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Immune and lymphatic system > Diverse world of viruses > Flashcards

Diverse world of viruses Flashcards

1
Q

How much does the common cold cost the UK’s economy each year?

A

£14 billion, it is 33% of the reasons for sickness and absence

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2
Q

Which pathogens can cause common cold?

A

Influenza, parainfluenza, respiratory syncytial viruses, metapneumoviruses, coxsackie viruses, entero-viruses, adenoviruses, coronaviruses and rhinoviruses

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3
Q

Which mosquito transmits Zika?

A

Aedes

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4
Q

Why is it important to learn about Zika?

A

In 20 years, temperatures rising mean that areas in the south etc will become habitable for the mosquitos

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5
Q

How is herpes transmitted?

A

Via type I or II herpes simplex virus

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6
Q

How is type I HSV transmitted?

A

Oral contact - oral-genital contact can transmit to genitals

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7
Q

Symptoms of type I HSV infection

A

Infection around mouth

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8
Q

How is type II HSV transmitted?

A

Sexually

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9
Q

Symptoms of type II HSV

A

Genital infection

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10
Q

How do you get secondary herpes?

A

Immunosuppression predisposes you to get infected with other pathogens

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11
Q

What is herpes simplex keratitis?

A

Secondary herpes leading to corneal infection

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12
Q

Symptoms of HPV

A

Genital and planar warts and cancer

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13
Q

How does HPV cause warts to form?

A

Infects keratinocytes on skin

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14
Q

Symptoms of HPV types 6 and 11

A

Verrucous carcinoma of genitalia

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15
Q

What does herpes simplex encephalitis result in?

A

Cerebral dysfunction

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16
Q

How is HSE transmitted?

A

Trigeminal or olfactory nerve transmits it from periphery to brain

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17
Q

How does the lipid envelope form?

A

A viral particle exits a host cell. It tears off part of the cell membrane and ‘cloaks’ itself with it

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18
Q

What are naked viruses?

A

Don’t steal cell membrane - they burst out of cell

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19
Q

How do makes viruses attach to subsequent cells?

A

Displaying viral proteins on capsids (capsid spikes)

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20
Q

What do the pre-translated proteins in the capsid of a virus do?

A

Aid virus to infect subsequent cells

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21
Q

What shape is influenza?

A

Helical

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22
Q

What shape are rhinovirus and adenovirus?

A

Icosahedral

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23
Q

How many sides does an icosahedral bacterium have?

24
Q

What 3 shapes can viruses be?

A

Helical
Icosahedral
Complex

25
Q

What are the four phases of viral replication?

A

Attachment
Penetration
Uncoating and synthesis
Assembly and release of new viruses

26
Q

What happens when viruses attach to host cells?

A

Virus particle attaches to cell surface. Viral proteins responsible for binding form either projections (glycoprotein spikes/fibers) or depressions in the virus’ surface

27
Q

What happens when viruses penetrate cells?

A

Virus penetrates cell by either fusing with cell membrane or by priming the host cell signaling pathway leading to endocytosis

28
Q

What happens during the uncoating and synthesis stage of viral replication?

A

Shell of capsid disintegrates and reverse transcriptase turns RNA into DNA. Viral DNA transported to nucleus where integrase integrates HIV DNA into host’s DNA. The host’s normal transcription machinery transcribes HIV DNA into multiple copes of new HIV RNA

29
Q

What happens when new viruses are assembled and released?

A

Some of replicated RNA becomes genome of new viruses, whilst the cell uses other copies of RNA to make new HIV proteins. New viral RNA and HIV proteins move to cell surface where immature HIV forms. Finally, virus is released from cell and protease cleaves newly synthesized polyproteins to create mature infectious virus

30
Q

What is classification?

A

Arranging organisms into taxonomic groups according to their observed similarities

31
Q

What are the categories of the Linnaean hierarchical system?

A 
Domain
Kingdom
Phylum
Class
Order
Family
Genus
Species
32
Q

How does the Baltimore classification group viruses?

A

According to how mRNA is produced during replicative cycle of virus

33
Q

What is the positive strand of DNA identical to?

34
Q

How did viruses used to be categorised?

A
  • Associated disease
  • Type of disease caused
  • Sites in body affected
  • Place where they were first isolated
  • Scientists who discovered them
  • Common cultural perceptions
35
Q

What is the overall aim of viruses in a host cell?

A

Produce mRNA and translate that mRNA using the host cell’s ribosomes

36
Q

Genomic material of class I viruses and how they replicate

A

Double stranded DNA viruses (e.g. HPV, herpes). Class I viruses transcribe DNA into mRNA using RNA polymerase and that mRNA is translated into proteins

37
Q

Genomic material of class II viruses and how they replicate

A

Single stranded DNA, can be positive or negative strand (e.g. adeno-associated viruses). To replicate, they use DNA polymerase to form double stranded DNA molecule. This is transcribed using RNA polymerase into mRNA, which is translated into proteins

38
Q

Genomic material of class III viruses and how they replicate

A

Double stranded RNA (e.g. reoviruses). Positive strand acts as mRNA, which is translated into proteins

39
Q

Genomic material of class IV viruses and how they replicate

A

Single stranded RNA (positive strand), e.g. SARS/ Hep A and hep C. However, must replicate genomic material for daughter cell. Replicate by using RNA dependent RNA polymerase to replicate ssRNA+ into ssRNA-. ssRNA- used as template by RNA dependent RNA polymerase to produce another strand of ssRNA+. When enough ssRNA+ produced, goes to ribosome to be translated into proteins

40
Q

Genomic material of class V viruses and how they replicate

A

Single stranded RNA (negative strand), e.g. influenza/ebola. Use RNA dependent RNA polymerase to produce ssRNA+, which is then turned back into ssRNA- which goes ribosomes to make protein

41
Q

Genomic material of class VI viruses and how they replicate

A

Single stranded RNA positive diploid (e.g. HIV). Diploid = contains 2 copies of the ssRNA+. To replicate, they use reverse transcriptase to produce DNA. This makes a DNA/RNA hybrid. RNA disintegrates (unstable). Single DNA strand left, which is duplicated by DNA polymerase to produce dsDNA. DsDNA inserted into host genome using integrase, which is transcribed into mRNA using RNA polymerase

42
Q

Genomic material of class VII viruses and how they replicate

A

Gapped dsDNA (e.g. Hep B). Part of genome is double stranded and part is single stranded. To repair gaps, they use DNA polymerase to form dsDNA. DsDNA undergoes transcription to produce mRNA which is translated to protein.

43
Q

Why is it important to make more class VII molecules using reverse transcriptase?

A

There wouldn’t be enough genetic material for daughter viruses

44
Q

Why do viruses have a high mutation rate?

A

Flu viruses change through small genetic changes that are passed down to daughter generations through ‘reassortment’. This mixes larger genetic segments from several viral strains to create a new virus. This causes antigenic variability

45
Q

What is antigenic drift?

A
  • Mutations accumulate - protein structure is changed so antigens are different and antibodies can’t bind
  • New vaccines must be developed frequently
  • Vaccines made in advance working on prediction - may not always be accurate
46
Q

What is antigenic shift?

A
  • Viruses present in two different species
  • Infect a ‘mixing vessel’ - can have multiple viruses from different species
  • When in mixing vessels, the two viruses exchange large amounts of genetic materials (reassortment)
  • This culminates in creation of new viruses which are new to original organism’s immune system
47
Q

What does Saquinavar target?

A

Protein synthesis

48
Q

Molecular base of Saquinavar

A

In HIV, mRna is translated into inert poly proteins. Viral protease then cleaves them into functional proteins during budding of the virus from the host cell. HIV protease inhibitors prevent this

49
Q

Indications for saquinavar use

A

HIV infection, in combination with other retroviral drugs

50
Q

What does acyclovir target?

A

Nucleoside analogue

51
Q

Molecular base of acyclovir

A

Phosphorylated to the monophosphate by a viral enzyme (thymidine kinase) only in cells infected with HSV or VZV, which provides selectivity, then further phosphorylated by cellular kinases to acyclovir triphosphate. This competes for the viral DNA polymerase, becomes incorporated into the growing viral DNA chain and terminates it

52
Q

Indications for acyclovir use

A

Systemic and topic treatment of HSV. Systemic treatment of varicella zoster
Prevention of recurrence and prophylaxis in immunocompromised

53
Q

Target of amatadine

A

Viral uncoating

54
Q

Molecular basis of amatadine

A

Blocks an ion channel which is formed by membrane protein of influenza A, thus preventing viral uncoating within cell

55
Q

Indications for amatadine use

A

Prophylaxis and treatment of influenza A

Immune and lymphatic system (27 decks)

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