Pestiviruses
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- Created by: fionnualamaire94
- Created on: 29-11-16 12:22
Members of the flaviviridae family
Pestiviruses - very important group of animal pathogens
Flaviviruses - arthropod borne, important human pathogens
Hepatoviruses - hepatitis C virus
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Flaviviridae molecular biology
morphology -
- 60-80nm icosahedral particles composed of a single capsid protein (C) surrounded by a tightly adherent envelope
- particles are not very stable in the environment
- particles contain an 11-12Kb single stranded +ve sense RNA genome
- Envelope consists of 3 viral glycoproteins - E1, E2 and E3 (Erns in BVDV)
- genome encodes single large polyprotein - proteolyticllay processed by combination of viral and host proteases
- protein Npro - potent interferon response antagonist
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Pestivirus diseases of animals
Bovine viral diarrhoea virus genotype 1 (BVDV 1) - infects cattle sheep and deer
Bovine viral diarrhoea virus genotype 2 (BVDV 2) - infects cattle and sheep and can cause more severe acute disease than BVDV1
Border Disease virus - distinct variant of BVDV that infects sheep
Classial Swine Fever virus - (Hog cholera virus) - infects swine
All four are serologically related and are all immunosuppresive
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Bovine Viral Diarrhoea virus 1
Causes 2 distinct diseases:
- acute bovine viral diarrhoea (BVD)
- mucosal disease (MD)
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Bovine Viral Diarrhoea
- majority of infections are sub-clinical even in non-immune cattle
- usually causes trivial illness lasting a few days
- high morbidity, low mortality
- coughing and diarrhoea
- immunosuppressive action of virus during times of stress predisposes to mixed infection with Pasteurella hemolytica, exacerbates the respiratory disease - stress induced pneumonia or shipping fever - very severe brochopneumonia
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Bovine Viral Diarrhoea Pathogenesis
- Incubation 4-7 days. Duration ~10 days post infection.
- primary replication in oral mucosa, transmission to the palatine tonsil
- widespread dissemination via blood as free virus or infected lymphocytes and monocytes to many tissues - especially lymphoid organs
- causes mild fever, leukopenia and diarrhoea
- virulent strains (BVDV 2 strains) cause severe thrombocytopenia and associated haemorrhagic consequences
- BVDV antigen can be detected in many tissues of infected animal and is primarily associated with monocytes and follicular dendritic cells
- most deleterious consequences of BVDV infections are associated with one, or more aspects of the reproductive physiology
- conception rates can be reduced by 50% following BVDV infection - abortion, reabsorption, infection of ovaries and oviduct cells, reduced eostradiol secretion and LH burst - loss of milk production - congential defects - persistently infected calves
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Cytopathic and Non-cytopathic biotypes
- Most BVDV viruses grow in cell culture without causing CPE and are designated noncytopathic strains
- some strains are cytopathic and are particularly associated with mucosal disease
- only ncp strains can cause persistent infections as they are able to inhibit induction of IFN by dsRNA during infection - enables them to establish persistent infection in the foetus
- cp strains cant do this and will usually cause abortion or foetal damage depending on stage of gestation
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Consequences of in utero infection
- <18dpc (pre-implanted) infection does not occur
- <25dpc (early pregnancy) leads to embryonic death and reabsorption (cp/ncp strains)
- 25-90 days - retarded growth/look normal but are persistently infected (PI) and tolerant - excrete large quantities of virus
- only ncp strains can do this
- occurs in window of opportunity where foetus's acquired immunity is developing - viral antigen is recognised as host antigen
- 80-125 days - congential defects of the eye and CNS effects (retinal dysplasia and cerebral hypoplasia)
- 125 - 180 days - calves may survive, develop neutralising antibody and clear virus, high incidence of congential abnormalities - late gestation infections result in clinically normal calves with high levels of pre-colostral antibodies - immune for life but prone to other disease
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Significance of PI animals
- small and unthrifty but not always
- never seroconvert (create Ab) to virus they are carrying - may partially respond to antigenically distinct strains
- likely to succumb to mucosal disease eventually - many die between 6-24 months as maternal antibody wanes
- extremely efficient transmitters of infection to non-immune animals
- provide long-term reservoir for maintaining the virus in the population, hence ncp strains predominate
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Transmission of BVDV
- rate of spread depends on stocking density and prevalence of PI animals
- transmission from PI animals is much more efficient than from acutely infected animals
- occurs by direct contact - 1hr nose to nose contact sufficient - contact with feed contaminated with urine, nasal secretions, faeces, aborted foetuses and placentas
- can be transmitted iatrogenically - contaminated gloves
- semen from PI bulls is highly infectious - rarely but can lead to PI offspring, embryos from PI or acutely infected animals can be infected
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Mucosal Disease (1)
- only occurs in PI animals
- extensive ulceration of GI tract, necrotic lesions in the mouth, profuse diarrhoea containing fresh or clotted blood
- death 2 weeks after onset of clinical signs - 100%
- animals are infected with cp and ncp strains simultaneously - "virus pair" - results from spontaneous mutation of ncp strain to cp form in PI animals - antigenically very similar/identical
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Mucosal Disease (2)
- cp mutation increases the expression of viral protein NS3 - serine protease, helicase and NTPase
- unrestrained replication, high levels of dsRNA and apoptosis - resulting cell death manifests as mucosal disease
- transmission of cp virus to other PI animals leads to mucosal disease storm
- transmission to PI animals with antigenically distinct strain produces slower progressing form of the disease - chronic MD - partial immune response but death is still inevitable (when cp and ncp strains recombine usually)
- MD may also be triggered by live-attenuated vaccines which are usually based on cp variants
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Summary of Events leading to MD
- non-immune pregnant cow becomes infected with ncp strain of BVDV
- virus readily crosses placenta to infect the foetus
- cow mounts a successful immune response and recovers (life long immunity)
- ncp virus evades foetal innate immunity by blocking IFN expression. Immature immune system of foetus becomes tolerant to virus
- persistently infected calf is born - never seroconverts and sheds virus all its life
- ncp virus mutates to cp phenotype or calf is infected with virus from another source
- inability of PI animal to respond to cp virus infection leads to extensive tissue damage and death from mucosal disease
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Severe acute BVD
- second genotype of BVDV recognised in recent years - BVDV2
- associated with more severe primary acute infection - esp. Canada/USA
- acute disease caused by virulent strains of BVDV2 is characterised by fever, diarrhoea, thrombocytopaenia, haemorrhages, respiratory disorders, high abortion and mortality rates
- UK strain of BVDV2 is less virulent
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Epidemiology
- introduction of infected animals into naive herd results in rapid spread and dramatic losses (50% of calves lost in first year due to MD) - following year stable equilibrium is reached - 85% animals are immune and 1-2% PI - outbreaks of BVD occur when non-immune animals are born or introduced from outside the herd
Routes of introduction:
- purchase of new stock - PI animals, acutely infected animals, trojan horses - convalescent dam carrying PI foetus
- infected semen/embryos - PI bull, acutely infected bull, bull infected at puberty
- deer and sheep
- breakdown of biosecurity
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Control
- Desirable but expensive:
- eliminate PIs
- prevent reintroduction by quarantine, or by only introducing immune animals
- identification of PI animals requires individual ELISA tests for Ab (negative) and Ag (positive)
- bulk milk tests for antibodies indicates the proportion of the herd that has seroconverted - milk tests for virus (PCR) suggests prescence of PI animals or newly introduced acute infection
- Compromise solution:
- vaccinate heifers before service on an annual basis - boosters
- live vaccines are effective but may induce MD and can infect foetuses
- hinders serological assessment of herd status
- despite large antigenic differences - immunisation of cattle with vaccines employing only BVDV1 mitigates against acute BVDV2 disease, but may not provide complete foetal protection
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Diagnosis of BVDV
- based on clinical history, signs and examination of reproductive records
- history of abortions, stillborns, weak calves, and infertility problems
- lab diagnosis is based on virus isolation, in situ hibridisation, antigen detection, PCR and serology on paired sera
- BVDV1 and 2 are antigenically distinguishable using monoclonal antibodies and in neutralisation assays with antiserum
- specimens include faeces, urine, blood, nasal secretions, skin biopsies and post-mortem tissues
- differential daignosis from FMDV, malignant catarrhal fever, salmonellosis, Rinderpest and Ibaraki disease
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