Lec 6 - Viral interactions with the host Flashcards

1
Q

3 requirenments for successful infection

A
  • sufficient viral particles (shedding)
  • cells at site if infection must be accessbile, susceptible and permissive
  • host antiviral defences must be absent or defective
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2
Q

why could H5N1 have genetic factors in terms of how its spread

A

No large scale person to person transmission as observed in other influenza virus outbreaks.
When virus cirulating, only 3 examples of person to person spread and they all occurred in families. Usually Mother/father to children, but not wife/husband which suggests a genetic component to H5N1 susceptibility.

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3
Q

how can viral replication prevent virus from causing disease

A

Mistakes in viral replication can generate viruses incapable of completing an infectious cycle – particularly true of RNA virus which have no proof reading activity and acquire mutations.

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4
Q

dilution effect of viruses when leaving host

A

sunlight, desiccation, chemical enviornment

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5
Q

what are some viral defences ot hostile environemtns

A
  • some are stable at low pH and protease resistant
    (e.g. GI viruses)
  • if trans by insect vector, then no exposure to environment
  • or by direct phsyical contact
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6
Q

how does systemic infection work

A
  • viral replication at primary site of infection
  • disseminated via blood, lymph, nerves to secondary site
  • more replication
  • virus back into bloodstream
  • more dissemination
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7
Q

diff in incubation period for local infection vs systemic infection

A
  • local = short (e.g. influenza)
  • systemic = long (e.g. measles)
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8
Q

virus entry points

A
  • eyes
  • resp tract
  • GI tract
  • urinal tract
  • sexual transmission
  • skin (not common, via scratch or injury)
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9
Q

why is skin not supportive for viral infection

A

Epidermis:
- dead keratinised cell
- devoid of blood/lymphatics
- products from commensal bacteria = not good for viral growth

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10
Q

what layer of skin can virus infect

A

dermis and subdermal tissue
- highly vascularised

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11
Q

most common route of viral entry

A

respiratory tract

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12
Q

defence mechanisms in respiratory tract

A
  • hairs in nose
  • mucociliary escalator (ciliary, goblet cells)
  • alveolar macrophages in lower resp tract
  • immunoglobulin A (an anitbody in the resp tract that can neutralise some viruses)
  • saliva in throat = goes to stomach, destroyed
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13
Q

what type of virus cant infect GI tract

A

enveloped (Except for coronavirus)
= intesine is alkaline w/ bile salts
so would destroy plasma membrane

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14
Q

what are peyers patches

A
  • small bits of lymphatic tissue in ileum
  • monitor microorganisms and producing antibodies against the antigens in the gut lumen
    = BUT these can act as a ‘portal’ from gut lumen to bloodstream via lymphatic system
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15
Q

what is female urogenital system protected by

A

mucus and low pH

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16
Q

what increases risk of urogenital infection

A

abrasions in mucosal tissue from sexual activity

17
Q

systemic urogential tract infections

A

HIV
hepatitis
herpes simplex

18
Q

how can lymphatic system be involved in systemic spread

A
  • infection of epithelial cells
  • can lead to inflammation of basement membrane
  • lymph capillaries will take up virus into lymph system
  • deposits into GREAT VEIN
  • virus can now be spread systemically
18
Q

local urogential infection

A

HPV

19
Q

why lymphatic system easier for virus to get into

A

lymphatic capillaries more permeable than circc sysem capillaries

20
Q

where does lymph nodes deposit everything

A

great vein

21
Q

process of virus getting into bloodstream via lymphatic sys

A
  • infection at mucosal layer (e.g. skin, resp tract etc)
    -basememnt membrane damaged
  • virus taken up into lymph
  • taken into blood stream (PRIMARY VIREMIA)
  • either stays here OR
  • replicates in another organ
  • then back into blood (SECONDARY VIREMIA)
  • and into another replication site, released somehow
22
Q

what is active viremia

A

virus replicates in a tissue
gets passed into bloodstream

23
Q

what is passive viremia

A

DONT replicate in bloodstream at all
use it as a form of travel almost
to get from inital place to another

disseminated spread

24
Q

what is primary viremia

A

release of small number virions after replicating at an initial site in the bloodstream
(allows spread to seoncdary sites of replciation)

25
Q

what is secondary viremia

A

large number of virus into bloodstream with spread to organs

26
Q

example of passive viremia

A

bunya viruss

27
Q
A