Lecture notes
viral infection
- Module
- Mechanisms of pathology
- Institution
- Aston University, Birmingham (Aston)
in depth immunology notes
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Viral infections- human papillomavirus.Human papilloma virus.
Non-enveloped small icosahedral (viruses) viruses.
Small 52-55 nm diameter.
Double stranded DNA virus. Only codes 9-10 genes.
Infect squamous epithelial cells
Mode of transmission for these viruses is either skin-to-skin contact, vaginal, anal
and oral sex.
Most common sexually transmitted infection in UK. However not all HPVs will cause
sexually transmitted diseases.
Usually go away without a treatment.
There are more than 200 genotypes of HPV, about 40 types are sexually transmitted.
They are categorised based on their genotype, so if a new HPV is discovered it would
have to be sequenced and all the differences are on different types of genotypes.
1/ of HPVS are sexually transmitted and There are several different categorising of
HPV within that group.
We can also categorise them based on if they are low risk (do not cause a serious
disease) or high risk (cause cancers).
HPV can cause different lesions, they can form warts, verrucas, genital warts and
cancers.
Because HPV are non-enveloped, they are resistant to environmental factors, so they
can survive for many moths outside a host at low temperatures.
HPV can be associated with: cervical cancer, oral cancer, penile cancer, vaginal
cancer etc.
HPV is usually associated with causing cancers in places where there is a mucus
membrane present, so it infects the mucus membrane.
HPV genome.
HPV has a double stranded DNA genome, which is circular in size.
There are several regions within the genome, E1-E7 genes, are in the early region
and this is based on when these genes are expressed during the infection cycle of
HPV.
Early region genes have different regulatory functions when they enter the
epithelium.
This infection cycle of HPV is closely linked to the differentiation cycle of
keratinocyte.
There is also a late region, there are only two genes expressed here, L1 and L2. These
are both capsid proteins. L1 forms the major capsid protein, so the majority of that.
L2- is the minor capsid protein. L stands for late because they are expressed late in
the infection cycle.
Long control region (LCR)- this is important for controlling viral replication and
transcription.
HPV life cycle.
, HPV infects the basal epithelial cells of the squamous epithelium, this is because
these are the only dividing cells and these are the only ones that are going to divide
and eventually keratinocytes will differentiate from them.
They are the closest ones to the basement membrane and an important factor for
HPV to be successful in infecting is that it needs contact with the basal membrane
for infecting, so therefore some microabrasion needs to happen that is exposing the
basal membrane. And only then can the HPV infection be successful.
So, HPV infection occurs via trauma to the epithelium that exposes segments of the
basement membrane.
And HPV then binds to receptors at the basement membrane and receptors on the
cell surface, so it needs several factors for the attachment and for the infection cycle
to happen.
L1, capsid protein, needs to interact with heparin sulphate proteoglycans.
And it also needs secondary receptors, so it will use extracellular matrix proteins or
other receptors that are available.
This virus is specific, so different types of viruses will be infecting specific tissues, so
one type of virus will only be able to infect a specific type of tissue.
It is a multi-step process, that requires secondary receptors.
Once this attachment is established, the cell will enter the cell via endocytosis.
Through the endosomes it will travel through the trans Golgi network and it will gain
entry into the nucleus at some point.
Because it is a DNA containing virus, and it infects human cells, DNA viruses need
specific enzymes that are provided by host cells. Especially for the replication of their
genomic information, they need the access to the nucleus.
So, some viruses might be able to enter the nucleus through the nuclear pores, so
they will not be dependent on the cell cycle however, HPV does require the
breakdown of the nuclear envelope therefore it needs mitotically active cells.
Therefore, it can only infect the cells that are dividing like basal epithelium cells,
which are mitotically active during mitosis when the nuclear envelop breaks down
this is when it can enter the nucleus.
When it comes to synthesis and assembly, some viruses will stay outside the genome
as episomes so they will not integrate into the genome. But some HPV types are able
to integrate into the host cell genome.
Next step, when the synthesis and replication of the viruses is happening, the
assembly of virions also takes place in the nucleus. Normally we associate this
happening in the cytoplasm, but this particular type of virus is going to assemble the
virions in the nucleus.
When it is released, it happens as the keratinocytes differentiate so they move from
the basement membrane to the top surface of the skin. And the top surface of our
skin is formed of these dead cells, and it does not have an active process of getting
out, but it is released from the dead cells that are shed with the epithelium surface.
HPV infection cycle summarised.
The HPV life cycle very strictly follows the differentiation program of the host
keratinocyte.
So, HPV does need to infect at the basal membrane where there is actively dividing
cells and as it infects initially it was start expressing those early genes.
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