Morbillivirus

1. Morbillivirus • Rinderpest –

2. Newcastle Disease

3. Newcastle Disease

4. Pathogenesis – special affinity for epithelial cells of the URT, GIT and both T and B lymphocytes • Replicates in tonsils and l.n. mandibular and pharyngeal l.n. • Viremia 2-3 days after which

6. rinderpest

7. Rinderpest

8. Rinderpest

9. Rinderpest

10. Rinderpest • Lung lesions

11. Rinderpest • For few that survive, solid immunity • Routine vaccination • Only one antigenic type – totally different from foot and mouth – 7 types • Reduced incidence of disease – VACCINATION

12. Genus PneumovirusBovine Respiratory Synctial Disease • Extremely fragile – cannot even freeze specimen • Mild to severe respiratory tract disease • Cattle and sheep • Worldwide • Etiologic agent – Bovine Pneumovirus • High morbidity, low mortality • 2nd bacterial infections increase severity of the disease • Contribute to Shipping Fever • Independently not major problems • Clinically – not pathognomonic

13. Bovine Respiratory Syncytial Dz. • Diagnosis – isolation difficult • FA staining of lung lavage • Gross and histopath • Paired serum samples – VN and ELISA • Control – inactivated and modified virus vaccines

14. Orthomyxoviridae - hemagglutination • Avian influenza virus – proventriculus • Genera – Influenzavirus A – pathogens for humans, horses, fowl, mink, seals and whales • Classification – • Type or species – based on antigenic characteristics of ribonucleoprotein RNP and matrix protein – M1 • Subtypes – based on the two enveloped proteins, hemagglutinin and neuraminidase • 1. HA/H – Hemagglutinin – bind to sialic acid moietites of a glycoprotein or glycolipid receptors on cell surface – ABs to HA proteins neutralize infectivity of virions

15. 2. Neuraminidase – NA – enhances pinching off and release of virions by destroygin sialic acid receptors on the cell membrane which would otherwise recapture the progeny virions and hold them at the cell surface • Abs to NA decrease the amount of virions released from the infected cells • DO NOT NEUTRALIZE FREE VIRIONS

16. Replication • Adsorption and penetration – endocytosis • Uncoating – low pH in endosomes induces conformational change in HA --- fusion of viral envelope with endosomal membrane. • Protons pass into the virion via M2 ion channel – uncoat the influenza virus • Passage of the M2 channel, H+ cannot enter – UNCOATING CANNOT TAKE PLACE • THEREFORE IMPEDING MULTIPLICATION – VACCINE STRATEGY • The RNPs transported to nucleus where transcription and replication of viral RNA occur • “cap snatching” – viral endonuclease cleaves the 5’methylguanosine cap with 10-15 NT from host cell mRNA – used for a primer for transcription by viral RNA polymerase • Each gene separately transcribed • After RNA replication – M1 enters nucleus and binds to the nucleoprotein-transcriptase negative sense RNA complex – down regulates transcription and allows export from nucleus into cytoplasm before assembly into virions • HA,NA, M2 migrate to plasma membrane of apical surface of cell • M1 recognition and binding to cytoplasmic portion of the HA and budding occurs • After budding, NA facilitates virion release from cell surface

17. Influenza A Viruses • Every influenza began as an avian influenza virus • HA/NA subtypes – • Horses • Swine • Humans • Poultry • Nomenclature – Influenza viruses codified as to the type, host species, geographic location, strain no., year of isolation nad parenthesis by subtype • Ex. A/equine/Prague/1/56(H7N7)

18. Genetic changes in Influenza A viruses • Antigenic shift – major antigenic change - involves new gene for new HA or NA – genetic reassortment • In nature, human strain of influenza A infects a pig infected with avian influenza A virus – both avian and human strains replicate effectively in pigs • Reassortmetn containing mainly genes from human virus, buteh HA derived from the avian virus can infect humans and initiate a pandemic

19. Genetic changes cont. / Equine Influenza • Antigenic drift – minor change • Point mutations in HA or NA subtype • Affect neutralizing epitopes that produce strains that are slightly antigenically different from its predecessor • Equine Influenza • Acute, extremely contagious, febrile respiratory disease • Etiologic agent – influenza A virus; Two antigenically distinct forms • A/equine/Prague/1/56 (H7N7) – Equine influenza virus 1- last outbreak 1979 • A/equine/Miami/1/63 (H3N8) – Equine influenza virus – 2 has been associated with all recent outbreaks – undergone a MINOR ANTIGENIC DRIFT since isolation in 1963 • VIRUS IS VERY UNSTABLE UNDER ORDINARY ENVIRONMENTAL CONDITIONS

20. Equine influenza virus Distribution, Transmission, Pathogenesis • Worldwide – except Australia, NZ and Iceland • Transmission – aerosol • No CARRIER STATE – may shed virus for up to one week after recovery • Pathogenesis – replicates in the epithelial cells of RT • Lesions – may include laryngitis, tracheitits, bronchitis, interstitial pneumonia, pleuropneumonia, interstitial myocardiditis – RARE • Clinical features – IP – 1-3 days • Sudden onset, rapid spread, high fever, conjunctivitis, reddening of the nasal mucosa, increased nasal and conjunctival exudates • Dry, hacking, paroxysmal cough – abortion associated with high fever • Recovery 7-10 days • Mortality is rare- occurs with high fever

21. Equine Influenza – Diagnosis and Control • Diagnosis - • Virus isolation – nasal mucosa and lungs- embryonated eggs – allantioc or amniotic routes and cell culture • HIA • HI test – paired serum test • Control – vaccinated with bivalent inactivated vaccine antigens

22. Swine influenza • A. suum can contribute to secondary infections for swine influenza - A. suum at left • Similar to African swine fever, in that migrating water fowl are the reservoir hosts – resistant to influenza – harbor and spread to the domestic poultry population • Significant between mammalian and avian species – viremia is a MAIN PHASE – CNS, resp. or GI • Differential diagnosis – Newcastle Dz. • Highly pathogenic Avian influenza -

23. Avian Influenza – Fowl plagueNO VACCINE • Hemorrhagic lesions dominant feature on PM exam