Viral Persistence 2 Flashcards
Imm tolerance as mech for persistance BVD eg
Normally a trivial acute disease lasting a few days
In utero can result as persistant infection resulting in mucosal disease charac by high mortality low morbidity rates, spec imm tolerance and immsuppression first clinically recog in herd by fever anorexia watery diarrhoea and erosive stomatitis
Outcome dep on infection time, non pregnant causes BVD. Pregnant cause dam to foetal transmission due to high freq transplacental spread outcome of infect dep on period of gestation of infection
Outcomes of in utero BVD infection
Pre 100d result in destructive lesions and growth retardation of organs and tissues normally causing abortion or mummification
100-150d during imm dev can affect organogenesis of the eye and cns. Surviving calves tolerised to viral antigens so dont mount spec imm resp so persistant tolerant ibfection. Calves remain sero-ve and shed large amounts of infectious virus in all body secr and excr and are very efficient at transmitting to suscept cows. High prob of dev mucosal disease and dying
Post imm dev/post approx 125d may result in some pathological dan but animals mount an imm resp and completely clear virus
Latent infection of herpes
In lymphoid cells for beta and gamma herpes. And in nervous syst for alpha
Latent alpha herpes eg BHV1
Primary ibfection usually early in life and causes mild illness, following initial repl in muc tissue it enters periph nerve endings and travels by retrograde axonal transport up axon to berve body. There it establishes a transient productive infection before subsiding into latent state where it remains prod no virus until it is induced to reactivate by some ext stimuli where react virus travels down axon and causes vesicular eruption at site innervated by the axon (site of initial infection. React or recrudescence is typical of a latent infection
What can reactivate latent alpha herpes virus
Uv light
Menstruation
Stress
Gamma herpes EBV latency eg
Establish latent infection in b lymphocytes. 2 patterns of latent gene expression described: latency 1 and latency 3
3 can be targetted by cytotox t cells regulating level of latent infection
All have EBNA1 like pro that tethers the virus genome to host chromosomes ensuring virus is passed to progeny cells
React during immsuppression showing importance of imm syst in maintaining latency
TSE
Eg scrapie Bse Kuru Cjd Agent not a classical virus beleived to be an infectious pro 'prion' theory some still beleive in existence of virus theory implying some nucleic acid pro complex
TSE prion pro
Prion pro exists as normal pro of cells eg neurons as PrPc
Scrapie infected contains aberrant prion pro PrPsc which is largely protease res and less soluble
PrPsc catalyse more PrPc to change to PrPsc. Complexes can emerge in cns producing scrapie assoc fibrils They have the same aa struct but diff 3D shape
PrPc req for dis, if no PrP gene then they are res
TSE prion pri entry
Via abrasion or orally
DC implicated as transporter of infection to spleen where amplification occurs
Time to cns varies with strain can be less than 150d or more than 350d
Diff species also extends time
Some sheep scrapie res due to diff aa at certain position in gene: british sheep scrapie plan
