Intro to viruses Flashcards
Why are viruses considered to be intracelluar obligate parasites
- They depend on the host cell for raw materials and energy.
- They can only replciateom host cell
- They exist as either an extracellular virion containing DNA or RNA virus genome
- or as nucleic acid inside the host cell.
What is the general structure of viruses
- always contained in capsid: protects nucleic acid
- some viruses have an envelope: take part of the cells plasma membrane (smart things)
- makes it easier for it to infiltrate a human cell
- a bit like a trojan horse
How do we classify viruses
Hard to do so,
but we use baltimore’s classification (this is based on nucleic acids and how they transcribe mRNA
What are the steps of virus lifecycles
pssst there’s 12
2.Adsorption
- have specific glycoprotiens, which interact with specific proteins on the cell
- for example EBV is only specific for b cells
- Entry
- can directly fuse with plasma membrane
- or via endocytosis
- Capsid transport to the nucleus
- Transcription
- Translation
- Replication
- needs to replicate new viral proteins, like capsid proteins, so new nucleic acids can be encapsulated for new virions
- Capsid assembly
- Glycosylation
- Glycoprotein export to the cell surface
- Endocytosis of glycoprotein-containing plasma membrane
- Envelopment
- Virus release
Influenxa
Describe the structure of influenza
- it’s a segmented negative sense single stranded RNA virus
- its a segmented virus
- it has 8 segments
Influenza
How does being segmented help influenza
- gives it an advantage
-Why? - each segment codes for 1 or 2 proteins
- for example RNA polymerase which will help turn the negative sense genome into a positive sense to make proteins
Influenza
What are the three types of influenza
not really like scientfic names, think broad
A
The one that causes pandemics (infects humans, pigs, birds, horses)
B
the one that causes easonal epidemics (only infects humans)
C
The one that causes mild resiportiry illness (only humans and pigs)
Influenza
How do we divide influenza
it;s based on viral proteins
- Haemagglutinin (H1 – H18)
- Neuraminidase (N1 – N11)
we can class them as avain, swine or other types of influenza
Influenza
How does influenza get into target cells
- influenza interacts with the cell surface to help the virus enter the cell
- in humans the virus can interact with alpha 2,6 sialic acid which is found in the airway epithelium
Influenza
Influenza is a acute virus
what does this mean?
-once you get it, you make antibodies
-these neutrailsing antibodies block the interaction between the haemagglutinin and the cell surface
Influenza
Why do we get infected a lot with influenza
-its because its an RNA virus
-RNA viruses really unstable,
-can get mutations really quickly
What is meant by antigenic drift
- Everytime influenza replicates,
- there’s no proofreading
- so it will accumulate mutations
- the mutations can make be meh, great or bad
- small changes happen in the genes over time, as the virus replicates
- These mutaions accumulate over time.
- Eventually this will generate proteins no longer recognised by the immune system
- so the mutations alter epitomes in haemagglutinin so that neutralsing antivodies no longer binds
Influenza
Why does influenza mutate so much
- RNA viruses must replicate their genomes using RNA polymerase
- RNA polymerase lacks the proofreading ability (DNA polymerase does have this ablity thoughO
- RNA viruses mutate more than DNA viruses
- RNA viruses can alter antigenic epitopes targeted by the immune system.
How does antigenic drift result from replication errors
- In vitro, a single cell infected with poliovirus can yield 10 to the power of 5 virus particles
- In vivo, an HIV-infected person may produce 10 to power of 9 virus particles/day
Basically you make bare viruses each day
What is antigenic shift
-causes a major change in influenza A viruses
-makes new haemagglutinin/or new neuraminidase proteins
-this makes new influenza A subtype
-influenza A has a segemnted genome, so if you get an infection of one cell with two different virusese,
-there can be swap RNA segements between the different viral strains
-results in creation of new virus with new proteins
-therefore you have no cross protective immunity to the virus
-which can cause a pandemic
How does antigenic shifts happen
-there’s a less chance that birds will pass on influneza to humans because of the different places the alpha 2,3 SA recpetor are (humans at base of lungs, birds high up respiratory tract)
Pigs however,
this flashacrds needs helppp
Hepatitis B virus
How many peopel around the world have a HBV infection
2 billion people have HBV infection
Hepatitis B virus
Describe the structure of hepatitis B virus
- tiny virus
- genome partly DNA and RNA
- there are 8 genotypes
Hep B
How is Hep B transmitted
- Perinatal transmission (mother to child at birth)
- Parenteral transmission (blood, blood products)
- Needlestick injury, tattooing, piercing
- Sexual
- Infected body fluids (saliva, menstrual, vaginal, seminal fluids)
- Medical/surgical/dental instrument
Hep B
Who is most at risk of contracting Hep B
- Health care workers
- Men who have sex with men/people who have multiple sex partners/sex workers
- Blood transfusion recipients
- I.V. drug users
- Infants of HBV carrier mothers
- Recipients of solid organ transplants
Hep B
Describe the Hep B virus incubation period, severity, chronic infection
the incubation period
-is between 30-180 days (av is 75 days)
Acute
-usually mild, but 30-50% of adults can present with jaundice and hepatitis
Chronic
can be chronic
Severity
-can be asympotamatic to fatal
Hep B
Acute hepatitis
Chronic Hep B
Hepatitis C
Is there a cure for Hep C
-there’s a cure for hep C
-but there’s no vaccine
Hep C
Describe Hep C and how it infects our cells
- small virus
- their envelope glycoproteins are small, so not efficient enough to interact with the cell surface
- so a small virus like this needs to overcome electrostatic forces to get to the cell
- but hep c isn’t great at that
- so hep c said WHERE THERE IS A WILL THERE IS A WAY
- and that WILL was these low-density lipoproteins
- these proteins can overcome the electrostatic forces of the cell
- which allows hep c to be in close contact with the cell, so that it can get in
Hep C
How is Hep C transmitted
it’s bloodborne
- Injecting drug use/sharing injection equipment
- Reuse or inadequate sterilization of medical/surgical/dental equipment (esp syringes/needles)
- Transfusion of unscreened blood and blood products
- Sexual practices that lead to exposure to blood
- Perinatal transmission (mother to child at birth) → less common
What is the incubation for Hep C
2 weeks to 6 months
What symtoms of an acute infection
80% are asymptomatic
20% have
-fever
-fatigue
-decreased appetite
-nausea
-vomiting
-abdominal pain
-dark urine
-joint pain
-jaundice
Hep C
How severe is Hep C
it can be asymptomatic to fatal
Hep C
How does the chronic infection affect people with Hep C
some people chronically imfected will develop cirrhosis and/or liver cancer
this happens to about 20-30% of people
How do we test/diagnose hep C
- You can do antibody testing (for historical infection)
- Viral nucleic acid testing (it can tell you there’s a current infection)
- At the beginning there’s lots of virus replication
- if they are reactive, then the hep C virus is present → this means there is HCV
- once it reaches threshold, symptoms will begin
- but it takes long for antibodies to develop
- if they are then there is no HCV infection, cant see RNA
Why is there not a vaccine that is immune against Hep V
there are many genotypes that are in different parts of the world
Herpesviruses
How would we describe the structure herpesviruses
DNA virus in envelope
there’s 8 herpes viruses
How do herpes viruses infect people
herpes viruses are masters of invading the immune system
- they have proteins that inactive the inate immune system
- this allows for enough time to get into the cell, go to the neuclus , reprogramme and then replicate
How do herpes viruses transmit
-Herpes infections are most contagious when symptoms are present
-can be transmitted oral to oral contact (HSV-1)
- genital to genital contact (HSV-2);
- oral to genital (HSV-1/2)
- via sores, saliva, surfaces in or around the mouth/genitals
Are herpesviruses symoptamatic, asymptomatic
Most oral and genital herpes infections are asymptomatic.
What’s the lifecycle of a herpes simplex 1 virus
Lytic virus
-infect mucoepithelial cells
-they replicate in the cells
-they then release the virus
But then they become latent
-this is immunological silent infection
-they then re-activate
-they replicate in the cells
-and then release
when a virus is latent it means they will stay with us forever
Where do simplex viruses go latent
- they go latent in trigeminal ganglion
- and HSV 2 goes in the sacral ganglia
What does neurovirulence mean
- Invade and replicate in the CNS
- Profound disease
- Severe neurologic devastation
- Meningitis/encephalitis
How does the virus spread when latent
when the immune system is preoccupied, they take their chance
Who does VZV effect
- Infants
- Adolescents
- Adults
- Pregnant women
- People with HIV/AIDS or cancer
- Patients who have had transplants
- People on chemotherapy, immunosuppression, long-term steroids.
What are the complications of VZV
aka chickenpox
Serious complications from chickenpox include:
- Bacterial infections of the skin and soft tissues, including Group A
streptococcal infections (Necrotising faciitis)
- Pneumonia
- Encephalitis, cerebellar ataxia
- Haemorrhagic complications
- Sepsis
is there a cure of VZV
there’s a vaccine
Cytomegalovirus infection
How do we transmit cytomegalovirus infection
via body fluids, urine, breast milk sexual, blood proudcts, organ donations, bone marrow
Cytomegalovirus infection
Is the infection symptomatic
usually its asymptomatic
but it can sometimes be symptomatic: can cause fevers, mononucleosis, hepatitis
Cytomegalovirus infection
What can happen in utero
You can get infections in mutiple body systems
like pneumonia, hepatitis, encephalitis
Epistein Barr virus
How is it transmitted
Salvia (via kissing)
Epistein Barr virus
Tell me about the primary and secondary infection
incubation peroid, sympyoms, where it replicates, who it affects
usually asymptomatic
has a 4-7 week incubation period
replicates in oropharengeal epithelial cells and B cells
happens during childhood
about 95% of people have it during adulthood
Symptoms, delayed infection can cuase glandular fever
-fever, pharyngitis, swollen lymph nodes, hepatitis
Epistein Barr virus
Where does it become latent
In B cells
expresses viral proteims, non codingmRNA,
Epistein Barr virus
EBV has a complication, what is it
EBV can cause a whole bunch of virus associated maligances
-B cell maligances (hodgkins lymphoma)
-epithelilal cells malaginices
T and NK cell maligancies
Epistein Barr virus
What is EBV complaications are associated with those that are immunocomprimised
Hodgekins lymphoma (post transplant)
-pneumonia, hepatitis (post transplant disease)
-Burkitt lymphoma, diffuse large B cell lymphoma (EVB and HIV related lymphoas)
What type of sarcima is associated with herpesviruses
not mentioned in lecture, but on slides
Kaposi sarcoma
latenxy in B cells and endoletjlail cells
