Virology Flashcards
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
b) A
c) A
d) A and D
e) D
f) Pigs A, B, C and D
e) A, B, C and D
Influenza
Important features
a) Polymerase
b) Genome
a) Error-prone polymerase - so generates considerable genetic diversity
b) Segmented genome - allowing reassortment during mixed infections (antigenic shift)
Influenza
Important features
a) HA
b) NA
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
Influenza
Influenza strains
a) Poultry
b) Pigs
c) Humans
d) Horses
e) Cattle
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
Influenza
Sialic acid variation between species and what this means
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
Influenza
Flu evolution
a) Meaning of hit and run strategy
b) How maintained
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)
Influenza
a) Antigenic drift
b) Antigenic shift
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
Influenza
Seasonality
a) What is observed
b) Mechanisms underlying
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
Influenza
Swine flu
a) Main strains responsible
b) Observed antigenic drift
c) Seasonality
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
Influenza
Eqine flu
a) Strain responsible
b) Vaccination
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
Influenza
Poultry
a) HPAI
b) LPAI
c) What is responsible for the difference in virulence
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
Herpes
a) What is modulated in the host by the virus
b) Example of SuHV1
a) Inflammatory, innate and specific immune responses
b) Bind and inhibit chemokines, blocks complement-mediated lysis, interfere with IFN patheways
Herpes
Virus structure
a) Size and structure of genome
b) How changes with replication
c) Virus structure (lable diagram)
a) Large, linear dsDNA genome, 70-100 genes
b) Genome circularises upon replication, genome is episomal during latency
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)
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
Herpes
Detection of viruses (5)
- Serology (ELISA)
- Isolation of virus by tissue culture
- Histopathology
- Immunohistochemistry (IHC) or fluorescent antibody (FA)
- DNA detection (PCR)
Herpes
Infectious bovine tracheitis (BoHV1)
a) Pathogenesis (5)
b) Clinical signs (7)
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
Herpes
Infectious pustular vulvovaginitis (BoHV1)
a) Pathogenesis (3)
b) Clinical signs (5)
a)
- Sexual transmission
- Ganglionic neuronal latency
- Mucosal and neural tissues infected
b)
- Fever
- Balanoposthitis
- Vulval labia inflammation
- Reddened mucosa with pustules
- Vulvar discharge
Herpes
BoHV1 vaccines available (4)
- Attenuated - may be abortigenic
- Modified live
- Non-replicating
- Subunit gD
Cannot prevent latent infection or reactivation from a wild-type
Herpes
Bovine encephalitis virus (BoHV5)
Pathogenesis (2)
- 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
Herpes
Malignant Catarrhal fever
a) Two viruses that cause disease
b) Pathogenesis (3)
c) Clinical signs (6)
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
Herpes
Aujeszky’s disease pathogenesis - SuHV1
a) Transmission
b) Invasion and translocation
c) Main host
d) Pathogenicity
e) Latency
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)
Herpes
Aujeszky’s disease (SuHV1) - clinical signs
a) Piglets
b) Fatteners
c) Sows/Boars
d) Pregnant sows
e) Dogs
f) Other species
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
Herpes
Marek’s Disease (MDHV1)
a) Characteristics of infection
b) Diagnosis criteria
c) Pathogenesis
d) Vaccination
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
Pestivirus
Bovine viral diarrhoea virus
a) BVDV-1 vs BVDV-2
b) Bovine viral diarrhoea disease summary
c) Mucosal disease summary
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.
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)
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
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
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
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)
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)
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
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
