Viral infection and Pathogenesis 1 Flashcards
Methods of breaching the skin to cause infection
Abrasion- pox, papilloma
Bite- rabies
Injection- arbo eg west nile
Local skin infection eg
Papilloma virus -DNA, non enveloped, wide host range
Doesn’t breach BM so no blood supply or imm resp so not elim
Rare to spread towards BM usually spread away as it needs the cell in cell cycle to repl and cells mature and go into cell cycle as they move away from the BM
Major GI tract barriers and eg viruses
Low pH
Proteases
Bile
Rota, parvo, corona, calici, astro
GIT route of transmission
Faeces/diarrhoea eg enteric
Saliva in licking, grooming, biting eg herpes and rabies
Local gut infection eg
Rotavirus rna virus nonenveloped
Infects cells at tips of villi in small intestine that absorb fluid and causes diarrhoea
Villi shorten as preferentialy infects the tips and kills the tip cells which grow back post infection
Major resp tract barriers and eg viruses
Ciliated epi
Mucous lining
Temp
Influenza, rhino, RSV
Local Resp tract infection transmission routes
Saliva
Coughs
Sneezes causing airborne droplets
Local Resp tract infection influences
Less than 5mM persist longer and penetrate deep in lung
Over 5mM cleared from lung
Temp influence as rhinovirus infect cooler regions of upper resp tract whereas RSV infect lower regions of resp tract (warmer regions)
Entry into blood system
Directly eg via arthropod vector or via lymphatics (common route)
Lymphatic spread to blood
Virus traverse epi and exposed to tissue macro can enter lymphatic syst
Carried to local lymph nodes and exposed to further macro at each stage virus may be engulfed, degraded and antigens presented to t cells to initiate imm resp, but some viruses repl inside macrophages eg FIPV, canine distemper, maedi-visna causing incr virus output. Some virions will pass straight through the lymphatics into the blood
Viremia
Presence of virus in the blood. Once in blood can localise to any body part in minutes
Either cell free - FMD, flavi, toga, entero
Or cell assoc; mono (maedi-visna), lympho (CDV), neutro (FeLV), macro (african swine fever)
Cells encountered by virus in blood that determine pathogenesis
Reticulo-endo cells (eg macro)
Vascular endo cells
Virus interaction with RE cells
Maybe phagocyt, sestroyed and presented to imm syst (v efficient so viremia only maintained if virions enter blood as quickly as they are removed)
May res phagocyt causing prolonged viremia
Post phagocyt virus could repl in macro causing incr viremia
Virus interaction with endo cells
Vasc endo is blood-tissue interface and so is barrier for particles eg virions
Parenchymal invasion by virus in most organs dep on localisation of birus in capillary and venule endo cells where barrier is thinnest
Virions can passively transfer accross or may infect endo cells to pass through
Mouse pox description
Dna virus with several hijacked genes from host cells (key virulence determinants)