communication when as enough fat?

Answer 18

LEPTIN (resist obesity) -> hypothalamus ->decrease food intake and increase E expenditure

Question 19

Obesity and inflammation/atherosclerosis?

Answer 19

ADIPONECTIN release from adipocytes -> reduce inflam.

Obesity ->deficiency in adiponectin ->increase vascular inflam. ->increase athero.