Sexually transmitted infections Flashcards

1
Q

Describe the structure Human Immunodeficiency virus

what is around the virus? what is present on this? important ones?

what is the viral nucleic acid? how many copies?

important proteins (3)

A

Virus has an envelope
Viral proteins are present on the envelope
Important ones are glycoprotein 120 and glycoprotein 41
There are some host cell proteins on the envelope
Viral nucleic acid is RNA
There are two copies of the RNA
Other important proteins include reverse transcriptase, integrase, protease

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2
Q

Describe replication cycle of Human Immunodeficiency virus

what does HIV bind to? what other receptor too?
what viral protein is used for attachment? what then changes shape? effect of this?

now what happens? what is lost?

how does the rna use reverse transciptase? effect of this?

what is made? what does it become? where does it go and what does it do there?

what is the effect of this and what is made? where? where do they go next?

A

HIV binds to the CD4 receptor on cells
Another receptor, the chemokine receptor, is also used
The viral protein used for attachment is the gp120
Then the gp41 changes shape and helps the virus to fuse with cell membrane

Virion enters cell
Loses envelope

Viral RNA is reverse transcribed to DNA
Complementary DNA, cDNA, is made

The cDNA is made into a double stranded copy
This becomes circular
Travels to nucleus
Integrates into host DNA

Viral messenger RNA made
In cytoplasm translated to proteins
Virus capsid made
Some proteins glycosylated
Travel to cytoplasmic membrane
Virus buds off
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3
Q

How does the virus kill cells

what does the virus mainly infect?
what brings attention to TH attention?

what recognise these atnigens?

what is made once recognised? what else is made? what happens to cell?

what speeds up virus replication? outcome of this?

A

Virus mainly infects Thelper cells.
There are cells that function as assistants to Th cells
Antigen presenting cells
They bring the antigen to Th cells attention

The Th cells use molecules on their surface called T cell receptors to touch and recognise these antigens

Once they recognise the antigens they make interleukins IL2
They also make interleukin receptors
The cell is activated

If this cell is infected with HIV and the cell is activated, virus starts to replicate fast.
Virus proteins are made fast
Out come is cell death

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4
Q

Diagnosis of HIV

A
General clinical manifestations
Fever
Lethargy
Malaise
Headache
Sore throat
myalgia
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5
Q

clinical diagnosis (too general)

A
Headache
Other neurological symptoms
Gastrointestinal 
diarrhea
Rash
Urticaria
Loss of hair
Ulcerations in mucocutaneous areas
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6
Q

Lab diagnosis
what is detected? (2)
if positive what do you do?
whats the next test?

A

Fourth Generation HIV test.
Detects HIV antibodies and an HIV antigen p24
If positive, do a second assay to confirm
Then carry out a PCR to look for viral RNA

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7
Q

Learning Objective - Outline the epidemiology of sexually transmitted virus infections

what is distrubution like?
difference over the years?

A

The key point to learn about the statistical data shown is that worldwide there are a large number of HIV infected people.
The number has lowered in the last few years.
You don’t need to remember the numbers.
Remember there are some areas in the world that the incidence of infection is higher.
You don’t need to remember the exact locations.

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8
Q

Herpes simplex virus - durations

3 different phases?
duration of viral shedding?

recurrence - viral shedding? heal?

A

days 0 - 6 = vesicular pustule
days 6 - 12 = wet ulcer
days 12 - 20 = dry crusts

duration of viral shedding = 12 days

FOR RECURRENCE
viral shedding = 5 days
healed = 12 days

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9
Q

Herpes virus - how it works

what happens after the lesion is healed?
what causes a recurrent infection?

A

After the lesions have healed, there is establishment of the latent infection in the dorsal root ganglia innervating the mucosal areas involved in acute infection

The virus is on the skin until it migrates up inside the axon to the dorsal root ganglion. Then, at any time, the virus can start replicating again and migrates back down the axon towards the skin where it causes a recurrent infection

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10
Q

Herpes virus - latency + activation

what is latency?
what is reacrtivation?

A

Latency- Virus replication stops and very few virus proteins are made

Reactivation- There is release of the latent virus from the infected ganglia, this causes infection of the epithelial cells, leading to a recurrent infection, clinical or subclinical.

You can get infected with herpes simplex 1, even if you only have one sexual partner, the more sexual partners the higher the risk of infection with HSV-1.

Some individuals will not have any recurrences, while others may have over 15.

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11
Q

Herpes structure and types

types?
envelope?
size?
seen under light microscope?
what is inside the envelope? what is made of? structure?
what is between this and the envelope?

describe the virus

A

There is a herpes simplex type 1 and type 2.

They are enveloped and around 120-300nm in size.

They cannot be seen under a light microscope.

There is a nucleocapsid inside the enveloped structure and the nucleocapsid is made of capsomeres.

The nucleocapsid has an icosahedral structure.

In between the nucleocapsid and the envelope there is the tegument.

The virus is a double stranded DNA virus, the DNA is linear and codes for more than 70 polypeptides.

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12
Q

Herpes diagnosis

lab based apporach

A

based on symtoms

lab based = take a swab and use the sample for pcr amplification of the viral dna

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13
Q

Herpes viral infection

where does it attach?
what fuses?
what enters cell and what is lost?
where does it go? what happens here? what is made?

what happens in the cytoplasm? what goes from here to the nucleus?
what happens to these and where do they go next?

A

Attachment to cell epithelial
Use of specific receptors. Which one uncertain.
Fusion of viral envelope with cell envelope.
Penetration
Lose envelope in the process
Nucleocapsid enters cell
Transport of the nucleocapsid through the cytoplasm to the nucleus
Viral DNA released in the nucleus
Viral DNA becomes circular
Replication of viral DNA in the nucleus
mRNA generated
The translation process takes place in the cytoplasm
Viral capsids assemble in the cytoplasm
Capsids transported to the nucleus
DNA packaged into empty capsid
Nucleocapsid containing DNA buds through the inner lamella of the nuclear membrane
Virus egress through the cell

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14
Q

Papillomavirus

structure?
enevlope?
genome?
what does it lead to? what is available for this?

A
Non enveloped - Icosahedral
DNA genome -circular genome
Family Papovaviridae
Vaccination programme available 
Cervical cancer
diagnosis = clincial and lab based

Papilloma virus infection is common in the population and not everyone infected will show symptoms

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15
Q

Papillomavirus - clinical course

how long can it incubate for?
how long is active growth and host containment?

what can the patient end up with?

A

The clinical course of the disease is as follows, it can incubate for a many months until the first lesion appears. ( 1 - 8 months)

There is then active growth and host containment of the disease, it then moves into late stage. (3 - 6 months)

Patient can end up with sustained clinical remission or persistent or recurrent disease.

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16
Q

Hepatitis B virus - structure

what are incomplete particles?
where can they be found?

A

The complete viral particles are 42nm, however not all particles are the complete virus.

The incomplete particles are surface antigen proteins (so lack a core) and can be found in serum of infected individuals.

17
Q

Clinical and epidemiologic features of hepatitis B

incubation? mean?
age preference?
transmission? (3) what can it not be?

A

Incubation (days) – 35 to 150, mean is 75
Onset can be insidious or acute
Age preference is young adults, babies and toddlers
Transmission can’t be foecal-oral
Transmission can be percutaneous (e.g. needles), perinatal (from mother-baby), or sexual

Occasionally severe -> 0.1-1% of cases
Fulminant in 5% of cases
Chronicity is unpredictable, 0.1%-30% chance
Carrier (+neonatal infection)
Resulting in cancer, 0.5-2%
18
Q

Diagnosis of hep B

3 ways?

A

Look for viral antigens in serum
Test for antibodies to viral proteins
Look for viral DNA in the serum

19
Q

hep B transmission

main contributors?
what has caused infections to go down?

A

Transmission as stated earlier could be through, heterosexual activity, transfusion or dialysis, homosexual activity, health care employment, household contact, intravenous drug use or unknown.

Sexual contact and intravenous drug use are main contributors.

There are some high risk areas of the world for Hep B, including Africa, Indonesia

Hep B immunisations (as well as introduction of testing and treatment) have caused the number of infected cases going down.