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Phase 2a - ICS > Viruses > Flashcards

Viruses Flashcards

1
Q

Viruses that cause miscarriage and birth defects

A

Cytomegalovirus
Varicella Zoster Virus
Herpes Simplex Virus
Rubella

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2
Q

Viruses that cause outbreaks

A

Influenza
Measles
Mumps
Norovirus
SARS-CoV-2

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3
Q

Viruses that cause CA

A

EBV = lymphoma
Hep B/C = hepatocellular carcinoma
HPV

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4
Q

Key point 1

A

Viruses are a common and significant cause of human disease globally, and nationally in the UK

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5
Q

Viruses can be seen under what?

A

Electron microscope

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6
Q

Size of viruses

A

They range in size from 20nm to 260nm.

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7
Q

Definition of a virus

A

An infectious, obligate intracellular parasite

Comprising genetic material
(DNA or RNA) surrounded by aprotein coat and/or a membrane.

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8
Q

Do viruses have cell wall?

A

No - Bacteria does.

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9
Q

Do viruses have organelles?

A

No - Bacteria does.

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10
Q

Do viruses have DNA and RNA?

A

No - Bacteria does.

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11
Q

Are viruses dependant on host cell?

A

Yes, Bacteria is not.

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12
Q

Are viruses alive?

A

No - bacteria is.

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13
Q

What are the different shapes of viruses?

A

Helical - influenza

Icosahedral - adenovirus

Complex

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14
Q

True or false?

A

Virions can exist outside of a host for a variable amount of time (depending on the virus and the environment), but cannot replicate unless they are within a host.

True.

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15
Q

Virions consist of:

A

Genetic material (DNA or RNA).
Protein coat (capsid).

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16
Q

Viruses can be enveloped and non-enveloped:

A

Enveloped: influenza, HIV

Non-enveloped: adenovirus and parvovirus.

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17
Q

Key point 2

A

Viruses are very small, and consist of genetic material surrounded by a protein coat.

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18
Q

What do viruses need to replicate?

A

Viruses require a cell and it’s machinery in order to replicate.

19
Q

Viral attachment:

A

Viral and cell receptors viruses need specific receptors to attach to cells and enter cells- this dictates the type of cells that viruses can infect. e.g. HIV (gp120 and CD4 receptor on T cells).

20
Q

Viral cell entry:

A

Uncoating of virion within cell. Only central viral ‘core’ carrying the nucleic acid and some associated proteins enter host cell.

21
Q

Virus and host cell interaction and replication:

A

Migration ofgenome tocell nucleus.

Transcription to mRNA using host materials.

Use cell materials (enzymes, amino acids, nucleotides) for their replication; subvert host cell defence mechanisms.

22
Q

What do viruses use to interact and replicate with the host cell?

A

Host ribosome.

Host nucleotides and host enzymes and AAs.

23
Q

What does the translation of viral mRNA produce?

A

Structural proteins.

Viral genome.

Non-structural proteins: enzymes.

24
Q

Assembly of a virion.

A

Occurs in different locations depending on virus:

-Nucleus (e.g. herpes viruses)
-Cytoplasm (e.g. poliovirus)
-At cell membrane (e.g. influenza virus).

25
Types of release of new virus particles:
1. Bursts out - cell death (i.e. rhinovirus). 2. Budding/exocytosis - HIV, influenza.
26
Key point 3
A virus is completely dependent on its host cell’s machinery to replicate.
27
What are the ways viruses can cause disease?
1. Direct destruction host cells. 2. Modification of host cell. 3. Over-reactivity of immune system. 4. Damage through cell proliferation. 5. Evasion of host defences. Viruses cause disease through multiple methods!
28
Example of direct destruction of host cells:
Poliovirus - host cell lysis and death after a viral replication period of 4 hours. (Lysis of neurones = paralysis).
29
Examples of modification of host cells:
Rotavirus (resistant to acidic pH) - atrophies villi and flattens epithelial cells. - decreases small intestine SA - nutrients including sugar is not absorbed - hyperosmotic state -profuse diarrhoea
30
Examples of over-reactivity of immune system:
Hepatitis B - destruction of hepatocytes. - jaundice - pale stool - dark urine - RUQ pain - fever and malaise - itching In chronic HBV, there is sustained viral replication and liver cell destruction but at a lower level, therefore fewer clinical symptoms.
31
Examples of damage through cell proliferation:
HPV - cervical CA - Acquisition through contact - Partial viral replication and expression of some HPV proteins - Continuous expression of oncoproteins causing cellular DNA mutations. - Dysplasia and neoplasia - Local and metastatic spread.
32
HPV and CA formation
HPV associated with cervical, penile, anal, vaginal, vulval and head/neck cancer HPV (types 16 or 18) infection of suprabasal layer. Partial viral replication including transcription and expression of several early viral gene products. Gradual movement of basal cells to mucosal surface through natural wear and tear. At some point the HPV genome may become integrated into the host cell chromosome. Mutagenic agents (eg nicotine) may increase the chance of this happening. Following integration, control of viral gene expression is lost and the HPV E6 and E7 proteins may be expressed. Two cell growth and proliferation suppressor proteins, Rb (retinoblastoma) and p53 are prevented from operating. Excessive cell growth and proliferation occurs and cervical cell carcinoma results.
33
Example of evasion of host defences at cellular level:
- Latency (herpesviridae) After primary disease, virus not detectable but viral DNA lies latent and can reactivate, particularly at times of lower immune control (illness/immunosuppression/advancing age) Nerve root ganglion (VZV) Lymphoid cells – T cells, B cells, NK cells (HHV-8) Myeloid cells – monocytes, macrophages, neutrophils, basophils, eosinophils etc (HHV-6)
34
What is the primary and reactivation diseases called by VZV?
Primary = chickenpox Reactivation = shingles/herpes zoster
35
Evasion of host defences, cell-cell spread:
Measles, HIV. Direct cell to cell spread has multiple advantages Avoids random release into the environment Increased speed of spread within tissues Avoiding immune system
36
Evasion of the host defences - molecular level:
Antigenic variability: influenza, HIV, rhinovirus. Ability to change the surface antigens in order to evade the host’s immune system. Explains: - how a host can be re-infected with the same virus e.g. common cold - why with influenza vaccination is required annually, as each season a different viral strain is circulating.
37
Evasion of host defences - prevention of host cell apoptosis.
Herpesviridae. In response to a viral infection, many cells undergo apoptosis, which reduces the amount of virus released from the cell Prevention of host cell apoptosis allows the virus to continue replicating within it, so more virus is produced and then released. It also has an essential role into how some viruses are oncogenic (cancer causing).
38
Evasion of host defences - downregulation of interferon and other intracellular host defence proteins.
If interferon synthesis is stimulated, this activates the antiviral state in neighbouring cells. When this is blocked = neighbouring cells are susceptible to infection.
39
Evasion of host defences - interference with host cell antigen processing pathways.
Herpesviridae, measles, HIV.
40
Key point 4.
Recognising how viruses cause disease allows us to: 1. Understand transmission and natural history 2. Know who is most at risk 3. Develop treatments and “preventative” drugs
41
Key point 5.
Viruses vary wildly in the range of clinical syndromes they can cause, due to: - Different host cells and tissues that they can infect - Different methods of interaction with the host cell.
42
Herpes simplex virus:
Skin: Orofacial herpes, Genital herpes, Herpetic whitlow, Erythema multiforme, Herpes gladiatorum Visceral: Oesophagitis, Pneumonitis, Hepatitis CNS: Meningitis, Encephalitis, Transverse myelitis Eye:Conjunctivitis, Keratitis
43
JC virus (Human polyomavirus 2; John Cunningham),
CNS: Progressive multifocal leukoencephalopathy
44
What are diagnostic techniques for viral infections?
PCR Serology Histopathology Electronmicroscope

Phase 2a - ICS (43 decks)

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