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128 Cards in this Set
- Front
- Back
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What is the genome of herpesviridae? |
dsDNA, linear |
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What is the morphology of herpesviridae? |
enveloped icosahedral symmetry has a tegument, a space between capsid and envelope |
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How does herpesvirus get into the cell? |
receptor mediated endocytosis host receptors = heparan sulphate, TNF, NGF, herpesvirus entery mediator (HVEM) viral glycoproteins |
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Herpesvirus gene expression is broken into three phases. What is made in each phase? |
Immediate early genes = virus transcription Early genes = non-structural regulatory proteins Late genes = structural proteins |
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What factors are important for herpesvirus virulence? |
immune evasion (complement inactivation, suppress antigen presentation, inactivate cytokines, avoid apoptosis, latency) virokines (thymidine kinases) |
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How are the three subfamilies of herpesviridae divided? |
Alpha, Beta, and Gamma are divided based on biological activity |
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What is characteristic of alphaherpesvirinae? |
grows rapidly lyses infected cells latency in sensory neurons |
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What is characteristic of betaherpesvirinae? |
grows slowly
cell lysis does not occur until several days after infection latency in salivary glands, kidneys, lymphocytes |
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What is characteristic of gammaherpesvirinae? |
grow slowly replicate in lymphoid cells latency in lymphoid cells lymphoproliferative diseases, transform cells (tumors) |
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What kind of pathology is seen in adults vs. puppies who contract CHV-1? |
Adults = usually contracted via genital contact, typically asymptomatic Puppies = cell-associated viremia (virus within RBCs) --> hemorrhagic disease --> highly fatal |
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What is the presentation of feline herpes virus? |
upper respiratory tract infection conjunctivitis, oral ulcers, corneal ulcers abortion in pregnant adults |
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How is management different between canine and feline herpesviruses? |
No vaccine for canine herpesvirus (just try and keep puppies warm, not much you can do for them) Vaccine for feline herpesvirus (treat chronically infected animals with antivirals) |
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What is latent infection? |
viral genome is dormant in latently infected cells virion particles or proteins are NOT present in the host |
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What is the difference is eye diseases between FIP and FHV? |
FIP = uveal tract lesions due to accumulation of immune complexes (cloudy) FHV = corneal ulcers due to viral replication in epithelial cells, inflammation |
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You see a cat with oral ulcers. What are your top viral differentials? |
Calicivirus and herpesvirus |
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What is the difference between EHV-1 and EHV-4? |
Tissue tropism EHV-1 = respiratory disease, abortion, paresis, neuological disease EHV-4 = respiratory disease |
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What is characteristic of the primary infection associated with both EHV1 and EHV4? |
Incubation period = 2-10 days primary infection = biphasic fever, nasal discharge, cough typically uncomplicated, complete recovery in 1-2 weeks |
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With EHV1, are abortions typically associated with primary infection or the re-emergence of latent virus? |
latent virus typically a few weeks to several months after respiratory outbreak |
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What feature is central to the pathogenesis of EHV-1? |
viremia infection of T lymphocytes --> latent/persistent in lymphocytes --> neutropenia and lymphopenia |
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Where will you find EHV-1 DNA in an animal with a latent EHV infection? |
trigeminal ganglion and T cells |
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What is characteristic of the neurological mutant of EHV-1? |
ataxia, inability to empty bladder, weakness of tail, paralysis |
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How does the horse immune system respond to EHV-1? How effective is it? |
strong humoral immune response protection from re-infection is short lived (no correlation between circulating antibody levels and protection from reinfection) |
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How can EHV-1 infections be prevented? |
vaccine is available, but only provides short-lived immunity. Reduces the severity but does not prevent the disease |
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What are the two forms of BHV-1? |
Infectious bovine rhinotracheitis (IBR) = "red nose disease" Infectious pustular vulvovaginitis (IPV) |
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How can BHV-1 be transmitted? |
aerosol or sexually (natural coitus or artificial insemination) |
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What are some possible complications associated with BHV-1 infections? |
abortions encephalitis fatal disease in newborn calves shipping fever (bronchopneumonia) |
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Are BHV-1 diseases associated with acute infections or the reactivation of latent infections? |
reactivation of latent infections (this is different from CHV in which disease was associated with acute infection) |
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where does BHV-1 become latent? |
peripheral nervous system (this is different from EHV and FHV which became latent in the trigeminal ganglion) |
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What is bovine mammillitis-pseudo lumpy skin disease? |
BHV-2 localized infection of teats/udder systemic infection is rare (but possible) transmission via milking machine or arthropod vector |
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What sample should you take from an animal if you suspect it is infected with BHV-2? |
take skin scrapings from lesions diagnosis = predominately immunofluorescence and immunohistochemistry |
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What two alphaherpesviruses infect poultry? |
Avian infectious layngotracheitis Marek's disease ("range paralysis") |
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How is the tissue tropism different between Avian infectious laryngotracheitis and Marek's disease? |
AIL = respiratory epithelium Marek's = respiratory epithelium, neurons, feather follicle epithelium, macrophages, (lymphoblastoid cells semi-permissive) |
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What are the two forms of Marek's disease? |
Nervous form (paralysis) Visceral form (lymphoid tumors, induces T cell proliferation) |
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What are two examples of betaherpesviruses? |
Porcine cytomegalovirus = "inclusion body rhinitis" Elephant Herpesvirus |
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What is obviously the most important and fascinating virus that we've studied so far? |
Elephant herpesvirus |
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If an elephant contracts the herpesvirus that has co-evolved with the other elephant species, what symptoms will you see? (asian strain--> african elephant or african strain --> asian elephant) |
fatal hemorrhagic disease widespread capillary damage from virus replication in endothelium lethal pericardial, thoracic, and abdominal effusions |
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What symptoms do you see in an elephant infected with it's species specific strain of herpesvirus? |
pinkish skin lesions (trunk, head, genitals) pulmonary nodules localized skin papillomas |
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What important gammaherpesvirus is particularly pathogenic to American Bison? |
Malignant Catarrhal fever |
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What are the clinical features associated with malignant catarrhal fever? |
everything goes wrong nasal and ocular discharge, diarrhea, fever, respiratory problems, painful urination, erosive and ulcerative stomatitis, CNS lesions, vasculitis, death |
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What alphaherpesviruses cause problems in pregnant animals? |
EHV-1 and BHV-1 |
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What herpesvirus infects primarily B cells? What type of herpesvirus is this? |
Marmoset lymphoctryptovirus gammaherpesvirus |
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What viruses are involved in canine infectious respiratory disease complex? |
canine adenovirus type 2 (CAV-2) canine parainfluenza virus (CPiV) canine influenza canine herpesvirus canine respiratory coronavirus |
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What order is paramyxoviridae part of? What is the common genome, replication, and morphology shared by this order? |
Mononegavirales enveloped, many shapes of nucleocapsid -ssRNA genome (non-segmented) |
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What is RNA editing? |
when the RDRP enzyme inserts extra residues into the mRNA when its being synthesized *creates a frame-shift, altering the amino acid sequence encoded by the mRNA *mechanism to produce multiple proteins from one gene |
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What surface proteins are important for paramyxoviridae cell entry? |
HN glycoprotein (combination hemagglutinin/neuraminidase) Fusion (F) glycoproteins |
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These two bovine parainfluenzavirus commonly co-infects hosts with: Bovine adenovirus BVDV (bovine viral diarrhea v.) IBR (infectious bovine rhinotracheitis, bovine herpesvirus 1) Bovine coronavirus |
Bovine parainfluenza virus 3 Bovine respiratory syncytial virus causing shipping fever |
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What is Simian Virus 5 (SV5)? What animal(s) can it infect? |
Canine parainfluenza virus 2 Can also infect humans, monkeys, cattle, swine, cat, chickens |
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What are the three strains of Newcastle disease, and what tissues do they infect? |
Velogenic = neurotropic, enterotropic, lymphoid Mesogenic = neurotropic, pneumotropic, lymphoid cells Lentogenic = neurotropic pneumotropic, lymphoid cells |
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How is Newcastle disease transmitted? |
direct contact with secretions contaminated feed, water, implements, premises, human clothing, especially feces |
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What are the clinical signs of velogenic Newcastle disease? |
neurological signs, severe depression, edema of the head and eyes *may see death with no detected sign of prior illness, 10-15% of the flock may be lost in 24hrs |
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How many hens were culled in the 2007 VND outbreak? |
trololol You don't need to know that! (but it was 200,000) |
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Are there vaccines available for Newcastle disease? |
Yes! Live vaccine (drinking water or aerosol form) Inactivated vaccine (expensive, IM or SQ) Ovo vaccine (injected into eggs before they hatch) |
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What virus family does Canine Distemper Virus belong to? |
Paramyxoviridae |
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What is the tissue tropism of canine distemper? |
respiratory system GI system CNS ***leukocytes!!! |
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What are the symptoms of acute and peracute canine distemper? |
peracute = sudden fever and sudden death acute form = biphasic fever, leukopenia, anorexia, catarrhal inflammation of bronchi, conjunctivitis, depression, pustules on abdomen and thighs, hyperkeratosis of digital cushion |
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What virus might cause hyperkeratosis of the digital cushion in dogs? |
canine distemper virus |
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What two viruses cause severe leukopenia and diarrhea in dogs? |
Parvovirus and Distermper |
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What is old dog encephalitis? what virus is it caused by? |
Canine distemper virus progressive loss of neurological functions, localized twitching of muscles, paresis or paralysis, petit mal convulsions |
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What disease is the major initiating factor in Shipping Fever in cattle? |
Bovine respiratory sycytial virus |
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What are common clinical signs from CDV and NDV? |
behavior change paralysis coughing discharge diarrhea |
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What are systems affected by CDV and NDV? |
CNS GI Respiratory ***leukocytes!!! |
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What species is infected by Blue Eye Paramyxovirus? |
Pigs new emerging disease In piglets: respiratory symptoms, encephalitis, death. In adults: reproductive disease Respiratory transmission |
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How is the virus genome and morphology different for para- and orthomyxoviridae? |
paramyxoviridae = -ssRNA, non-segmented, enveloped, spherical othromyxoviridae = -ssRNA, segmented, enveloped, helical |
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Where does replication occur for paramyxovirus? orthomyxovirus? (think about what kind of virus they are!) |
paramyxovirus = cytoplasm (-ssRNA, this makes sense) orthomyxovirus = nucleus (-ssRNA, so this makes... no sense... why's it do that? 5' CAP STEALING, can only happen in the nucleus) |
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What is essential for hemagglutinin to work? What enzyme completes this step? |
HA cleavage --> HA1 + HA2 done by host cell proteases |
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What is the main determinant of orthomyxovirus host range, and also the main determinant of host range? |
HA |
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How does orthomyxoviridae exit the host cell? |
budding from the cell surface (no cytolysis) NA is crucial to this step |
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How are orthomyxoviruses classified? How many genome segments are in each class? |
Type A - 8 segments Type B - 8 segments Type C - 7 segments |
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What do the three orthomyxovirus classes have in common? What is different between them? What can vary within a class? |
All classes share = morphology, genome, replication Same within one class = nucleocapsid (NP), Matrix (M) proteins, and other antigens Different within one class = HA and NA |
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Which influenza virus type is of greatest importance to veterinary medicine? |
Type A |
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How many HA and NA subtypes are there within Type A influenza? |
17 known HAs 10 known NAs |
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All subtypes of Influenza Type A are found in which species? |
birds |
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Is antigen drift or antigen shift responsible for: The reason we need a new flu vaccine every year? The emergence of a new pandemic? |
Antigen drift = new flu vaccines because of small changes in NA and HA Antigen shifts = new pandemics. emergence of new NA or HA in a population that doesn't have any immunity to it |
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What is antigen drift? |
small point mutations in HA and NA few amino acid substitutions helps the virus immune surveillance |
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What protein has the highest mutation rate? |
HA1 |
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What is antigen shift? How does it happen? |
"new" HA or NA proteins, sudden big change *random reassortment of segmented RNA genomes *mixed infection of human and animal viruses *emergence of a dormant virus from an unknown reservoir |
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What kind of disease is caused by equine influenza? |
acute contagious respiratory disease |
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What is the HA and NA type of canine influenza virus? Does this help figure out where the disease came from? |
canine influenza virus = H3N8 This is the same stain as horses, crossed over at shared racecourses into greyhounds in 2004 |
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What's the difference between canine parainfluenza virus and canine influenza virus? |
parainfluenza = paramyxoviridae (non-segmented genome) Mild respiratory disease influenza = orthomyzoviridae (segmented genome) fever, wet cough, nasal discharge, high morbidity/low mortality |
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What is fowl plague? |
avian influenza highly lethal poultry disease respiratory distress, diarrhea, edema of head/face/neck, visceral hemorrhage |
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What two diseases of poultry can both present with edema of the head and face? |
Newcastle disease (paramyxoviridae) Avian Influenza (orthomyxoviridae) |
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What is the criteria for determining if a strain of avian influenza is highly pathogenic (HPAI)? |
1. strain kills 6,7, or 8/8 chickens 2. H5 or H7 strain that has HA cleavage site that is compatible with other HPAI viruses 3. strain is not H5 or H7, but kills 1-5 chickens and grows in cell culture in absence of trypsin |
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What two HA types are most commonly seen in HPAI? |
H5 and H7 |
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What is you differentials list for sudden high mortality in poultry? |
Newcastle disease Marek's disease Infectious laryngotracheitis (herpesvirus) Duck plague (herpes) IBDV (infectious bursal disease virus) |
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What made the 1918 pandemic influenza strain so deadly? |
exposure of immune system to brand new viral antigens --> overactive innate immune response --> aberrant and presistent activation of proinflammatory cytokines and chemokine responses |
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What is transformation? |
*the modification of host gene expression by the application of foreign DNA *conversion of normal eukaryotic cells to abnormal cells that have uncontrolled cell division |
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What are the three consistent features of transformed cells? |
No contact inhibition No dependence on exogenous growth factors No anchorage dependence |
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What are the three categories of oncogenes? |
1. cellular proto-oncogenes: normal host cell gene that regulates cell cycle 2. cellular oncogene (c-onc): mutated host gene activated in tumor cells 3. viral oncovene (v-onc): viral genes act as tumor inducers |
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What are the functions of proto-oncogene encoded proteins? |
1. control of DNA transcription 2. second messengers and signal transducers (tyrosine kinase, GTP-binding proteins) 3. growth factors 4. growth factor receptors |
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How do DNA and RNA viruses transform cells? |
DNA viral oncogenes: inactivation of cellular tumor-suppressor genes (p53, pRb) or inhibition of apoptosis RNA viral oncogenes: alter signal transduction process (growth factor expression, receptor expression, kinases, transcription factors) |
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What are the five classes of viral oncogenes? |
1. secreted growth factors 2. cell surface (growth) receptors 3. components of intracellular signal transduction 4. transcription factors and other DNA-binding nuclear proteins 5. components of cyclin network: cyclins, cyclin-dependent kinases, kinase inhibitors |
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What is the role of E6 in papilloma viruses? |
normal p53 --> activates p21 --> inhibits kinases E6 binds p53 --> inactive p53 --> inactive p21 --> active kinases --> loss of cell cycle inhibition |
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What is the role of E7 in papilloma viruses? |
normally E2F cell-cycle activator is inhibited by Rb E7 binds to Rb --> release E2F --> stimulation of cell cycle |
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E6 and E7 were the important viral oncogenes in papilloma viruses. What are the key oncogenes in adenoviruses? Polyomavirus SV40? |
Adenoviruses: E1A (binds Rb) and E1B (binds p53) SV40: Large T antigen binds both Rb and p53 |
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What subfamily of herpesviruses can be associated with tumors? |
gammaherpesviruses, possibly betaherpesviruses |
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What is an example of an alphaherpesvirus that causes tumors? |
Merek's virus in chickens lymphoid tumors |
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What virus causes Burkitt's lymphoma? What is the mechanism? |
Epstein-Barr virus proto-oncogene c-myc is constitutively activated --> prevents apoptosis |
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For DNA tumor viruses, which genes are transcribed during transformation? |
ONLY early genes |
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What are the three ways that retroviruses produce tumors? |
transducing retrovirus (v-onc+): introduce v-onc gene into cell chromosome cis-activating retrovirus (v-onc-): transform cells by becoming integrated in host cell DNA close to c-onc gene trans-activating retrovirus (v-onc-): gene codes for regulatory protein that may increase or decrease transcription of host genes |
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What are two ways that cis-activating retroviruses cause tumors? |
1. Insert upstream of a host gene (such as myc, which prevents apoptosis) to cause increased expression 2. Insert in the middle of a gene (such as Rb, which is a tumor suppressor gene), prohibiting normal expression |
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Oncogenic retroviruses can be classified as acute or slow transforming viruses. What's the difference? |
Acute transforming viruses carry a viral oncogene (v-onc+) Slow transforming viruses are v-onc- and act either through cis- or trans-activating pathways |
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Why are acute transforming viruses/transducing retroviruses considered defective? |
They have to infect with another virus because they don't have the genes necessary for their own replication. |
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What are the four most common families of DNA viruses that cause tumors? |
papilloma adenovirus herpesvirus hepatitis |
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What is the basic morphology and genome of Retroviridae |
enveloped, isometric or rod-shaped capsids +ssRNA |
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What is contained in the nucleocapsid of a Retrovirus? |
2 +ssRNA genomes 2 Reverse Transcripases (RTs) 2 tRNA primers (replication primers) |
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What are the two main proteins that can be used to identify Retroviruses? |
envelope glycoproteins (major antigens, used in FIV testing) capsid proteins (group specific and virus specific, used in FeLV testing) |
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What three forms does the Retrovirus genome go through during replication? |
1. +ssRNA (diploid, 2 copies) 2. linear ds DNA intermediate 3. integrated dsDNA provirus (integrated into host genome) |
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What acts as the genetic template for making more viral genomes for replication? |
integrated dsDNA |
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What are the three important groups of genes present in all Retrovirus genomes? |
Gag = structural proteins (matrix, capsid, nucleoproteins) Pol = viral replication (RT, integrase, RNaseH, protease) Env = envelope proteins (surface glycoproteins and transmembrane polyproteins) |
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What are the three distinct enzymatic activities of reverse transcriptase? |
1. RNA-dependent DNA polymerase 2. RNAse H (cleavage and degradation) 3. DNA-dependent DNA polymerase |
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What is required for retroviral genome integration into the host genome? |
Integrase enzyme 5 base pair inverted terminal repeat sequence (LTR) |
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Is the retroviral genome infectious? Why/why not? |
No, requires RT enzyme |
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What are three possible outcomes from retrovirus infection? |
1. productive infection 2. latent infection 3. transformation (may be V-onc+ or V-onc-) |
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How are retroviruses transmitted? |
Endogenous = behave like cellular genes, vertically transmitted Exogenous = infectious agents (may be horizontal or vertical) |
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What are the characteristics of Lentiviruses |
1. chronic 2. slow progression (lente = slow) 3. don't require dividing cells to support their replication 4. horizontal transmission |
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Where do retroviruses integrate into the host genome? |
Integration in host genome at: 1. 5bp nucleotide match 2. LTR 3. "att" site *chromosomal regions rich in expressed genes (transcription initiation sites [MLV] or sites of active transcription [HIV]) |
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How does the host immune system respond to retroviral infections? |
Endogenous retroviruses and vertically transmitted exogenous retroviruses are not detected (not recognized as foreign) Horizontally transmitted exogenous virus in immunocompetent host = transient viremia in immunoincompetent host = viremia, persistent infection |
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What are three ways that retroviruses produce tumors? (this is a repeat question because it appears more than once in her slides, so I assume it's important) |
1. transducing retrovirus (V-onc+, fast) 2. cis-activating retrovirus (V-onc-, slow) 3. trans-activating retrovirus (V-onc-, slow) |
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What are FeLV and FeSV? What kind of retroviruses are they? |
FeSV: V-onc+, transducing retrovirus, replication defective, requires co-infection with helper virus FeLV FeLV: V-onc- |
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What are the clinical forms of disease in FeLV/FeSV? |
Proliferative (neoplastic) disease Degenerative disease |
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What is the cell tropism of FeLV/FeSV? |
WBC stem cells (especially CD4 T cells) Thrombocytes |
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How is FeLV transmitted? |
Horizontal transmission: contact with infectious saliva or urine (shared litter pans, bites from infected cast, mutual grooming, nose-to-nose contact, oronasal) Vertical transmission in utero |
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Where are FeSV virus particles found? |
Present almost entirely within the tumor itself Recombinant of FeLV with host genome |
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What does the tissue tropism of FeLV suggest about the clinical form of the disease? |
FeLV infects WBCs and thrombocytes --> immunosuppression |
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What are the subgroups of FeLV? What changes between subgroups? |
FeLV-A: severe immunosuppression (100% of cats infected with FeLV) FeLV-B: neoplastic disease (50%) FeLV-C: severe anemia (1%) Differences due to Env genes = surface glycoproteins |
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What is the host immune response to FeLV? |
A good immune response can control the infection (stress may induce re-emergence of latent infection and produce viremia and active virus shedding) poor immunological response = persistent infection (viremic, shedding virus) limited immune response = viremic, protracted shedding, degenerative disease |
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Can FeLV be vaccinated against? |
Yes! FOCMA (feline oncovirus membrane associated antigen): virus-specific nonstructural protein expressed on the surface of infected cells. FOCMA antibody binds and induces ADCC of infected cells. Vaccine is protective against FeLV-induced tumors |
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What are potential side effects of FeLV vaccination? |
FOCMA vaccine at injection site = sarcomas due to the adjuvant = highly invasive tumors |
