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Virus host interactions
Terms in this set (18)
Routes of virus infection
• respiratory tract
(e.g. influenza - easy to reinfect due to coughing up )
• oral cavity (e.g. hep A uses
• genital tract
(e.g. some herpesviruses, HIV)
• skin (e.g. rabies,
-The resporatory tract is more complicated with different levels.
Human influenza viruses (B and C)are yearly epidemics, antibody protections to some extent exist in the body.
Avian influenza(A) is less common, so more pathogenic.
-Most human influenza viruses effect the top, making them easy to be passed on as they are coughed up.
-Spread from year to year with little death.
-Bird ones affect lower down in the respiratory tract
-More pathogenic,as not developed a degree of antibody resistance.
-But as low down less easy to contract.
- initial target site
-often no symptoms are caused at sites of entry
- The replicated virus particles spread through the body
- These principle routes are circulatory and nerve systems
- To the target organ
- Biten by animal
-Rabies virus in the saliva,
-The target organ is the salivary glands
-Primary viremia is the muscle and skin cells replicating
-Track through the central nervous system(secondary viremia)
-To the salivary glands.
-pathogenesis generally occurs by direct cytopathic effects on cells in the target organ.
-This means that you kill enough cells in the target organ to become ill.
-Target organ is same as
portal of entry
- e.g. influenza
virus does not tract round the body, it stays in the same place.
Infection of the target organ
Migration of cells in various ways
1.sliding along mucus membrane
2.jumping from cell to cell inside the cell
- to spread the virus in the environment again.
One virus may not be enough to infect you.
Target audience is not the same as the portal of entry
-Dissemination in the blood is an example of viral migration from entry portal to target organs
- (e.g. smallpox)
-The target organs in smallpox are respiratory mucosa, spleen,
bone marrow, lymph node.
The virus won't get to the target organ without a replication.
- This is because the immune system will kill enough virus that a really infectious dose is needed to get to the target organ.
-At target organ there will be further rounds of replication which leads to disease.
- There will then be a site of shedding, either the same or different to the target organ.
- This releases the virus back into the environment.
• the nervous system can also disseminate viruses
by similar mechanisms
Some plant viruses use insect vectors.
- Some plant viruses are so well adapted that they will tract through the insects body
-Replicating inside the insect aswell as the plant.
- In some cases virus is not cleared from the organism.
-The host has the virus for a long period of time.
-Involves modulation of both virus, cell
and host immune response.
-Virus producing proteins to modulate itself, preventing it replicating
-Virus also prevent the immune system recognising and killing the virus.
-Persistent infections can be latent and
then become reactivated.
-Waiting for a suitable environment to become reactivated.
How does the virus sense this suitable environment and reactivate?
- latent virus not expressing proteins
-The host is modulated.
-Might reactivate due to stress, immunodeficiency, another virus infection.
- How does the virus recognise this?
Viruses have a lot of Transcription factor binding sites.
-These sense the external environment of the cell.
-If the composition of transcription factors changes in response to one of the above causes the virus will detect it and begin replication.
Persistent infections are often found by
viruses infecting the immune system,
nervous system or digestive system.
-The most persistent is HIV
-Integrates into the DNA of the host in a macrophage or WBC.
- When integrated, it down regulates proteins on the cell surface.
-This means that it cannot be recognised by the immune system of the host.
-Some of these populations of macrophages act as deep reservoirs, where it is difficult to get rid of the virus.
-The virus cannot be removed.
How can they
How to viruses avoid the immune system of the host.
-avoidance of neutralising antibodies by spreading directly from cell to cell.
-budding into cytoplasmic vacuoles
-genetic variation (quasispecies)
-inhibition of immune and nonspecific defences
Viral persistence in the
- integrates into the cell DNA
-Mechanism of antigenic variation,and restricted viral cell factors( viral cells not recognised easily by viral t cells.
-Leading the the reactivation syndrome of AIDS.
-Episomal (maintaining the viral DNA)
-Maintaing the virus as an episome in the nucleus.
-Persisting, and latent, needs to divide when the cell divides because there will probably be markers on the host cell marking it as infected.
-As alot of viruses leave envelope proteins of surface when invade the host.
How does the virus divide when the cell divides to avoid detection?
eg Epstein Barr virus
- uses EBNA protein, encoded by the virus
-To down regulate most of the other viral genes.
- Not many of the genes are expressed.
-This restricts expression of most EBV genes but maintains the EBV DNA making sure it is not lost when the cell divides.
EBV also causes the expression of LM ( latent membrane )proteins .
-these interfere with the binding of the cell to t cells.
-The T cell cannot recognise the cell as being infected so they cannot kill it.
Natural Killer cells at the end might recognise it.
This is an example which is physically in a place that is able to be recognised.
Virus in a cell which is physically not able to be recognised by the immune system.
Herpes simplex virus
-HSV is an example of a virus
maintained in the nervous system
-Latent in ganglion, restricted expression
-Not seen by the immune system as hidden in the nervous cells.
-Look at the factors which will activate the expression of the virus.
-Virus will tract down the nerve cell into the mouth.
- Replication in the mouth cells.
-Colds sores will form.
The immune system recognised the cold sore infected cells and kills them off.
-But still persisting in the nervous system.
_persisting for a long time with the reservoir in the ganglion cell.
General host defences against viral infection
• several types of general defence including
non-specific defences and induced defences
• non-specific defences include anatomic barriers,
non-specific inhibitors, fever, inflammation and
-saturative, if you have enough you can inhibit the virus.
• more specific and induced defences include NK cells
and interferon production
• fever reduces mortality/replication for many viral infections
-At higher temperatures, the percentage survival of the host increases.
-Compared to lower temperatures.
Why should a fever act as a defence?
- Changing a small degree of temperature will severely change the replication effect of the virus.
- The virus requires a specific temperature to replicate at.
-more effective against bacteria than viruses
-Virus taken up by the phagocyte
-Many viruses have evolved resistance to this, requiring the phagocyte to engulf them as part of their life cycle.
-Another example of subverting the immune system.
-Wait to be engulfed so that they can replicate.
Inteferons and Natural Killer (NK) cells
Natural killer cells,
-non specific viral killing cells.
-Do not require antigenic presentation.
-activate natural killer cells.
-increase MHC class 1 expression
Inteferons and Natural Killer (NK) cells
-infection by a virus, showing the virus titre at different time points.
-Eventually titre killed off due to T cells and K cells.
-Activation of T cells takes a few days, once activated they are efficients as killing infecting cells off
-unless the virus cell has an defence mechanism.
Before the activation of the T cells, the NK cells are activated.
-By IFN alpha or beta
-NK cells kill virus early on
- Reduce the viral titre, not to zero but so that it is not so high.
-They do not kill all viruses.
How do Natural killer cells work?
Natural killer cells have activation ligands , these are host cell proteins.
Interferons increase the amount of MHC class one in the cells.
When a lot of MHC class one in the cell, this causes a negative signal which means that the Natural killer cell doesn't kill that cell.
In order to survive and natural killer cell you need a lot of MHC in the cell.
In a virally affected cell, there is altered MHC one.
-This means that there is no negative signal.
-So the natural killer cell will kill the virally infected cell.
Viruses, often down regulate or change the MHC one on the surface of the cell.
MHC one is required for CTL killing.
-Viruses try to get rid of the MHC1 from the surface, then they cannot be killed CTL.
-If they do this they then leave themselves open to being killed by natural killer cells.
-NO way to win :D
Although NK cells
and the immune system is
highly effective, viruses
have evolved many
mechanisms to avoid them.
A lot of different genes involved in the different defences.
-Evolved from the arms race.
THIS SET IS OFTEN IN FOLDERS WITH...
Effector mechanisms in the immune system
Unit 6 -Laboratory Diagnosis of Viral Infection
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