Viral Infection Flashcards
Influenza is which type of virus?
RNA virus.
How much Influenza virus type is there?
3 (A,B,C)
Key properties of the Infulenza virus:
- 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)
What differentiate Type A from the others:
- 8 RNA segments, neuraminidase, and hemagglutinin.
- Undergoes antigenic drift and antigenic shift.
What differentiate Type B from the others:
- RNA segments, neuraminidase, and hemagglutinin.
- Only undergoes antigenic drift.
What differentiate Type C from the others:
- 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)
Antigenic Variation is
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.
Antigenic Drift:
Small mutation in the same virus.
Antigenic Shift:
- Creates an entirely new strain of the virus
- Genetic Recombination (of 2 different strains of influenza –> human + Avian infection)
Role of the immune system toward antigenic drift:
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)
Steps Genetic recombination of the Influenza:
- 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..)
Lifecycle of Influenza:
- Absorption: Virus link to the ligand on the surface of the cell via hemagglutinin (sialic acid on the hemagglutinin)
- Endocytosis
- Fusion
- Transcription and Replication
- Assembly
- Budding and release
M2 protein is important for the influenza type A virus bc:
is needed for the virus to be able to escape the endosomal vesicle.
Drugs blocking the M2 protein (block virus to escape the endosomal vesicle):
Amantadine
Neuraminidase is important for the virus bc:
free the virus from the plasma membrane of the cell after the replication (cleave the sialic acid groups from host glycoproteins)
Sialic acid is important for the virus bc:
this allows the virus to enter the endosome and get into the cell.
Sialic Acid is linked to a sugar galactose for human this is in the airways epithelial cell. The linkage is:
alpha2-6 linkage (upper airways)
alpha 2-3 linkage (lower airways)
The difference between the A/H3N2 flu from Switzerland and A/H3N2 flu from Hong Kong is:
Antigenic shift
Amantadine ( Symmetrel) and Rimantadine drugs:
- 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.
Oseltamivir and Zanamivir drugs:
- Neuraminidase Inhibitors
- Tx and Prevent both types A and B.
Herpes viruses:
DNA genome
Herpes common properties:
- Cause Cell Lysis
- Latency and reactivation
Herpes virus targets:
- Neurons (neurotropic)
2. Leukocytes (blood-borne)
HHV-1 transmission (pathways):
- 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
Why is our body do not get ride of HHV-1 during latent phase>
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)
Why is the coldsore do not spread out?
Bc T cell will kill the infected skin cell.
Whitlow is:
Herpes simplex on the hands and fingers.
Reactivation of HHV-3 (Varicella Zoster)
Herpes zoster (shingles–>lesion close together)
HHV-3 spread out (pathway)
- 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.
Herpes Zoster can cause:
Post-Herpetic neuralgia, bc cause damage to these neurons when reactivated, make them hypersensibility..
HHV-4 (Epstein Barr Virus) affect (pathways):
- 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.
HHV-5 (cytomegalovirus) affects:
- 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.
HHV-6 (Roseola Virus) symptoms:
Rash with mild fever.. can be reactivated…
HHV-8 (Kaposi’s Sarcoma) related with:
Cancer when immunocompromised (AIDS)
