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Virology Flashcards

1
Q

Influenza

Host specificity - what strains are applicable for the following species
a) Canines
b) Felines
c) Poultry
d) Equids
e) Ruminants
f) Pigs
g) Humans

A

a) A
b) A
c) A
d) A and D
e) D
f) Pigs A, B, C and D
e) A, B, C and D

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2
Q

Influenza

Important features
a) Polymerase
b) Genome

A

a) Error-prone polymerase - so generates considerable genetic diversity
b) Segmented genome - allowing reassortment during mixed infections (antigenic shift)

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3
Q

Influenza

Important features
a) HA
b) NA

A

a) Receptor-binding protein with affinity for terminal sialic acid residues on host cell glycoproteins/glycolipids. Binding of HA allows membrane fusion and entry. 18 HA sub types
b) Receptor-destroying enzyme, allowing virus to exit and reinfect. 11 NA subtypes

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4
Q

Influenza

Influenza strains
a) Poultry
b) Pigs
c) Humans
d) Horses
e) Cattle

A

a) Domestic poutlry described as a bridging species: H1-H13, N1-N9
b) Bridging species from avian to humans
c) H1N1, H3N2
d) H3N8
e) Recent H5N1 infection from poultry

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5
Q

Influenza

Sialic acid variation between species and what this means

A

Humans, pigs and chickens have α2-6 linkage
Pigs, chickens, aquatic birds, horses, cattle (and human lower resp tract) have α2-3 linkage
As pigs and chickens have both sialic acid linkages, they have potential to act as adaptive hosts for the virus. Also allow coinfection with a human strain, producing reassortments

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6
Q

Influenza

Flu evolution
a) Meaning of hit and run strategy
b) How maintained

A

a) Short duration infection cycle (high titre, rapid transmission) and no persistent infection
b) Continued cycling of the virus, rapid replenishment of susceptible hosts, rapid antigenic evolution (drift and shift)

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7
Q

Influenza

a) Antigenic drift
b) Antigenic shift

A

a) Error-prone polymerase and rapid turnover and large number of progeny viruses means antigens are changing over time. Erods herd and vaccine immunity
b) Segmented genome means coinfection allows reassortment of genome, producing new strains of influenza

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8
Q

Influenza

Seasonality
a) What is observed
b) Mechanisms underlying

A

a) Temperate climates show strong association with winter months. Subtropical climates have continuous circulation, peaks at rainy periods
b) Mostly unexplained, but contact patterns, survivability of the virus (eg sunlight may destroy) and host suscebtibility are important

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9
Q

Influenza

Swine flu
a) Main strains responsible
b) Observed antigenic drift
c) Seasonality

A

a) H1N2 dominant in UK, H1N1 in Europe - not notifiable or reportable
b) Limited: reduced selective pressure from herd immunity due to short lifespan of hosts, inefficient vaccines
c) More prevalent in winter months

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10
Q

Influenza

Eqine flu
a) Strain responsible
b) Vaccination

A

a) H3N8 (historically was H7N7, but that is now extinct)
b) Inactivated polyvalent field strain matched vaccine. Multiple doses and boosters needed. Vaccine prevents clinical disease, but not infection. Mandatory schedule for racehorses

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11
Q

Influenza

Poultry
a) HPAI
b) LPAI
c) What is responsible for the difference in virulence

A

a) Highly pathogenic avian influenza - H5 and H7 responsible. Cause viraemic and systemic disease, sudden death of massive flock populations. Notifiable. No UK vaccines
b) Low pathogenicity avian influenza. Underreported, affecting intestinal tract and respiratory system. Causing production losses, anorexia
c) HA cleavage (must be cleaved to be active). If the usually monobasic cleavage site becomes multibasic (from stepwise mutation or non-homologous recombination), it can establish infection in more tissues than just respiratory epithelium ot gut.
Monobasic site can only be cleaved by trypsin-like proteases (only present in gut/ resp system)
Multibasic site can be cleaved by furin which is present throughout body

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12
Q

Herpes

a) What is modulated in the host by the virus
b) Example of SuHV1

A

a) Inflammatory, innate and specific immune responses
b) Bind and inhibit chemokines, blocks complement-mediated lysis, interfere with IFN patheways

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13
Q

Herpes

Virus structure
a) Size and structure of genome
b) How changes with replication
c) Virus structure (lable diagram)

c)
A

a) Large, linear dsDNA genome, 70-100 genes
b) Genome circularises upon replication, genome is episomal during latency

c)
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14
Q

Herpes

Bovine herpesvirus
a) What are the three herpesviruses responsible for bovine disease
b) What is the most important of these
c) Which have vaccinations available

A

a)
1. BoHV1 (α herpesvirus) - infective bovine tracheitis (IBR) and infective pustular vaginovulvitis
2. BoHV5 (α herpesvirus) - bovine encephalitis
3. OvHV2 (γ herpesvirus) - bovine catarrhal fever

b) BoHV1
c) BoHV1 is the only one with vaccines available, but they are not very effective

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15
Q

Herpes

Detection of viruses (5)

A
  1. Serology (ELISA)
  2. Isolation of virus by tissue culture
  3. Histopathology
  4. Immunohistochemistry (IHC) or fluorescent antibody (FA)
  5. DNA detection (PCR)
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16
Q

Herpes

Infectious bovine tracheitis (BoHV1)
a) Pathogenesis (5)
b) Clinical signs (7)

A

a)
- Aerosol transmission
- Incubation period 2 – 3 days
- Clinical signs may be worse during stressful periods
- Ganglionic neuronal latency
- Mucosal and neural tissues infected

b)
- Coughing is the first sign
- Fever (for 7-10 days)
- Excess salivation
- Serous to mucopurulent nasal discharge
- Vesicles on the muzzle and nares (ulcerative)
- Abortion at 4 – 7 months
- Upper respiratory tract infection symptoms

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17
Q

Herpes

Infectious pustular vulvovaginitis (BoHV1)
a) Pathogenesis (3)
b) Clinical signs (5)

A

a)
- Sexual transmission
- Ganglionic neuronal latency
- Mucosal and neural tissues infected

b)
- Fever
- Balanoposthitis
- Vulval labia inflammation
- Reddened mucosa with pustules
- Vulvar discharge

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18
Q

Herpes

BoHV1 vaccines available (4)

A
  1. Attenuated - may be abortigenic
  2. Modified live
  3. Non-replicating
  4. Subunit gD

Cannot prevent latent infection or reactivation from a wild-type

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19
Q

Herpes

Bovine encephalitis virus (BoHV5)
Pathogenesis (2)

A
  • Direct neural spread from nasal cavity, pharynx, tonsils via maxillary and mandibular branches of CN V (Trigeminal Nerve)
  • Lesions in the midbrain and entire brain
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20
Q

Herpes

Malignant Catarrhal fever
a) Two viruses that cause disease
b) Pathogenesis (3)
c) Clinical signs (6)

A

a) AlHV1 (zoos) OvHV2 (UK)
b)
- Disease of both sheep, cattle, wild ruminants and pigs
- Common in farming systems with both sheep and cattle
- OvHV2 reservoir is sheep that infect in-contact cattle via nasal secretions all year round
- AlHV1 reservoir is wildebeest that shed virus especially around calving
c)
- Bilateral corneal opacity (distinguishes from BoHV1!!)
- Severe fatal lymphoproliferative disease in cattle
- Fever
- Erosive, crust lesions on the muzzle and oral cavity
- Nasal and ocular discharges
- Death by 2 days to several weeks after clinical signs

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21
Q

Herpes

Aujeszky’s disease pathogenesis - SuHV1
a) Transmission
b) Invasion and translocation
c) Main host
d) Pathogenicity
e) Latency

A

a) Transmitted by aerosol, saliva and nasal discharge
b) Virus invades epithelial cells of the upper respiratory tract. Translocates via axons of sensory nerves to infect neurons (ganglionitis latency), CNS, and lymphoid tissue
c) Pig major host and reservoir
d) Highly pathogenic, extremely lytic, rapid replication
cycle. Highly neurotropic. Fatal in other species
e) Latency in neurons and lymphoid tissue (seropositive animals are latently infected)

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22
Q

Herpes

Aujeszky’s disease (SuHV1) - clinical signs
a) Piglets
b) Fatteners
c) Sows/Boars
d) Pregnant sows
e) Dogs
f) Other species

A

a) Convulsions, neurological signs, death
b) Growth retardation, respiratory stress
c) Profuse salivation
d) Abortion, premature partuition with abnormal litters
e) Pseudorabies - paralysis of jaws and pharynx, drooling, but non-aggressive
f) Pruritis and self-mutilation

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23
Q

Herpes

Marek’s Disease (MDHV1)
a) Characteristics of infection
b) Diagnosis criteria
c) Pathogenesis
d) Vaccination

A

a) Highly contagious disease of poultry. T-cell lymphomas, peripheral nerve damage
b) History, clinical signs, gross necropsy, histopahtology
c)
- virus released in feather dander (epithelial cells)
- Inhalation of infected dander
- Highly cell associated
- Oncogenic - CD4+ T-lymphocytes transformed
d) Vaccination in ovo or at hatching is highly protective against disease

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24
Q

Pestivirus

Bovine viral diarrhoea virus
a) BVDV-1 vs BVDV-2
b) Bovine viral diarrhoea disease summary
c) Mucosal disease summary

A

a) BVDV-1 (pestivirus A) and BVDV-2 (pestivirus B) infect cattle and sheep, with BVDV-2 capable of causing a more severe acute infection
b) An acute transient disease. Usually only lasts a few days, low mortality, although there are more virulent strains (especially BVDV-2). Symptoms include coughing and diarrhoea. Most significant economically with reproduction losses and immunosuppression
c) 100% fatal, haemorrhagic enteric disease, only infecting presistently infected (PI) calves.

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25
# Pestivirus BVDV pathogenesis
- primary replication in oral mucosa, transmission to palatine tonsil - causes mild fever, leukopenia, diarrhoea (although virulent strains can cause severe thrombocytopenia and haemorrhage - serious impact on reproductive physiology (conception rates down by 50%, high foetal death rates, endocrine dysfunction) and congenital defects (arthrogryposis, cerebral hypoplasia)
26
# Pestivirus BVDV cytopathic vs non-cytopathic strains
- Most pestivures (>90%) are non-cytopathic (ncp) - Cytopathic strains particularly associated with mucosal disease - Only ncp strains give rise to PI calves
27
# Pestivirus BVDV consequences of in utero infection at days post conception (dpc) a) Pre-implantation (< 18dpc) b) Early pregancy (< 25dpc) c) 25-90 dpc d) 80-125 dpc e) 125-180 dpc f) late gestation
a) No infection of pre-implanted embryo as virus cannot penetrate zona pellucida b) Embryonic death and reabsorption (cp and ncp strains) c) Infection by ncp strains (not cp) may result in retarded growth or look normal, but calves will be born persistently infected and tolerant to the virus (no antibody response) and excrete large quantities of virus d) Congenital defects of eye and cerebral hypoplasia e) Calves can develop antibodies against virus to clear infection, but still high incidence of congenital abnormalities f) Clincially normal calves with high levels of antibodies. But may be partially immunocompromised
28
# Pestivirus BVDV - significance of PI animals
- extremely efficient transmitters of infection to other non-immune animals - long-term reservoir essential for maintaining virus in population - all PI animals will eventually die from mucosal disease - PI dams will always produce PI calves
29
# Pestivirus BVDV mucosal disease
- only occurs in PI animals - ulceration of GI tract, necrotic mouth lesions - profuse diarrhoea with fresh/clotted blood - death within 2 weeks of clincal signs - animals carry ncp and cp virus strains (either ncp virus mutates to cp, or animal is infected with a cp virus from another source)
30
# Pestivirus Diagnosis of BVDV
- history of abortions, infertility problems, calves with congenital defects, signs of mucosal disease - bulk milk sample for herd-level detection in dairy - ear punch sample for detecting PIs (only PI will have enough viral Ag to get a positive result, so can identify these animals) - lab diagnosis (antigen detection by ELISA, PCR or serology)
31
# Pestivirus Classical swine fever virus (CSF) a) pathogenesis b) transmission
a) - pigs and wild boar are the only natural reservoir - notifiable disease - high mortality rate b) - incubation period 2-10 days - oronasal pig-to-pig - manual transfer - contaminated transport vehicles - artificial insemination with contaminated serum - local spread up to 1km - transplacental
32
# pestivirus Classical swine fever virus a) Acute infection b) Sub-acute infection
a) - death within 2-3 weeks - high fever, depression, anorexia - conjunctivitis - purple skin (petechial haemorrhage) b) - persistently infected offspring (life expectancy < 1 year) - button ulcers in colon (necrosis) - prolongued disease - abortion
33
# Complex viral disease Canine infectious tracheobronchitis pathogens (4)
- Canine parainfluenza virus 2 - Canine adenovirus-2 - Bordetella bronchiseptica - Secondary opportunistic infection (canine respiratory coronavirus, canine influenza virus)
34
# Complex viral disease Canine infectious tracheobronchitis - pathogenesis of a) Primary infection by CPiV or CAV-2 b) Primary infection by Bordatella bronchoseptica
a) - viral damage to epithelium - interference with immune responses (CPiV viral proteins inhibit interferon response, CAV evade immune system) b) - upper resp tract commensal or pathogen - regulates its virulence state - grows on and infects ciliated epithelium - releases toxins (decrease neutrophil function)
35
# Complex viral disease Canine infectious tracheobronchitis a) How is disease spread (4) b) Clinical disease incubation c) Clinical signs
a) - Direct contact - Aerosol - Mechanical transmission - Common in weaning puppies b) 3-10 days c) - show after 10-20 days - fever - sneezing, coughing fits - coughing induced with pressure on trachea or during exercise
36
# Complex viral disease Respiratory syndrome of calves a) What calves affected b) Morbidity and fatality c) Clinical signs (3)
a) < 6months, peak 2-10 weeks old (when there is decreased maternal immunity b) 100% morbidity, 20% fatality c) - fever - coughing - nasal discharge - conjunctivitis - production losses
37
# Complex viral disease Respiratory syndrome of calves a) What are the primary infection viruses (3) b) What are important secondary infection pathogens
a) - bovine respiratory syncytial virus (BRSV) - most important - bovine parainfluenza virus-3 (PiV-3) - bovine viral diarrhoea virus (BVDV) b) - Pasteurella multocida - Histophilus somni - Mycoplasma bovis
38
# Complex viral disease Respiratory syndrome of calves Pathology of primary infection with BRSV
- Infection of ciliated epithelial cells, type II pneumocytes (can cause necrosis and apoptosis of epithelial cells, syncytial formation) - Damages cilia - Induces inflammatory response (F protein/TLR4 -> NFκB activation) - Antagonises IFN responses (NS2 protein)
39
# Complex viral disease Respiratory syndrome of calves Pathology of primary infection with PiV-3
- Infection of epithelial cells of URT and LRT - Damages cilia - Decreases alveolar macrophage function
40
# Complex viral disease Respiratory syndrome of calves Pathology of primary infection with BVDV
- Diarrhoea, erosive lesions of the GI tract, mild pneumonia - Targets lymphocytes and macrophages (leukopenia) - Decreased proliferation and cytokine responses of leukocytes - Neutrophil function decreased
41
# Complex viral disease Respiratory syndrome of calves Pathology of secondary infection with Pasteurella multocida
- Ubiquitous in ruminants, commensal in nasopharynx - Opportunistic pathogen - Need prolonged impaired defense mechanisms for lung colonisation - Fibrinous pleuropneumonia
42
# Complex viral disease Porcine circovirus disease a) Causative virus b) What pathologies can occur from infection (3)
a) Pocine circovirus type 2 (PCV-2) b) - post weaning multisystemic wasting syndrome (PMWS) - porcine dermatitis and nephropathy syndrome (PDNS) - porcine respiratory disease complex
43
# Complex viral disease Porcine circovirus disease a) PCV-2 virus structure b) PCV-2 methods of immunosuppression
a) - stable, non-enveloped capsid - circular ssDNA - requires host DNA polymerase for replication b) - infection of T-lymphocytes - host becomes lymphopenic due to apoptosis - antigen found in macrophages due to phagocytosis - microbiocidal activity of macrophages reduced
44
# Complex viral disease Porcine circovirus disease a) PMWS clinical features b) PMWS mortality determinants
a) - post-weaning mortality - wasting in piglets 6-14 weeks - anaemia, enteritis, hepatitis, pulmonary change - enlarged lymph nodes - moderate to high morbidity b) - High mortality in poor herd health status all year round - Peak mortality in spring in good herd health status - Not all PCV-2 +ve pigs show clinical disease
45
# Arboviruses a) Define Arbovirus b) Examples of arthropods that act as vectors (3) c) What is necessary for infection to persist in a region (2)
a) Virus transmitted by biting insects, where the virus infects and replicates in the insect b) 1. Mosquitos 2. Ticks 3. Biting flies/midges c) - continual cycling between host and vector - transovarial infection (allows permanent maintenance in vector population)
46
# Arboviruses What makes a good arthropod vector (4)
1. Co-incident and common (found in the geographic range of disease, sufficient numbers to sustain transmission) 2. Perference for host species concerned 3. Susceptible to infection via oral route 4. Transmission competent (bite introduces an infectious dose - amplification in salivary glands)
47
# Arboviruses Seasonality of arboviruses a) Vector populations b) Vector competence
a) - Rainfall provides breeding sites for insect - temperature effects mobility and vector viability - colder weather = decreasing number of vectors b) - Vectors are cold-blooded, so as virus replication is temperature dependent, extrinsic incubation period (EIP) and viral titres vary accordingly - EIP defines the time it takes for a vector to become infectious following exposure to an arbovirus - Colder weater = decreasing vector competence
47
# Arbovirus Mechanisms of arbovirus persistence in overwintering (5)
1. With transovarial transmission, can reside in eggs or larvae, which enter diapause in winter (hatch when temperature rises) 2. Survive in adult insects if they move indoors 3. Persistent infection in alternative host 4. Transplacentally infected animals leading to persistent infection 5. Long-lived alternative insect vector
48
# Arboviruses Bluetongue virus a) What transmits the virus b) What animals are infected
a) Culicoides midges (only contagious with a midge vector) b) Sheep and cattle - sheep show moderate clinical signs - cattle show mild symptoms/asymptomatic and can act as overwintering reservoir
49
# Arboviruses Pathogenesis of Bluetongue virus (BTV) in sheep Primary replication of the virus
- primary replication in local endothelial cells and leukocytes - migrate to regional lymph nodes - amplification in lymphocytes and dendritic cells - free virus disappears rapidly from plasma as antibodies appear
50
# Arboviruses Pathogenesis of Bluetongue virus (BTV) in sheep a) How is damage caused to the host b) How long is infectious virus detetable in the blood of sheep vs cattle c) How long is virus detectable in blood of sheep by PCR vs cattle
a) - extent of infection of endothelial cells correlates with severity of disease - virus destroys endothelial cells, vascular smooth muscle cells and pericytes - causes haemorrhage and disseminated vascular coagulation b) Sheep - 5 weeks. Cattle - 8 weeks c) Sheep - 14 weeks. Cattle - 20 weeks
51
# Arboviruses Clinical signs of Bluetongue in sheep (9)
1. Abortion 2. Excess salivation and frothing due to cyanotic tongue 3. Swelling of mouth, head and neck 4. Conjunctivitis and ocular discharge 5. Haemorrhagic nasal discharge 6. Fever for several days 7. Hyperaemia and oedema of the buccal and nasal mucosa 8. Coronary band inflammation 9. Stiffness, lameness
52
# Arboviruses Bluetongue overwintering mechanisms a) Transovarial transmission in insects b) Role of cattle c) Role of T cells d) Transplacental transmission
a) No infectioun of eggs or larvae, so when the adult insect dies, the virus will die. Also no evidence for low level cycling in winter b) Viraemic phase is longer in cattle, so could act as a reservoir c) Virus may lay dormant in T cells - local inflammation at bite sites activate T cells d) Some persistently infected (late gestation) animals, but not a typical feature
53
# Oncogenic viruses a) Define oncogenesis b) What 4 types of genes are damaged c) What are the main oncogenic virus types (3)
a) Dysregulated growth of cells from a genetically altered progenitor cell b) - Oncogenes: activate growth and differentiation - Tumour suppressor genes: regulate cell cycle - Genes regulating apoptosis - Genes mediating DNA repair c) - Oncoretroviruses (RNA virus) - Papillomaviruses (DNA virus) - Herpesviruses (DNA virus)
54
# Oncogenic viruses Retrovirus features a) Virion structure b) Stability and spread c) Genome
a) 80-100nm enveloped virus b) Relatively unstable. Requires prolongued close contact or blood contact for spread c) Diploid ssRNA (+ve sense). Simple retroviruses have just 3 genes (gag, pol and env), complex retroviruses have additional accessory genes
55
# Oncogenic viruses a) Retrovirus replication b) What cells do oncoretroviruses require
a) - Replicate through a dsDNA intermediate - Reverse transcriptase produces a provirus - Provirus integrates into host genome - Provirus long terminal repeat (LTR) contains promoter/enhancer elements b) Require dividing cells for provirus/nucleocapsid complex to enter nucleus - usually infect haemipoietic stem cells / lymphocytes (cause tumours of haemopoietic/lymphoid origin)
56
# Oncogenic viruses Mechanisms of retroviral oncogenesis (3)
1. Encoding v-onc (an oncogene picked up by the virus) - Seen in rapidly oncogenic viruses - may contain mutations that alter normal protein function or regulation - may be a fusion product with a viral protein, modifying function or location - v-onc expression isn't controlled the same way as normal host oncogenes as they aren't affected by cellular regulatory factors 2. Activation of a cellular oncogene - Seen in weakly oncogenic viruses - Provirus inserts close to a cellular oncogene - LTR or promotor enhancer effect on cellular oncogene 3. Essential virus protein interferes with oncogene expression and cell cycle - Seen in weakly oncogenic viruses with a very long incubation - Provirus protein expressed can be an up-regulator of cellular promotors responsible for cellular oncogene expression
57
# Oncogenic viruses Feline leukaemia virus a) How is it oncogenic (2) b) How is virus shed c) Transmission (3)
a) - Oncoretrovirus - T-cell tumours caused by active virus replication produce severe immunosuppression - Myeloproliferative diseases due to active virus responsible for many clinical signs b) Excreted in saliva, tears and urine c) - prolongued contact - biting - iatrogenic
58
# Oncogenic viruses Pathogenesis of feline leukaemia virus a) Feautres of latent infection or cleared infection b) Features of persistently infected
a) Antibody positive, antigen negative b) - antibody and antigen positive - virus repicates in bone marrow stem cells, travels through peripheral blood to replicate in epithelial cells of salivary gland - clinical signs of immunosuppression manifest months to years later - death within 3 to 4 years
59
# Oncogenic viruses Papillomaviruses a) Features of the virus (4) b) What can it cause c) Transmission
a) - icosahedral - no envelope - circular dsDNA - stable b) - Benign infectious papillomatoses (warts) - Squamous cell carcinoma tumours c) - direct contact - contaminated equipment (indirect contact) - viruses are species specific, except for ungulate viruses
60
# Oncogenic viruses Mechanisms of transformation by papillomaviruses
- E6 interferes with p53 function and causes p53 degradation - E7 interacts with RB and inhibits its interaction with E2F-1, allowing cell cycle progression - E5 inhibits MHC class I expression - Co-factors also impact
61
# Oncogenic viruses Canine oral papillomavirus (COPV) a) What is caused b) Features of infection
a) Oral warts (conjunctiva, eyelid, skin around nose and mouth) b) - 1-2 month incubation, then regression after 1-2 months - Most adults are resistant - Squamous cell carcinoma are rare
62
# Oncogenic viruses Gallid herpesvirus 2 (GaHV2) - Marek's disease virus type 1 a) Lytic infection b) Latent infection c) Disease caused d) Transmission e) Effect of vaccination
a) Lytic infection of B cells, CD4+ T lymphocytes are transformed b) Latency in CD4+ T lymphocytes, telomere integration establishes this latency c) Lymphoproliferative disease of chickens within 2-6 weeks of infection, visceral, skeletal muscle and cutaneous lymphomas d) Inhalation of dander e) Has reduced disease but not infection
63
# Oncogenic viruses Major transforming molecules of Gallid herpesvirus 2 (4)
1. Meq - Transforms cells - Inhibits lytic replication - Activates T cell proliferation (p53) 2. viral telomerase RNA (vTR) - maintains transformed cells - interacts with telomerase reverse transcriptase - Relocalises RPL22 to nucleoplasm (a cellular factor involved in T-cell development) 3. viral interleukin 8 - recruits B cells and CD4+ T cells 4. microRNA miR-M4 - orthologue of cellular miR-155 - implicated in cancers
64
# Gastroenteritis viruses a) Enteric viruses that enter via the GI tract (3) b) Viruses that cause enteritis but are spread by systemic infection (2)
a) - Reoviridae (rotavirus) - Calciviridae (norovirus) - Coronaviridae (coronavirus) b) - Parvoviridae (parvovirus) - Circoviridae (circovirus)
65
# Gastroenteritis viruses Rotavirus a) Features of virion b) Effect of proteolytic cleavage c) What cells are infected d) Transmission
a) - 11 segments, dsRNA genome - triple layered capsid - non-enveloped - stable - resistant to wide pH range b) Increases infectivity (chymotrypsin cleaves VP4) c) Infects terminally differentiated enterocytes (high proportion of these in neonates, leading to villous atrophy) d) Faeco-oral transmission and water-borne
66
# Gastroenteritis viruses Rotavirus NSP-4
- only known viral enterotoxin - increases Cl- secretion - causes an increase in intracellular Ca2+ to inhibit disaccharidase release - inhibits glucose transport into enterocyte - activates enteric nervous system
67
# Gastrointestinal viruses Rotavirus - clinical signs of white scours/milk scours
- seen in calves, piglets, foals, lambs - incubation of 1-24hs - white, liquid faeces, may be mucoid - often continue to suckle, but reduced lactase (caused by virus) makes diarrhoea worse - more severe with lack of colostrum, co-infection or stress (cold, overcrowding) - usually recover within 3-4 days, but death by dehydration or secondary infection can occur
68
# Gastroenteritis viruses Caliciviridae - norovirus a) Features of virus b) What cells infected c) Clinical disease
a) Linear, ssRNA (+ve sense) b) Differentiated enterocytes, leading to villous atrophy and crypt hyperplasia in proximal small intestine c) - 12-16h incubation - yellow/green watery diarrhoea with mucus
69
# Gastroenteritis viruses Coronavirus a) Virus features b) What is it resistant to c) Replication d) Diseases caused (4)
a) - ssRNA (+ve sense) - enveloped - prominent glycoprotein spikes b) Resistant to trypsin and low pH c) Replicates in cytoplasm of epithelial and endothelial cells, and macrophages. d) - enteritis - respiratory disease - hepatitis - neurological disease
70
# Gastroenteritis viruses Transmissible gastroenteritis virus (TGEV) a) Type of virus b) Incubation c) Mortality of young pigs d) Cells infected and pathogenesis
a) Coronavirus b) 2-7 days c) < 2 weeks old, high mortality. > 5 weeks, low mortality. Causes diarrhoea and vomiting d) Intestinal terminally differentiated epithelial cells - direct virus damage to villi causing blunting - loss of lactase and disaccharidases -> watery diarrhoea including undigested milk
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# Gastroenteritis viruses Parvoviruses and circoviruses a) Virus structure b) Replication c) Diseases caused (4)
a) - small, ssDNA genome - parvo - linear, circo - circular - non-enveloped - do not encode DNA polymerase b) Must replicate in cycling cells (S or G2) - bone marrow (lymphoid) - gut epithelium - foetal or neonatal c) - leukopenia - enteritis - foetal disease - wasting
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# Gastroenterits viruses Parvovirus a) Site of infection b) Diseases caused in cats and dogs c) Virus shedding in cats and dogs
a) - Oro-nasal (direct or indirect infection) - Primary replication in pharyngeal lymphoid tissue - Bone marrow and gut epithelial stem cells infected (cells in S phase) b) - Cats: panleukopenia (FPLV) - high mortality - Dogs: lymphopenia (CPV-2) - usually only fatal in puppies - Both: immunosuppression, enteritis (shortened villi, vomiting/diarrhoea) c) - Virus excreted in faeces, saliva, urine, vomit - Cats: shed for up to 6 weeks - Dogs: shed only during clinical disease (7-10 days)
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# Gastroenteritis viruses Circoviruses - porcine circovirus type 2 (PCV-2) a) what is this virus associated with b) Clinical signs c) Pathology
a) PCV-2 assocoated granulomatous enteritis b) - affects pigs 40-70 days old - yellow diarrhoea, becoming black as disease progresses - retardation of growth c) - inflammation and lymphoid depletion in Peyer's patches with intracytoplasmic inclusion bodies - epithelioid macrophages and multinucleated giant cells in lamina propria
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# Prions Differences between PrPC and PrPSc (4)
PrPC - mostly α-helical - monomeric - detergent-soluble - proteinase K-sensitive PrPSc - enriched in β-sheet - oligomeric - detergent-insoluble - proteinase K-resistant
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# Prions PrPC a) Structure b) Location
a) - a GPI-linked membrane protein - anchored to cell membranes via GPI protein b) - high levels expressed on neurons and follicular dendritic cells
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# Prions Classical scrapie a) Describe pathogenesis b) PrPC variants that are highly susceptible to disease (2) c) PrPC variant that is resistant to disease
a) - due to oral uptake of prions in feed - prions amplify in lymphoreticular system - prions are transmitted through the peripheral nervous system to the central nervous system - PrPSc amyloid plaques in brainstem b) VRQ (valine, arginine, glutamine) and ARQ (alanine, arginine, glutamine) c) ARR (alanine, arginine, arginine)
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# Prions Atypical scrapie a) Which PrPC variant is resistant to disease b) How does age of susceptible sheep differ to classical scrapie
a) VRQ (valine, arginine, glutamine) b) - Classical: young sheep - Atypical: old sheep
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# Prions Bovine spongiform encephalopathy (BSE) a) Source of infection b) Pathology
a) - ingestion of prions from feed - ruminant meat and spinal material was fed to livestock cattle to maximise growth (now banned) - allowed introduction of PrPSc to healthy cattle b) - Classical BSE: PrPSc in medulla oblongata - Atypical BSE: PrPSc in cerebellum
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# Prions Classical vs Atypical BSE in cattle a) Age of onset b) Behaviour c) Amyloid plaques d) Site of PrPSc
a) - Classical: 4-6 years old - Atypical: > 8 years old b) - Classical: Aggressive - Atypical: Placid c): - Classical: no plaques - Atypical: plaques present d): - Classical: medulla - Atypical: cerebrum
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# Prions Clinical signs of a) BSE b) Scrapie
a) - Aggressive behaviour - Hypermetria - Uncoordinated gait - Ataxia b) - Pruritus (itching) - Ataxia

PID (3 decks)

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