Viral Infection

Question 1

Influenza is which type of virus?

Answer 1

RNA virus.

Question 2

How much Influenza virus type is there?

Answer 2

3 (A,B,C)

Question 3

Key properties of the Infulenza virus:

Answer 3

• Hemagglutinin (allows the virus to recognize the airway epithelial cells and to it)
• Neuraminidase (enzyme )
• M2 ion channels on the surface(ONLY TYPE A), M1 in the surface of the capsule
• Genetic material: 8 separately coiled strands (called RNP)

Question 4

What differentiate Type A from the others:

Answer 4

• 8 RNA segments, neuraminidase, and hemagglutinin.

- Undergoes antigenic drift and antigenic shift.

Question 5

What differentiate Type B from the others:

Answer 5

• • RNA segments, neuraminidase, and hemagglutinin.

- Only undergoes antigenic drift.

Question 6

What differentiate Type C from the others:

Answer 6

• Only 7 RNA segments and do not have the neurominidase.
• You will become immune after getting the Influenza Type C.
• Type C is stable. (no antigenic variation)

Question 7

Antigenic Variation is

Answer 7

when viruses continuously mutate and change their genetic properties. As they mutate they change their antigenic properties so the immune system cannot recognize them as well.

Question 8

Antigenic Drift:

Answer 8

Small mutation in the same virus.

Question 9

Antigenic Shift:

Answer 9

• Creates an entirely new strain of the virus

- Genetic Recombination (of 2 different strains of influenza –> human + Avian infection)

Question 10

Role of the immune system toward antigenic drift:

Answer 10

Once we are expose to the virus, our antibodies are still effective and able to recognize partially the antigen (from the last exposure). These antibodies bind to the hemagglutinin, preventing the virus from entering the cell. (The infection are still there, but much more mild)

Question 11

Steps Genetic recombination of the Influenza:

Answer 11

• 2 different strains of influenza lock onto the hemogglutinin.
• Both strains force their RNA into cytoplasm of the cell.
• RNA strains recombination –> new virus
• Antibodies from humain cannot always recognize because (eg. hemogglutinin is avian hemogglutinin..)

Question 12

Lifecycle of Influenza:

Answer 12

1. Absorption: Virus link to the ligand on the surface of the cell via hemagglutinin (sialic acid on the hemagglutinin)
2. Endocytosis
3. Fusion
4. Transcription and Replication
5. Assembly
6. Budding and release

Question 13

M2 protein is important for the influenza type A virus bc:

Answer 13

is needed for the virus to be able to escape the endosomal vesicle.

Question 14

Drugs blocking the M2 protein (block virus to escape the endosomal vesicle):

Answer 14

Amantadine

Question 15

Neuraminidase is important for the virus bc:

Answer 15

free the virus from the plasma membrane of the cell after the replication (cleave the sialic acid groups from host glycoproteins)

Question 16

Sialic acid is important for the virus bc:

Answer 16

this allows the virus to enter the endosome and get into the cell.

Question 17

Sialic Acid is linked to a sugar galactose for human this is in the airways epithelial cell. The linkage is:

Answer 17

alpha2-6 linkage (upper airways)

alpha 2-3 linkage (lower airways)

Question 18

The difference between the A/H3N2 flu from Switzerland and A/H3N2 flu from Hong Kong is:

Answer 18

Antigenic shift

Question 19

Amantadine ( Symmetrel) and Rimantadine drugs:

Answer 19

• M2 protein blocker (which let the virus escape from the vesicle. )
• Use to prevent and tx type A influenza but NOT USE ANYMORE BC RESISTANCE DEVELOPED.

Question 20

Oseltamivir and Zanamivir drugs:

Answer 20

• Neuraminidase Inhibitors

- Tx and Prevent both types A and B.

Question 21

Herpes viruses:

Answer 21

DNA genome

Question 22

Herpes common properties:

Answer 22

• Cause Cell Lysis

- Latency and reactivation

Question 23

Herpes virus targets:

Answer 23

1. Neurons (neurotropic)

2. Leukocytes (blood-borne)

Question 24

HHV-1 transmission (pathways):

Answer 24

• Enter the skin, travels into sensory neuron (trigeminal ganglion)
• Stay in latent phase
• When reactivated, travels back to the skin, attack the skin
• causing lysis –> coldsore

Question 25

Why is our body do not get ride of HHV-1 during latent phase>

Answer 25

Bc the virus do not display anything on his surface so can not be recognized by the T cell. (good bc T cell would be destroying our trigeminal sensory neuron)

Question 26

Why is the coldsore do not spread out?

Answer 26

Bc T cell will kill the infected skin cell.

Question 27

Whitlow is:

Answer 27

Herpes simplex on the hands and fingers.

Question 28

Reactivation of HHV-3 (Varicella Zoster)

Answer 28

Herpes zoster (shingles–>lesion close together)

Question 29

HHV-3 spread out (pathway)

Answer 29

• Primary viremia: Replicate in the lymph nodes
• Secondary viremia: replicate in the liver, spleen and others organs
• Lesion appear on the skin.
• Latent phase: goes into the sensory ganglia then travel to the dorsal root ganglia.
• Reactivation: affect the dermatome, area in the skin that innervated by that specific ganglion.

Question 30

Herpes Zoster can cause:

Answer 30

Post-Herpetic neuralgia, bc cause damage to these neurons when reactivated, make them hypersensibility..

Question 31

HHV-4 (Epstein Barr Virus) affect (pathways):

Answer 31

• Epithelial cells in the pharynx and the B cells.
• It causes atypical lymphocytes.
• It causes changes in the Liver (hepatitis), spleen (larger) and swollen lymph nodes.
• Latent phase: in the B cells and in the epithelial cells of the pharynx.

Question 32

HHV-5 (cytomegalovirus) affects:

Answer 32

• Body reacts with cell-mediated response (CD4 T cells, CD8 T cells, B cells, neutrophils and NK cells.
• Asymptomatic usually except if at risk (immunocompromise, newborn…) –>hearing loss, newborn morbidity/abnormalities.

Question 33

HHV-6 (Roseola Virus) symptoms:

Answer 33

Rash with mild fever.. can be reactivated…

Question 34

HHV-8 (Kaposi’s Sarcoma) related with:

Answer 34

Cancer when immunocompromised (AIDS)