Lec 6 - Viral interactions with the host Flashcards
3 requirenments for successful infection
- sufficient viral particles (shedding)
- cells at site if infection must be accessbile, susceptible and permissive
- host antiviral defences must be absent or defective
why could H5N1 have genetic factors in terms of how its spread
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.
how can viral replication prevent virus from causing disease
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.
dilution effect of viruses when leaving host
sunlight, desiccation, chemical enviornment
what are some viral defences ot hostile environemtns
- 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
how does systemic infection work
- viral replication at primary site of infection
- disseminated via blood, lymph, nerves to secondary site
- more replication
- virus back into bloodstream
- more dissemination
diff in incubation period for local infection vs systemic infection
- local = short (e.g. influenza)
- systemic = long (e.g. measles)
virus entry points
- eyes
- resp tract
- GI tract
- urinal tract
- sexual transmission
- skin (not common, via scratch or injury)
why is skin not supportive for viral infection
Epidermis:
- dead keratinised cell
- devoid of blood/lymphatics
- products from commensal bacteria = not good for viral growth
what layer of skin can virus infect
dermis and subdermal tissue
- highly vascularised
most common route of viral entry
respiratory tract
defence mechanisms in respiratory tract
- 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
what type of virus cant infect GI tract
enveloped (Except for coronavirus)
= intesine is alkaline w/ bile salts
so would destroy plasma membrane
what are peyers patches
- 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
what is female urogenital system protected by
mucus and low pH
what increases risk of urogenital infection
abrasions in mucosal tissue from sexual activity
systemic urogential tract infections
HIV
hepatitis
herpes simplex
how can lymphatic system be involved in systemic spread
- 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
local urogential infection
HPV
why lymphatic system easier for virus to get into
lymphatic capillaries more permeable than circc sysem capillaries
where does lymph nodes deposit everything
great vein
process of virus getting into bloodstream via lymphatic sys
- 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
what is active viremia
virus replicates in a tissue
gets passed into bloodstream
what is passive viremia
DONT replicate in bloodstream at all
use it as a form of travel almost
to get from inital place to another
disseminated spread
