Virology Summary Flashcards

Question

Rabbit Haemorrhage Disease

Answer 1

Caliciviridae \* Highly contagious and often fatal disease of European rabbits \* Endemic in Europe, Central America, and Africa \* Biological control agent in AUS and NZ \* Resistant in the environment \* Epi: virus shed in all secretions \* Transmission: faecal oral route, inhalation, conjunctiva, mechanical transmission (mosquitoes and fleas), fomites \* Clinical signs: SUDDEN DEATH, short incubation 3 day \* Pathogenesis:

Answer 2

\* Transmission: Contaminated food, water or fomites \* Fluid accumulation in gut lumen = secretory diarrhoea and osmostic diarrhoea because reduced ability to break down disaccharides \* Pathogenesis: very high concentrations are shed in faeces (survives in faeces for months), infectious dose is small- widespread disease (MINIMAL CONTAMINATION = WIDESPREAD EFFECTS) \* SEVERE ENTERITIS: Affects intestinal epithelial cell destruction (APICAL CELLS- vs. parvo's crypt cells). LIKE CORONAVIRUS. \* Resistant to BLEACH and CHLORINE \* Control: Ab in milk (LACTOGENIC IMMUNITY: neutralizes pathogen and just passes because it is in the small intestine lumen), dehydration and electrolyte balance major cause of death, IMPROVED HYGIENE (want a vaccine that will induce a mucosal response) \* Major cause of diarrhoea in many domestic species \* Short incubation period- 12-24 hours \* Clinical signs: profuse watery diarrhoea, may stop suckling, low mortality (associated with dehydration or secondary bacterial infection) \* Disease seen in animals 1-8 weeks old (not in first week due to colostrum)

Answer 3

\* Enveloped \* Respiratory and/or GI epithelium \* Enteric disease, respiratory disease, immunopathological, and neurological

Answer 4

\* Second most common cause of diarrhoes in calves (after rotavirus) \* Less than 2 weeks old (lasts 4-5 days) \* Replication in epithelium of mature villi \* similar to rotavirus!!

Answer 5

Coronaviridae \* Epi- multi-cat households or catteries (15% of cats are persistently affected in affected households BUT infection does not always result in disease, EFFECTIVE CELL MEDIATED RESPONSE IN MOST KITTENS to eliminate) \* Cats of any age, but less than one year and older than 10 are most susceptible \* Transmission: faecal/ oral transmission OR respiratory \* FIPV exposure 3 possibilites (FIPV replicates in macrophages): 1. Effective CMI 2. Decreased CMI- Periodic FIPV replication and shedding (but subclinical) 3. Defective CMI- Continuous FIPV = B cell activation = immune complexes= IMMUNE MEDIATED VASCULITIS which either becomes DRY (pyogranulomatous lesions- survives for months) or WET (marked vascular permeability- lives for weeks) but both are fatal.

Answer 6

Coronaviridae \* Affects chickens- highly contagious- economically important disease worldwide \* Primary replication: Respiratory tract \* Viraemia within 1-2 days of exposure (= widespread distribution to oviducts, kidneys, and Bursa- severity of lesions depends on strain virulence) \* Transmission: Respiratory route (several weeks) OR faeces OR eggs of infected birds \* Clinical signs: most severe in young \< 3 weeks- gasping, nasal exudate, mortality from occluded bronchi, REDUCED EGG PRODUCTION, 7 days in individuals, 10-14 days in flock \* Diagnosis: PCR \* Vaccines- yes

Answer 7

\* Replicate in cytoplasm to very high titres in mammalian cells with severe cytopathic effects \* Togaviruses of veterinary importance are arboviruses \* Do not have a survive in the environment phase, either in the insect host or in the mammalian host

Answer 8

Togaviridae \* Epi- tend to be seasonal- late summer after heavy rainfall- due to mosquitoes \* Pathogenesis: mossie bite- replication in local cells- drains to local LNs- viraemia spreads to muscle and connective tissue and reticuloendothelial system --\> SECONDARY replication in these tissues leads to secondary viraemia of high titre to allow CNS invasion THEREFORE neural necrosis, phagocyte infiltration and interstitial oedema (VEE also involves resp. tract) \* Clinical signs: CNS disease- incubation 9 days- range from mild fever and depression to fatal febrile encephalomyelitis- head pressing, circling, ataxia, blindness, inability to swallow \* EEE and WEE- Bird (passerine)- mosquito, bird (passerine) -mosquito- then into incidental host: consider two incubation periods- inside the bird and inside the mosquito (intrinsic and extrinsic incubation periods) (NOT sufficient viraemia in incidental hosts to continue the EEE or WEE)- HUMANS are IH (horses too) \* VEE - viraemia in horses with sufficiently high titre for horses to be a source of virus for vectors (HORSES ARE AMPLIFYING HOST)- HORSES are IH \* Diagnosis- viraemia is transient so difficult-- also lots of infection BUT possibly not acute. Look for IgM!! therefore RECENT infection. Control: vaccination available in endemic areas (BEFORE SUMMER or insect breeding season maybe boosting again)- live and inactivated. AND vector control- insecticides, repellent, insect proof stabling. EXAMPLE OF SENTINEL CHICKENS or insect traps.

Answer 9

\* Viraemia in horses is sufficiently high titre for horses to be a source of virus for vectors (amplifying host) \* Small mammals and mossies are the endemic cycle \* Bridge vectors- less selective mossies \* Mutation in the virus \* Less specific mossies= horses and humans \* Vaccinating horses \* Febrile illness with 1% developing clinical encephalitis (humans)

Answer 10

\* Endemic cycle- passerine birds and ornithophilic mossies \* Bridge vectors are zoophilic mossies \* mammals, humans, and horses are IH \* EEE- case fatality rate of 50-75% (humans, similar in horses) \* WEE- cast fatality rate 3-10% (humans, similar in horses)

Answer 11

\* Ross River Virus & Flaviviruses (WNV, MV, RRV) \* widespread musculoskeletal (RRV) and neurological disease (encephalitis- Flaviviruses) reported in horses late summer and autumn (early February) \* Clinical signs- ataxia, headpressing, depression, hypermetria (funny walk) \* what was unique about 2011? Large weather events, unusually wet summer

Answer 12

Ross River Virus (Togaviridae)- people, horses Murray Valley Encephalitis Virus (Flaviviridae)- people and horses Kunjin/ WNV (Flaviviridae)- people, horses, dogs, donkey, alpacas

Answer 13

Flavivirus, Polyarthritis virus \* Clinical signs: Fever, rash, and often polyarthritis \* Diagnosis- IgM or IgG seroconversion/ PCR \* Subclinical infection- 60% of human cases \* Most common arboviral disease reported in AUS \* reservoir hosts: grey kangaroo and maybe bats

Answer 14

Flavivirus and Pestivirus (Flavivirus are arboviruses) \* Replicate in cytoplasm \* Do not tend to last outside the host (labile and sensitive) \* Stable in meat products for months

Answer 15

Flavivirus \* Exotic to Australia (we have had outbreaks in people and domestic animals)- SE Asia, India, Indonesia \* Pigs are important AMPLIFYING HOSTS (sufficient VIRAEMIA)- pigs tend to survive but with reproductive failure \* Endemic cycle- with birds and mossies- spillover into pigs- INCIDENTAL HOSTS: horse and humans (INSUFFIENT VIRAEMIA) \* OFTEN CAUSES FATAL ENCEPHALITIS but can have inapparent infections in other species \* Sentinel chickens- seronegative chickens- chickens seroconvert so if seropositive then you know it is in the envrionment at the moment \* Diagnosis: brain and tissue samples, blood for serology \* Vaccines: inactivated and live vaccines available EFFECTIVE

Answer 16

Flavivirus \* Mediterranean, Asia, and Africa, US (old world to new world- totally susceptible population) \* Bird and mossie cycle- closely related to Kunjin virus- essentially the same thing \* Follows bird migration routes \* DNA vaccines, recombinant vaccines now. At first killed. Better longer duration. \* One reason so fast and so widespread- COMPLETELY SUSCEPTIBLE- especially BIRDS, mosquitoes propagated the infection, people too. In Australia- would need unusual weather conditions- as we have some endemic already. Not completely susceptible population.

Answer 17

Flavivirus \* Mossies and birds-- horses and people

Answer 18

Flaviviridae, Pestivirus \* Acute disease- bovine virus diarrhoea (often undetected) \* Chronic disease- mucosal disease (persistent infection) \* Epi- non pregnant cattle- all ages susceptible, reduced production \* BUT IN PREGNANT animals: Infection of susceptible cattle- crosses the placenta- infects the foetus-- depends on stage of gestation \* Early gestation \< 80 days- SMEDI \* infection early in gestation 80-125 days- cytopathic strain of BVDV, foteal lesions, weak or dead calves. Non-cytopathic strain= tolerance (no response mounted)-- GO ON TO BECOME PERSISTENT CARRIES SO IF EXPOSED TO CYTOPATHIC VIRUS THEN MASSIVE AMPLIFIERS!!!! (therefore poor reproductive outcomes of the other cows they infect) \* Infection late in gestation \> 125- calf mounts own immune response. Develop Ab and survive. \*\* If mucosal disease--\> fatal \* Diagnosis: difficult- persistently infected- serologically negative but they are the biggest risk \* Vaccines- yes BUT you can induce mucosal disease REMOVE PERSISTENTLY INFECTED ANIMALS- however, how do you identify??

Answer 19

Flaviviridae Exotic \* highly contagious \* 2-10 day incubation period \* fever, hyperaemia, purpura \* convulsions, SUDDEN DEATH \* Neurological- paralysis \* there are more moderate strains and more virulent strains (more moderate cause reduced fertility) \* Transmission: Ingestion and inhalation- replicates in tonsils--\> LNs--\> endothelial cells \* HAEMORRHAGE, DIC

Answer 20

Picornaviridae, Aphthovirus \* high morbidity, low mortality \* Disease of economic importance DIRECT AND WITH TRADE (outbreak in a dairy herd, lactation stops and reduction for the rest of the cow's life AND reduced growth rate in pigs and cows) \* DISEASE OF CLOVEN HOOVED ANIMALS- DEER, ANTELOPE, PIGS, CALVES (NOT HORSES) \* FMD free (with vaccine or without vaccine) or FMD endemic \* If FMD free with vaccine- animals can still be infected and shed virus \* Clinical signs: 2-8 incubation, infects cloven hooves, vesicle develop less than 24 hours after first clinical signs, excessive salivation, fever, inappetance, MYOCARDITIS- SUDDEN DEATH \* Diagnosis: vesicles are laden with virus \* Transmission: Respiratory tract OR broken skin, low dose to initiate infection OR ORAL TRANSMISSION of pigs (fed infected meat) \* Pathogenesis: virus replicates in pharyngeal mucosa and draining LNs, viraemia- spread to other organs. VIRUS EXCRETION respiratory route: Ruminants excrete 120,000 TCID50 from resp tract/ day. PIGS- 4 Million TCID50 resp tract/ day. PIGS ARE AMPLIFIER HOST \* VIRUS EXCRETION- up to 4 days BEFORE CLINICAL SIGNS and stop 4-6 days after VESICLES APPEAR \* SHED IN ALL SECRETIONS AND EXCRETIONS \* 80% of ruminants become persistently infected\*\*\* \* Sample that is preferred is from the mouth- pharyngeal and uper oesophageal tissues. Pigs chewing on rope. \* Vaccines are SEROTYPE SPECIFIC... SEVEN different serotypes (only decreases clinical signs, does slightly cause less shedding) \* Control: FMD acid labile-- so less than 4 pH or higher than 11 \* Clinically indistinguishable from other vesicular disease from livestock- need to diagnose in lab (Swine vesicular disease (corona), Vesicular exanthema (calici), Vesicular stomatitis (rhabdo)) \* SKIN AROUND THE TOP OF THE VESICLE- not the fibinr PLUG!!! epithelium or vesicular fluid \* PCR \* Think of Netherlands with control- cull the infected, blanket/ ring vaccine around the outbreaks and then cull the vaccinated so you can become FMD free without vaccine again for export purposes (Cheese!)

Answer 21

Picornaviridae \* URT disease in horses \* Virus excreted from resp tract \* Viraemia develops with excretion in urine \* PCR

Answer 22

Picornaviridae, Cardiovirus, Genus: Enterovirus (aka Porcine enterovirus) \* Epi- rodents natural host (urine/ faeces excretion)--\> pigs acquire infect, HIGHLY CONTAGIOUS, HIGH MORTALITY 90%, LONG EXCRETION TIME 7 weeks, survives up to 4 weeks in environment \* Pathogenesis: viraemia after ingestion, high virus titres in myocardium, spleen, mesenteric LNs... OR repro strains: SMEDI \* Important exotic disease of pigs \* Clinical signs: fever, depression, anorexia, tremors, ataxia, hind limbs show signs first- progressive paralysis, CONVULSIONS, COMA, DEATH \* Vaccinations available- quarantine, hygiene \* Diagnosis- culture, experimental infection

Answer 23

Picornaviridae, Genus: Enterovirus \* Mild vesicular disease of pigs \* Occurs sporadically in Europe and Asia \* CLINICALLY INDISTINGUISHABLE FROM FMD \* Presents as lameness due to vesicles around feelt \* Diagnosis: Antigen detection in vesicular epithelium \* Fed pigs sea lion meat that was contaminated with this the virus

Answer 24

Non-enveloped (relatively stable in the environment) \* GI virus- would not be a good career move to have an envelope \* Resp disease too

Answer 25

\* systemic disease affecting dogs, foxes, wolves, skunks, other canids \* Transmission: via ingestion of urine, faeces, or saliva from infected animal \* Infection through nasopharyngeal, oral and conjunctival route of infection-- virus infects tonsillar crypts--\> spreads to regional LNs--\> bloodstream via thoracic duct--\> infection of endothelial parenchymal cells and many organs = HAEMORRHAGE AND NECROSIS especially of liver, kidneys, spleen, lungs \* VIRAEMIA--\> spreads to urine (infection of the kidney), faeces and saliva \* Clinical recovery about 10 days after infection if production of neutralizing antibody 3 Overlapping syndromes!! \* Incubation pd= 4-9 days \* History of sudden fever, collapse, and abdominal pain in young dogs is suggestive \* virus will continue to be shed for 6 months \* CAV 1 vaccine causes ocular oedema (immune complexes in the capillaries in the eye)- so use CAV 2 vaccine is used

Answer 26

\* Localized respiratory disease (part of kennel cough complex) \* Bronchitis and bronchiolitis \* No systemic infection \* provides complete homologous protection and cross protection against CAV 1 without side effects

Answer 27

\* Young horses- mostly asymptomatic or mild disease \* UNLESS Arabian foal with SCID (absence of B and T cells so unable to mount a response) \* So within 3 months of birth foal dies of adenovirus \* So high prevalence in the virus, but does not cause a major problem unless immocompromised

Answer 28

\* Non-enveloped- resistant in the environment (resistant to solvents, low pH and high temperature) \* cause papillomas (warts) \* replication linked to growth and differentiation of stratified squamous epithelium of skin and some mucous membranes \* May give rise to carcinomas \* Usually regress after a few weeks with CMI response

Answer 29

\* Cattle are more commonly affected, typically in young but all ages \* 10 different bovine papillomaviruses \* Transmission: Fomite transfer (equip used to restrain), sexual transmission of venereal warts \* More common in housed than at pasture \* Infection widespread but oftenw ithout any clinical signs \* Some cause enzootic haematuria- carcinogens and end up with carcinomas in the bladder which causes bleeding into the bladder \* Lesions in the alimentary tract from another papillomavirus

Answer 30

\* Aural plaques and cutaneous papillomas \* Young horses- muzzle typically \* Usually regress 1-9 months

Answer 31

\* the most common tumour of horses, mules, and donkeys \* More common \< 4 years old (unusual for a tumour) \* Occur singly or in groups \* Head, ventral abdomen, and limbs most commonly affected \* Locally aggressive, do not metastasize \* Superficial ulceration and secondary trauma are common \* Bovine papillomavirus found in the lesions-- but of course association does not equal causation

Answer 32

\* Non-enveloped- extremely resistant in the environment \* Replicate in the nucleus in RAPIDLY DIVIDING CELLS \* Bleach in a practical situation will not work because too much organic matter.

Answer 33

\* Highly contagious, systemic and enteric disease of cats \* Bone marrow suppression, GIT signs, cerebellar hypoplasia (foetus) \* One serotype- worldwide \* Endemic in unvaccinated cat populations- young cats affected (primarily in kitten as maternal antibodies wane) \* Transmissible infection in susceptible queens (in utero infection can cause cerebellar hypoplasia/ atrophy) AND in saliva, urine, and vomit (in acute stages) \* Incubation 5 days \* Seasonal disease pattern \* If survive, strong, longlasting immunity (severe cases die in peracute stage) \* Clinical signs: blood diarrhoea, dehydration, vomiting \* Pathogenesis: rapidly dividing cells- lymphoid tissue \* Treatment: supportive therapy, blood transfusions \* Vaccines- very EFFECTIVE

Answer 34

\* High morbidity and mortality in initial outbreak 1978 (all ages of dogs) \* Transmission: faecal oral route of infection following exposure to virus in contaminated faeces \* Severe disease in pups between 6 weeks and 6 months of age (waning maternal antibodies) \* Disease can be mild or sub-clinical if SUFFICIENT IMMUNITY \* Clinical signs: haemorrhagic gastroenteritis and vomiting, myocarditis (uncommon- in young pups because heart cells dividing rapidly \< 2 weeks) (severely affected animals die) \* Pathogenesis: crypt cells in the intestinal mucosa-- they are the key to the entire intestinal mucosa-- so you can end up with mucosal collapse (maldigestion and malabsorption and often severe haemorrhage- foetid smell) \* Diagnosis- PCR or faecal immunoassay, haemagglutination \* Treatment- supportive \* Vaccination- EFFECTIVE \* kennels and shelters- strict hygiene, quarantine, and disinfection required

Answer 35

Canine Distemper, Canine Parvo 2, Canine Adeno 2 \* no earlier than 6-8 weeks, 14-16 weeks, and 1 year of age \* Adult vaccination not more often than every 3 years \* Optional vaccines should only be used in animals at risk annually

Answer 36

We cannot predict when maternal antibodies will wane

Answer 37

How many progeny? Horses with one or cattle vs. a litter with dogs or cats? Is there enough? Quality, Quantity, Gut closure \* Giving colostrum from a different mother- if they've been running together likely to have been exposed to similar things

Answer 38

\* SMEDI!! (Stillbirth, Mummification, Embryonic Death, Infertility) \* Important cause of reproductive failure in swine worldwide) \* Single serotype \* Endemic in many herds- MORBIDITY reduced by VACCINATION \* Most significan if virus is introduced in non-endemic herd \* Transmission: Oronasal route \* Pathogenesis- replication in tonsilar lymphoid tissues--\> viraemia--\> transplacental \* \<30 days gestation: foetal death and resorption \* 30-70 days gestation: foetus fails to develop (mummification/ stillbirth) \* \>70 days gestation: stillbirth or normal piglet (depends on immune response) \* Diagnosis- infected foeti contains high levels or virus, haemagglutination, PCR \* Prevention- in endemic situation exposure of gilts prior to mating inducing immunity, vacciation available (limited opportunity to vaccinate guilts as they are bred at 7 months of age- waning maternal antibodies)

Answer 39

\* Non-enveloped \* Very stable in environment (stays in nesting boxes, shed in dander) \* require actively dividing cells \* persistent infection

Answer 40

\* Cockatoos, parrots, budgerigars \* Birds under 5 years old at greater risk \* Feather loss, feather deformities, beak and claw deformities \* Pathogenesis- virus replicates in the basal epithelial layer of feather follicles, beak, and claws \* Captivity- they can survive, but not in the wild- they can't eat \* Diagnosis- PCR, but not many things that make birds look the way they do when they have PBFD \* Experimental vaccine only \* Resistant in the environment- so difficult to eradicate- just get rid of cage and everything

Answer 41

\* Widespread in most pig populations \* Variety of clinical disease syndroms- wasting is most important NOT PUTTING ON WEIGHT \* 6 week old pigs present with weight loss and enlarge LNs and dyspnoea

Answer 42

\* Circoviridae \* 2-3 weeks of age, young birds develop aplastic anaemia and generalized lymphoid atrophy \* Transmission: horizonal by direct contact and fomites AND vertical \* Virus shed in faeces and feather dander

Answer 43

\* Non-enveloped \* segmented- important in reassortment \* Genus orbivirus: Bluetongue, African Horse Sickness, Equine Encephalosis (arboviruses- infectious not contagious)

Answer 44

Reoviridae, Orbivirus \* We have bluetongue virus in Australia, but do not have Bluetongue disease (comes from Indonesia and PNG)- in the North \* Disease of sheep, cattle, goats in subtropical and tropical regions \* Clinical signs: Hyperaemia of oral and buccal cavities, nasal discharge, congestion of oral mucosa, cyanosis of the tongue (congestion in the vessels), OEDEMA (head and neck) \* Pathogenesis- Cardiovascular system- clinical signs of VASCULAR FRAGILITY (endothelium) \* Incubation period about 1 week (immune status and nutritional status important)-- also incubation period in vector (so movement of animals may have occurred several weeks prior) \* 30% mortality rate, usually 2-8% \* Ewes affected during pregnancy often abort \* Transmission: Cuilicoides midge (1 midge lives for 70 days and could infect 20 animals) (overwintering- they may hole up with the cattle in the shed) \* Viraemia lasts 14-28 days (cows up to 10 weeks) \* \> 25 serotypes!!! IMMUNITY IS SEROTYPE SPECIFIC!!!

Answer 45

\* Reoviridae, Orbivirus \* Essentially Bluetongue in horses \* Equidae- horses, mules, donkeys, zebras \* GENERALIZED OEDEMA AND LESIONS OF VASCULAR FRAGILITY (endothelium)-- and regional lymphoid tissue-- AFFECTS EVERYTHING \* Peracute form: high fever \> 41C, sudden onset of dyspnoea, rapid abdominal breathing, coughing, pulmonary oedema (effectively drowning in their own pulmonary oedema), saw-horse stance, collapse and die within 4-24 hours \* Subacute: cardiac-- subcutaneous oedema, abdominal pain, cunjunctivitis (badly protruded conjunctiva) \* USUALLY ALL LESIONS OCCUR \* Mild or sub-clinical \* 9 SEROTYPES- IMMUNITY IS SEROTYPE SPECIFIC \* Vaccine is availabe \* Incubation period is 1 week \* Diagnosis- presumptive- clinical signs, rapid death \* Control- have been outbreaks outside of the South Africa with high mortality... if you use a live virus vaccine- you can end up spreading the disease through the Culicoides

Answer 46

\* Fragile enveloped viruses therefore prolonged close contact or intimate contact (blood or bodily fluids)... spread via respiratory-- you would need intensive conditions and close contact (some can be vertically transmitted) \*\*REVERSE TRANSCRIPTASE\*\* \* Like other RNA viruses- rapid replication and high rate of mutation (proteins on the surface are different, it keeps them one jump ahead of the immune system) & HIGH recombination rate (recombination, pseudotypes, and pseudodiploid) \* Immunosuppression and neoplasia \* Lifelong infection \* Long incubation period, chronic diseases \*\* 2 copies of the genome in each viral particle (within the nuclear capsid)... nearly all the other viruses have a single genome

Answer 47

\* contains 2 molecules of RNA- in other words... 2 copies of the genome sitting in the nucleus (nearly all other viruses have single copes of the genome) (called a diploid organism) \* get into a cell- reverse transcriptase already attached to RNA molecule starts replicating it and produces a DNA copy--\> that can be inserted into the hosts chromosome--\> a PROVIRUS (can be transmitted into the progeny or through secretions, prolonged close contact) \*\* The provirus serves as a template for new viral messenger RNA--\> turned into new proteins and generate the entire virus assembly process again--\> eventually new virus... OR \* Provirus can be inserted into the hosts chromosome in multiple spots- leads to gene transcription that leads to gene changes (IF INSERTED IN THE WRONG SPOT IT CAN LEAD TO NEOPLASTIC CHANGES) \* gag gene- production of thenuclear capsid \* pol genes- responsible for replication (reverse transcriptase) \* env genes- encode the envelope

Answer 48

Diploid genome- co infection by two different viruses in the same cell. What can happen: \* Pseudotyping- if one replicates more efficiently than the other- then you can have the genome of one virus coated with the capsid of the other virus (can result in changes in host cell range or host species range- retroviruses are therefore able to jump species easier than other viruses CAN ADAPT TO NEW CELL) \* Pseudodiploid- one copy of genome of one virus and one copy of the other. Two genomes transmitted at the same time therefore high likelihood of recombination. Can transmit the two viruses at the same time! HIGH LIKELIHOOD OF RECOMBINATION. \* Recombination- you can have proviruses already sitting in the chromosome- another one comes along and they can recombine with each other \*\* COMMON IN POULTRY

Answer 49

Retroviruses often cause lymphoid types of tumours e.g. Leukaemia. White cells in the blood stream or solid lymphoid tumours. Picture: Lymphosarcoma

Answer 50

\* Retroviridae \* Immunodeficiency viruses, slow virus diseases Examples: HIV, FIV, Visna, Equine Infectious Anaemia

Answer 51

Infection is more common than disease, infection for life, antibody commonly forms and persists. Especially important with individual pets. Only if you truly suspect retroviruses should you test (PCR, ELISA). \*\* using Ab test with a herd, might be okay if you suspect a retrovirus BUT \*\* you have to be careful dealing with individual animal-- don't use antibody test, for example with FIV-- the cat can sometimes eliminate the virus down to a point where they are not infectious to other cats. So you will still detect it (antibody will persist)... so you could give the owner the wrong advice.

Answer 52

\* Avian neoplastic diseases (avian tumour viruses). CONTROL: Eradicate from BREEDING STOCK. SELECT BIRDS FOR RESISTANCE (Certain MHC Haplotypes) 3 categories: - Replication incompetent - Replication competent (less capable of causing tumours) - Replication competent-- rapidly transforming (reproduce themselves and can cause neoplasia in host cells) \* Horizontal and vertical transmission (think of worlds meat chickens carrying alpharetrovirus due to pinching genetic stock of best breeding company in the world) \* Germ line common- usually see in the first few days of life \*\*\* If birds are infected after 5 days of age-- they will generally eliminate these diseases (the birds that are infected early are of the most danger because the virus is replicating unchecked) \*\* Immunotolerance (persistent infection with ++++ viral shedding) \* LYMPHOID TUMOURS-- ALL LYMPHOCYTES

Answer 53

Retroviridae, Beta retrovirus \*\* Breathless sheep \*\* \* Long incubation period (2-5 years) \* Multiple lung tumours ERADICATE BY REMOVAL OF AFFECTED SHEEP and progeny (because it is slow moving, this is effective- diagnosis is near impossible because recall infection is more common than disease and most sheep have retroviridae) (sheep are lagging behind-- CLINICAL SIGNS DIAGNOSIS) \*\* eventually die of their own secretions- lungs full of fluid \*\* TIP SHEEP UP YOU CAN POUR LUNG FLUID OUT OF THEIR NOSE INTO A DISH- loaded with virus... \*\* No diagnostic tests available- no immune response against virus.. so no Ab tests. All sheep have endogenous retroviruses (not producing virus but sitting in the chromosome) that are similar to Jaagsiekte, so you cannot distinguish with PCR

Answer 54

Retroviridae, Gamma retrovirus (similar to Jaagsiekte, Beta Retrovirus) \* Lymphosarcomas and leukaemia AND/OR \* Formation of Immune complexes and immunodeficiency \* Two outcomes of infection: -Virus neutralizating antibody can be present-- Feline Onco Virus Antibody (FOCMA) therefore knocked the virus down to a point where it is unlikely to be transmitted and does not cause disease OR - some cats have persistent viraemia without effective antibody which do spread disease and do cause disease in the infected cat \* A lot of cats become infected but do not progress to disease, LOW PREVALENCE in some cat populations (2% in Sydney in Australia), sometimes high prevalence in urban cat populations in other parts of the world

Answer 55

Deltaretrovirus \* CONTROL AND SPREAD: Horizonal infection (inefficient)- removal of affected animals can eradicate usually (because rate of infection relatively low) \* Most infections are subclinical- about 30% develop lymphocytosis and 10% of those develop lymphoid tumours after 4-8 years \* CAN AFFECT PRODUCTION \* Eradicate by tests for Ab and cull positives (for example, dairy cattle-- effective eradication program in a number of countries) \* Iatrogenic spread (VET!!!)

Answer 56

Lentivirus \* Long incubation (2+ years) \*\*RESPIRATORY SPREAD\*\* AND/OR \* Ewe to lamb transmission \* VISNA- immune attack of neural cells--paralysis and eventually muscles waste \* MAEDI- Chronic progressive pneumonia \* Strong immune response but this drives development of pathology, does not protect (Ab test is diagnostic) \*\* has been eradicated from some countries-- ICELAND-- completely depopulated large areas of sheep for 5 years\*\* \* Exotic to AUS and NZ but present most everywhere else

Answer 57

Lentivirus \* Leukoencephalomyelitis in goat kids \* Sometimes wasting \* Arthritis in adults (BIG KNEES) \* Lifelong infection \* Antibody present (does not eliminate virus) \* TRANSMISSION by colostrum \* CONTROL: achieved by serologic testing and culling AND by PASTEURIZING COLOSTRUM before giving it to goats (fragile virus) \*\* high prevalence in goats in Australia\*\*

Answer 58

Lentivirus ACUTE \*incubation period: 7-21 days \> fever \* Lifelong infection (can have recrudesence) \* Recurrent fever, jaundice, oedema, weakness, anaemia \* Antibody present (DIAGNOSTIC) \* VECTOR and iatrogenic transmission \*\* CONTROL WOULD BE SIMILAR TO ANY VECTOR BORNE VIRUS... but also vet measures

Answer 59

\* Worldwide distribution \* Domestic and other cats \* Five subtypes (vaccines not widely used) \* Initial acute disease, many months or years later: wasting, opportunistic infections, leukopaenia, behavioural change \* TRANSMISSION: Bites, cat fights (saliva) \* Lifelong infection \*\* Many infected cats remain disease free!! Not justified to recommend euthanasia for disease control.

Answer 60

\* Fatal disease in Balinese cattle in Indonesia \* Fever, panleukopenia, LN enlargement, haemorrhages \* Short incubation (5-12 days) (UNUSUAL)

Answer 61

\* Long incubation period but subacute disease because once they start showing signs they normally die fairly quickly \* Uniformly fatal \* Spongiform degenerative lesions (NO INFLAMMATORY response) \* Normal aging causes these type of lesions as well, so difficult to know if lesions are due to normal aging or disease \* Agent is about the same size of a virus, NO nucleic acid \* HIGHLY RESISTANT TO INACTIVATION \* LIPID ASSOCIATED (most viruses tend to be associated with the more aqeous parts of cells/ the brain) \* infectivity destroyed by protein disruption

Answer 62

\* Obvious strain differences \* No inflammation, adaptation to host species, very long incubation, EFFECT OF DOSE ON INCUBATION PERIOD \* Post-transationally modified variant of host's PrP= PrPsc (accumulates in infected cell and screws up the function, propagation of MISFOLDED PROTEIN slowly spreading cell to cell) \* Pruritis, tremors, ataxia, paralysis, wasting, subacute (most die in 4-6 weeks), generally 2-5 years old \* Control: aggressive slaughter campaigns, strict quarantine regulations on sheep, breeding resistant sheep (UK) BUT atypical scrapie occurs in sheep where previously thought resistant \* Pathogenesis: vacuolation and degeneration of neurones of CNS, hypertrophy of astrocytes, tonsils, spleen, LNs, probably in DCs, spinal cord, ascends the spinal cord to brain \* Transmission: Spread horizontally and maybe vertically, injection of infected material (louping ill)

Answer 63

Transmissible Spongiform Encephalopathy (aka Mad Cow Disease) \* Outbreak in the UK in 1986 (30,000 cases in 1994) \* Hyperaethetic, apprehensive, nervous, frenzied \* Eventually ataxic, then debility, recumbency and death \* Death in weeks to months \* Incubation period of several years \* Typical spongiform lesions \* Same sort of lesions in big cats in zoos (Perth) \* Epidemiology: Associated with FEED MEALS in the UK, LOWER TEMPERATURES IN PROCESSING, reduced use of lipid solvents, BAN ON FEEDING MEAT MEAL TO CATTLE \* Diagnosis of PrP by western blot ELISA \* Control: ban on feeding meat meal, fewer new cases occurred, slaughtered all suspected cases and progeny & siblings (BSE in humans- 228 worldwide)

Answer 64

\* Rare outbreaks in farmed mink \* Feeding scrapie infected sheep meat to mink \* mink eat each other

Answer 65

\* Mule deer and elk \* Captive deer and in free ranging animals \* Progressive weight loss, behavioural changes, salivation, polydipsia and polyuria \* Increasing incidence - infectivity in venison (concern for people who eat venison in the US)

Answer 66

TSE \* Progressive paralysis \* PNG- women and children, familial \* Ritual cannibalism practised on dead relatives

Answer 67

TSE \* Dementia of humans \* rare but worldwide \* Familial, iatrogenic or sporadic (contaminated instruments) \* corneal grafts, growth hormone

Answer 68

\* RNA viruses - Retroviruses - Flaviviruses \* DNA viruses - Poxviruses - Herpesviruses - Adenoviruses - Papillomaviruses - Hepadnaviruses

Answer 69

RNA viruses usually productive infection with progeny virions. While DNA viruses usually non-productive- integrated into cellular genome. Cancer can be regarded as failure of immunonological surveillance because they are normally eliminated by the immune system (there are tumour associated antigens on the surface).

Answer 70

\*\* Viral oncogenes- not necessary for viral replication (retroviruses had viral oncogenes- appeared to be resp. for transformation of cells- NOT found in all retroviruses). \*\* Cellular oncogenes- regulate cell function (sitting in the chromosome creating proteins that create tumours) \*\* Oncoproteins- soluble factors secreted by cells that stimulate other cells to grow -growth factors, growth factor receptors, intracellular signal transducers (downstream of this process- signal pathways that receive GF and signal cell to tell them to produce more genes), nuclear transcription factors (increase expression of certain genes)

Answer 71

These stop the cell cycle in the G1 phase OR they trigger apoptosis. If you remove these genes, then they continue to replicate OR they won't die when they are normally told to die. Viral infection may interfere with activity of these genes and proteins.

Answer 72

Exogenous (infect cell, go through lytic cycle, produce more virus that is then released) and Endogenous (DNA provirus in the chromosome of the host- never produce a virion- not all are a problem- can even be productive BUT can be capable of transforming cells- you would need a lot in order for them to end up going in the "wrong" cell- chance). Within exogenous: Replication competent and replication incompetent. Genes: gag- structure of the virion pol- replication (reverse transcriptase) env- proteins on outer surface

Answer 73

Either having the viral oncogene- nearly 100% of infected animals OR retroviruses sitting there for a long incubation period (proviruses) they usually do still cancer- just much later in life Replication incompetent endogenous retroviruses- if their env gene is replaced by viral oncogene= CANCER

Answer 74

Myeloid Leukemia Solid lymphoid tumours as well

Answer 75

\* Hepatitis C virus in humans causes chronic hepatitis--\> chronic inflammation may induce hepatocarcinoma \* unk in animals- may not live long enough or may just be undiscovered

Answer 76

\* Non-productive infection (need cell to survive infection). \* some contains analogues of oncogenes (genes that appear to be able to control cell growth- evolved these on their own)-- adenoviruses and papillomaviruses (increase cellular expression) \* Poxvirus analogue of epidermal growth factor (benign. Why? because it creates more cells for them to infect.) \* Squirrel- tend to be benign but can occur in a bad place that does not allow the animal to live \* BUT EXCEPTION fowl pox vaccine strain- picked up retro viral proviral genome inside the poxvirus genome- retrovirus came with the vaccine- so high rate of leukaemia associated with fowl pox strains (can travel with other viral genomes)

Answer 77

\* Benign warts (which are a tumour) plus co-factors CAN lead to neoplasia and carcinoma \* Bovine type 4 papillomavirus plus bracken fern = GIT and bladder carcinoma as a result of virus and carcinogens in the bracken fern \* Bovine Occular papillomavirus, lack of pigment plus UV exposure \* Also, Equine Sarcoid- do not metastasize but proliferate locally (BOVINE PAPILLOMAVIRUS)

Answer 78

\* Hepatic carcinomas \* Duck hepatitis virus, woodchuck hepatitis virus, human hepatitis B virus \* IN ducks, mycotoxin is co-factor and you do see tumours \* earlier in life infection occurs the greater the chance of developing hepatic carcinoma \* Expressed protein vaccine for hepatitis B (recombinant vaccine) \* Starts as RNA but when it infects the cell they become DNA- become proviruses sitting in the host chromosome

Answer 79

\* tumours affecting the nerves \* Rate of infection and mortality- 50% (high) \* See paralysis, tumours in feather follicles, bent necks, liver \* contains onco genes- do not appear to have origin in the host- developed by the virus (one induces increased transcription in the infected cell and a second onco gene which encodes a component of an enzyme that extends the telomeres) \* live virus vaccines- vaccines lack the v-onc gene (why they can induce protection)- used worldwide in poultry flocks- delivered by robots to get it in early enough to develop protection

Answer 80

\* Virus \* Susceptible host, genetic variation \* Immune status \* Co-factors (mutagens) (e.g. bracken fern and UV light) \* Oncogenes (brought in by virus OR c-onc (cellular oncogene) activated by virus which increases the virus expression) \* Interfere with cellular tumour suppressor genes

Answer 81

\* Developed to reduce the risk of cervical carcinoma \* Pre-pubescent women \* Likely to reduce general carcinogenesis of papillomavirus

Answer 82

Rhabdoviridae, Genus Lyssavirus \* Variable incubation period (replicates in muscle cells around the bite- enters the peripheral nervous system (very little replication in nerve cells) and makes its way slowly to the brain "retrograde axonal transport") (14-90 days (weeks to years): depends on species, virus strain, site inoculum)\*\* bites around the face or deep bites= shorter incubation period \* all warm blooded animals at risk \* Prodromal period: confused, disoriented \* Furious rabies (further spread within CNS (neocortex): increased aggressiveness hyper-excitable, roam long distances, bite inanimate objects \* Dumb rabies (reduced CNS function FURTHER spread- death due to respiratory arrest): muscle weakness, inability to swallow, salivation (hydrophobia- cannot swallow) \* Clinical signs- invariably fatal- seizures, coma, respiratory arrest, and death within two weeks of onset of clinical signs Transmission: bites (scratching and licking- unusual but aerosolized saliva from bats in a cave)... \*\*centrifugal spread in nerves- release from axon terminal and infection of non-nervous tissue- salilvary glands\*\* 1. Urban rabies in dogs (\>95% of human cases are from dog bites)- developing countries- stray dog control and vaccination programs (maintained when population density \> 4.5 dogs/km^2) 2. Sylvatic rabies in wildlife- North America (92% of reported cases), Europe, Africa \*\*\* Post mortem diagnosis (brain tissue immunofluorescence)- AT MOST RISK\*\*

Answer 83

\* Don't keep killing the strays- allows them to keep breeding because it opens up more room regarding resources \* Desexing, vaccine programs \*\* One vaccine is affective against all serotypes\*\*

Answer 84

\* aerial baiting with attenuated vaccine (fox)- chicken heads \* more difficult when multiple species are involved (they eat different things!) \* Requires money!! (Vaccination) \* In South Africa, for example, there are a number of different cycles- Mongoose & Canid \*\* One vaccine is affective against all serotypes\*\* \* Immune response- protective immunity involves both humoral and CMI-- Immune host will clear virus from site of entry BEFORE virus enters the nervous system (post exposure vaccination and RIG) \* Vaccines: inactivated in injections-- attenuated in chicken heads

Answer 85

Very similar to rabies (serologically)- vaccine will be the same

Answer 86

Rhabdoviridae, Genus Vesiculovirus \*\* Clinically indistinguishable from FMD \* Febrile disease of horses, cattle, and pigs- exotic to AUS \* Vesicular lesions: heal within 7-10 days Oral mucosa, teats, coronary band of cattle Spread by arthropod vectors

Answer 87

\* 3 day sickness \* transient- not serious BUT large animals laying down- they end up with nerve paralysis etc. \* Spread by culicoides midges and mossies \* Outbreaks occur when conditions favor vector movement or movement susceptible animals into an endemic area \* Incubation 4-7 days; 3-4 day duration of viraemia (neutrophilia: vasoactive amines cause increased permeability of serous membranes) \* Polyserositis and hypocalcaemia \* Neutralizing antibodies by day 3 after clinical signs \* HIGH MORBIDITY; low mortality \* Tropical regions- outbreaks occur after rainfall; in temperate regions- outbreaks in summer \* Solid immunity post infection- cases in uninfected animals \* Diagnosis by clinical signs \* Treatment with anti-inflammatories effective \* Inactivated vaccine available

Answer 88

Monitoring of sentinel herds, serological surveillance, insect traps \* Bluetongue, bovine ephemeral fever virus, Akabane virus \* trade assurance, early warning, risk management \* Mainly arc around Australia- not as much in the south

Answer 89

Bunyaviridae, Bunyavirus \* Cuilicoides brevitarsis- arbovirus of sheep and cattle \* Vertical transmission: foetal death, abortion, hydrancephaly, arthrogryposis \* Epi: tropical and sub-tropical regions in the Middle East, Asia, Australia, and Africa-- sporadic epidemics correspond with movement of vectors-- or movement susceptible animals into endemica area \* Disease in cattle, sheep, goats, and deer \* Previously unexposed dam is bitten by infected vector, virus crosses placenta from maternal circulation without producing clinical signs in the mother, severity of clinical sigsn in the foetus depend on stage of gestation when infected, primary foetal infection is an encephalomyelitis and polymyositis \* Pathogenesis: severely affected foetuses die and are aborted, survivors develop large cavitations in the cerebrum, hydrancephaly, and neurogenic arthrogryposis (kyphosis, scoliosis) \* Serological diagnosis- problem is everyone would be antibody positive but only the pregnant will have signs and symptoms, diagnosis is usually by gross pathological examination- virus is difficult to isolate from foetus/ newborn- caesarean \* GOOD immunity after infection \* Inactivated vaccines available in Japan and AUS

Answer 90

Bunyaviridae \* Shed in aerosolized urine and faeces of mice

Answer 91

Bovine parainfluenza virus (N. America) Newcastle Disease Rhinderpest Pest de Petit Ruminant Hendra

Answer 92

1. Haemagglutinin on the outside of virus 2. Neuraminidase protein \* role in attachment \* neutralizing antibodies are directed against HN 3. Fusion protein: cleavage of F protein essential for infectivity

Answer 93

Paramyxoviridae, Rubulavirus \* Virulence is variable \* Resp, GI, Circulatory, NS \* Incubation \*\*\*the more cleavable the F protein is (proteases by cells) the more virulent the virus is\*\*\* 1. Velogenic = high virulence (mortality rates approaching 100% in viscerotropic)--\> (haemorrhagic intestinal lesions and bright green diarrhoea--\>viscerotropic velogenic isolates) AND Neurotropic--\> mortality 10-20% resp signs, NS-- tremor, paralysis, torticollis 2. Mesogenic= intermediate (mild disease- mortality in young birds)--\> 10% mortality-- usually young- coughing, weight loss, reduced egg production 3. Lentogenic (in Australia)= low virulence (mild dx or inapparent infection) Pathogenesis: virus replication in epithelia of resp and GI-- HAEMATOGENOUS SPREAD FROM THESE SITES-- spleen and bone marrow. Secondary viraemia- infection of lung, intestinte, CNS Epi- WIDE RANGE OF BIRD SPECIES (not called Newcastle disease in wild birds-- Avian paramyxovirus 1)--- because Neutropic is defined as Newcastle disease?? Easily transmissible to commercial birds for example-- even if biosecurity is okay Transmission- inhalation of aerosols or ingestion of contaminated food or water. Would have to get rid of bedding and clean out the carcasses. Excreted in faeces, from resp tract- survives in carcasses for weeks. Wild birds act as reservoir- mutation at cleavage site. Diagnosis- virus isolation in embryonated eggs-- pathogenicity tests- mean death time for eggs- RT PCR and sequencing of fusion protein. Antibody detection by HAI Control: ND free countries: test and slaughter; ND endemic countries: attenuated live vaccines strains (V4 strain- endemic Australian strain, selected for temperature resistance, used to protect village poultry in Asia and Africa). Australia is a ND free disease WITH REGIONALIZATION. (ND is not an international trade barrier!!!) \* note diptheritic membrane on the inside of the trachea- which causes dyspnoea

Answer 94

Paramyxoviridae, Genus: Morbillivirus \* Eradicated 2011 \* acute fatal disease of domestic cattle, buffaloes, yaks \* high morbidity, high mortality (death within 12 days of dehydration and wasting, secondary infection) \* pyrexia, inflammation, and necrosis of mucous membranes (necrotic foci- become erosions), profuse haemorrhagic diarrhoea- lining of intestine comes out \* short incubation 3-5 days How did it maintain itself in the population? NO RESERVOIR- cow to cow. Transmission by inhalation. Epi- ONE SEROTYPE. Lots of strains but one vaccine ruled them all. One shot of the vaccine gave them lifelong protection. The vaccine covered any strain of Rinderpest that was out there. Virus is labile in the environment. No carrier state because they DIE.

Answer 95

Like Rinderpest but in goats Paramyxoviridae, Morbillivirus \* Africa, Central Asia \* Vaccines available- can also use Rinderpest vaccine \* Transmission by aerosol, requires close contact 70% mortality

Answer 96

Paramyxoviridae, Genus Morbillivirus \* highly contagious \* generalized infection affecting many organ systems \* there are cases in AUS but it is rare (it is worldwide) Epi- outbreaks in dogs, foxes, skunks, racoons, ferrets, lions Virus is labile in the env, Requires direct contact or close aerosol transmission, virus shed in expired air, faeces, urine, and other secretions \*\* urban dogs (young dogs as maternal Abs wane 3-6 months) vs. rural dogs (more susceptible because lower pop. pressure- if they are unvaccinated- fully susceptible- does not matter the age) Clinical signs- pyrexia, ocunasal discharge, pharyngitis, tonsillar enlargement, skin rash and pustules, hyperkeratosis of nose and footpads, cough, vomiting, diarrhoea, NEURO SIGNS (OLD DOG ENCEPH)--- GRAVE PROGNOSIS for dogs with neurological signs (even if they recover residual defecits) \*\* lifelong immunity if recover or vaccination.

Answer 97

Paramyxoviridae, Genus Henipavirus (initially thought African Horse Sickness- but in September so no culicoides) \* horses were tachypnoeic, tachycardic, ataxic, frothy nasal discharge, congestion, fluid filled lungs, (7 deaths within 12 hours)

Answer 98

Paramyxoviridae, Genus Henipavirus \* outbreak of viral encephalitis in people in Malaysia Sept 98 and April 99 \* Nipah closely related to Hendra \* Pteropid bats \* Hendravirus antibodies in each species of the Pteropid bat Do not know how it goes from bat to bat. Some evidence of horse to horse. No evidence of bat to human.

Answer 99

Influenza A (focus): \* horses, pigs, and poultry (and interface with humans) \* envelope, segmented RNA genome (each segment codes for a different protein in the virus) \* Haemagglutinin (HA) (attach virus to cell it is going to infect) \* Neuraminidase (NA) (responsible for getting the virus out of the infected cells) \* Based on HA and NA subtypes- is what creates different subtypes of Influenza A. (e.g. North American and European lineage-- further divided into strains) \*\*\* all subtypes found in wild water birds. Problem when it spreads to poultry (H7, H5), pigs (H1N1, H3N2), horses (H3N8), and humans (H1N1, H2N2, H3N2).

Answer 100

\* aerosolized- coughing or sneezing \* Virus attaches to cilia, trachea and bronchi- spreads through resp tract to alveoli 1-3 days \* fevere and pneumonia coincide with necrosis of epithelial cells in resp tract- create a nice env. for bacteria to grow

Answer 101

\* H1N1, H3N2 \* Seasonal \* Shed- 8-10 days \* subclinical infections \* High morbidity, low mortality \* Common interspecies transmission: horses, humans, birds \* Closely monitored as a source of potential pandemic viruses

Answer 102

H3N8 \* Fever, nasal discharge \* Harsh, dry cough \* need rest \* predisposes to Secondary bacterial infections (environment it sets up in the trachea) \* high morbidity- highly contagious

Answer 103

Resp and intestinal virus replication in birds. So virus is shed in high concentration in faeces and resp. secretions. 2 types of Avian influenza: LPAI and HPAI (HIGH virulence due to viraemia) \* LPAI- resp. signs more obvious. LOW VIRULENCE-- can originally be infected with LPAI and it can become the HPAI-- associated with rapid mutation of genes. \* HPAI- disease occurring suddenly-- sudden death. Watery diarrhoea, excessive thirst, inappetence, staggering gait

Answer 104

Prevent contact between infected and susceptible hosts Fomites Avian- wild waterbirds as reservoir- don't add new birds to a flock without measures \*\* Early detection and warning: \* biosecurity- movement control/ natural and articial boundaries/ management practices \* surveillance \*\* example with EI: ring vaccination around the border so the virus could not escape those areas.

Answer 105

\* Protective Abs directed to HA and NA-- variation causes Abs to be ineffective for different strains \* some cross reactivity between strains and subtypes in targets of cell mediated immunity

Answer 106

HA binds to Sialic Acid. HA resp. for entry. NA resp. for exit. Also HA and NA resp. for antigenic variation. HA resp for latching on and for fusion (fuse viral envelop with endosomal membrane- HA is resp for this). HA is the major target for protective Antibody. NA helps the virus get out of the cell- target for protective Ab as well (Tamiflu and Relenza, for example)- stop the virus from replicating (aka neutralize). Antigenic variation results in: Reduced efficacy of pre-existing Ab from previous infection or vaccination \*\* Drift- new strains, same subtype. Host has neut. Ab to HA or NA- infected virus has random mutation throughout genome, including HA and NA. Some neut. Ab no longer binds- mutants escaping neut. become more prominent= DARWIN!!! Survival advantage- therefore new strains within a subtype. Requires yearly update of vaccines in humans. (POSSIBLY driven by vaccines... no evidence) \*\* Shift- rapid new subtypes. More dramatic change. Emergence of new subtype in a population. 1) genetic reassortment between subtypes (requires coinfection of a single host cell... e.g. pigs as a MIXING VESSEL) e.g. Swine flu 2009- avian and human segmen 2) direct transfer of a subtype from one species to another - Avian to humans 3) re-emergence of a subtype that hasn't been around for sometime \*\* if new subtype is easily transmissible= pandemic or epidemic

Answer 107

\* high mortality in 15-34 year olds due to the fact that death was caused by a strong immune response \*\*Cytokine storm: systemic

Virology Summary Flashcards

(138 cards)