Retrovirus (IKKE FERDIG) Flashcards
Retroviruses are frequently carried lifelong
T
Retroviruses carry an integrase enzyme
T
Malignant transformation of host cells is a typical effect of several retroviruses
T
Retroviruses are enveloped, their resistance is low
T
The reverse transcriptase transforms DNA of the retroviruses to mRNA
F
Retroviruses are stable viruses; genetic changes are rare
F
Retroviruses are euryxemic agents
F
Retroviruses are frequently carried lifelong
T
Retroviruses are generally host specific viruses
T
Mutation of retroviruses is very rare
F
Immunosuppression is a typical effect of several retroviruses
T
Retroviruses can integrate into the genome of host cells
T
Reverse transcriptase is an important enzyme of retroviruses.
T
Retroviruses results in lifelong infection.
T
Retroviruses replicate mainly in the endothelial cells.
F
Several retroviruses can cause malignant transformation in the hosts
T
Retroviruses are generally species specific
T
Retroviruses are generally resistant, they can survive in the environment for several weeks
F
Retroviruses frequently cause permanent infection
T
Retroviruses are generally stable viruses, mutations are very rare
F
Retrovirus has weak resistance
T
Retrovirus has a wide host spectrum
F
Retrovirus has a good immunogenicity
T
Retrovirus infection is long-lasting
T
Retroviruses show high host specificity
T
Retroviruses are generally not carried for more than a month
F
Retroviruses generally cannot survive in the environment for a long time
T
Retroviruses are enveloped viruses
T
Retroviruses transcribe their nucleic acid to DNA
T
Frequent genetic changes of retroviruses are common
T
Retroviruses carry reverse transcriptase enzyme
T
Retroviruses generally cause long, frequently life-long infection
T
Retroviruses are generally genetically very stable.
F
The resistance of retroviruses is generally good, they survive in the environment well.
F
Reverse transcriptase is produced by retroviruses
T
The nucleic acid of retroviruses can be integrated into the genome of the host cell.
T
Retroviruses frequently cause immune suppression
T
Retroviruses are enveloped viruses
T
The host range of retroviruses is generally narrow
T
Reverse transcriptase converts RNA of retroviruses into DNA
T
Retroviruses are generally very stable viruses, mutations are exceptional in them.
F
Retroviruses are generally shed in infected lymphoid cells
T
Certain retroviruses can cause proliferation of the lymphoid cells
T
Retroviruses spread with infected lymphocytes
T
Retroviruses have a tegument or rind
F
You cannot multiply retrovirus artificially
F
Retroviruses can incorporate into the genome
T
Retroviruses cannot spread from animal to animal.
F
Retroviruses are widely distributed in Hungary
T
Retroviruses replicate mainly in endothelium cell
F
Retrovirus can replicate without helper retroviruses.
T
Retroviruses can integrate the cellular genome
T
The resistance of retroviruses is low, they cannot survive in the environment for a long time.
T
Retroviruses are generally good antigens.
T
Retroviruses have own metabolic enzymes
T
Antibodies against enzootic bovine leukosis virus can be detected 1-4 months after infection.
T
Antibodies against enzootic bovine leukosis virus can be detected only for 1-2 months after
infection
F
Maternal Antibodies against enzootic bovine leukosis virus can be detected only for 1-2
months
F
Lymphosarcoma can be seen postmortem in the case of enzootic bovine leukosis
T
Generation shift is the only way of eradication of enzootic bovine leukosis
F
Enzootic bovine leukosis virus does not spread from animal to animal.
F
Mild clinical signs can be seen in the incubation phase of enzootic bovine leukosis
F
Enzootic bovine leukosis virus is not shed in the colostrum
F
Enzootic bovine leukosis virus can be transmitted with blood
T
Enzootic bovine leukosis virus can spread from cattle to sheep, goats , and other ruminants
F
Enzootic bovine leukosis virus has uniform antigenic structure
T
In the case of Enzootic bovine leukosis the clinical signs appear at the age of 6-8 month
F
Enzootic bovine leukosis is carried lifelong
T
Enzootic bovine leukosis virus can be transmitted in tracheal discharge
T
Enzootic bovine leukosis occurs only in Holstein Friesian cattles
F
Enzootic bovine leukosis virus can infect foetuses of pregnant animals
T
Enzootic bovine leukosis virus has several serotypes and subtypes.
F
Enzootic bovine leukosis can spread by air within the herd
T
Enzootic bovine leukosis can spread by the veterinarian
T
Enzootic bovine leukosis virus cannot result tumour formation
F
Serological examinations cannot be used to the diagnosis of enzootic bovine leukosis
F
Immune tolerance can happen in the case of enzootic bovine leukosis
T
Selection cannot be used for eradication of enzootic bovine
F
Bovine enzootic leukosis infect only bovine
F
Bovine enzootic leukosis does not spread with excretion
F
Bovine enzootic leukosis spreads slow in the herd.
T
Bovine enzootic leukosis can be transmitted by blood
T
Bovine leukosis virus can give lifelong carriers.
T
Bovine leukosis virus causes seropositivity in latency period.
T
Enzootic bovine leukosis the pre-tumour phase usually in 6-10 months old animals
F
Enzootic bovine leukosis during pre-tumour phase causes lymphocytosis
T
Bovine enzootic leukosis virus can be transmitted with lymphoid cells
T
Iatrogenic infection is frequent in the epidemiology of bovine enzootic leukosis
T
The target cells of the bovine enzootic leukosis virus are the T-lymphocytes
F
The typical signs of bovine enzootic leukosis can be seen in cattle under 1 year of age
F
Antibodies against enzootic bovine leukosis virus can be detected in the ELISA test
T
Antibodies against enzootic bovine leukosis virus can be detected in the milk
T
Selection (test and slaughter) method cannot be used to eradicate enzootic bovine leukosis
virus
F
Generation shift method cannot be used to eradicate enzootic bovine leukosis virus
F
Enzootic bovine leukosis virus is spreading horizontally in a cattle herd
T
Enzootic bovine leukosis virus cannot infect foetuses
F
Enzootic bovine leukosis virus is passed to newborn calves mainly with colostrum in
endemically infected herds.
F
By the end of the incubation phase the animals become seropositive leukosis virus
T
Tumours can be seen in about 90% of the animals infected with enzootic bovine leukosis
virus
F
Antibodies in the milk against enzootic bovine leukosis virus can be detected with ELISA
T
Tumours caused by enzootic leukosis virus generally appear at the age of 6 months
F
The infection with enzootic leukosis virus is detected by AGP and ELISA
T
Enzootic bovine leukosis virus is zoonotic
F
Enzootic bovine leukosis virus is shed in lymphoid cells
T
Enzootic bovine leukosis virus cannot cause intrauterine infection
F
Enzootic bovine leukosis virus is spreading slowly in the herd.
T
The target cells of enzootic bovine leukosis virus are the B lymphocytes
T
Enzootic bovine leukosis virus is not shed by the infected animals
F
Enzootic bovine leukosis virus can be transmitted with organic infection.
T
Enzootic bovine leukosis virus can be transmitted with per os infection.
T
Clinical signs of enzootic bovine leukosis are seen mainly in 6-8-month-old calves
F
Enzootic bovine leukosis virus has several serotypes and subtypes
F
Enzootic bovine leukosis can spread by air within the herd
T
Enzootic bovine leukosis virus can not result in tumour formation.
F
Immune tolerance can happen in the case of enzootic bovine leucosis
T
During incubation phase of bovine enzootic leucosis the animal become seropositive.
T
The tumours in the case of bovine enzootic leucosis can be seen from the age of 6 months.
F
PCR is used for the detection of bovine enzootic leucosis in immunotolerant calves
T
Bovine enzootic leucosis can be eradicated with selection
T
Bovine enzootic leucosis virus has several serotypes
F
There is no horizontal spread in the case of bovine enzootic leucosis.
F
There is genetic predisposition in the case of bovine enzootic leucosis
T
Enzootic bovine leucosis occurs in all ruminant species.
F
Enzootic bovine leukosis virus can infect cattle, pigs and horses.
F
Iatrogenic infection can be important in the transmission of enzootic bovine leukosis virus.
T
Aerogenic infection occurs in the case of enzootic bovine leukosis virus
T
Enzootic bovine leucosis is spreading very fast in infected herd
F
Enzootic bovine leucosis virus can infect the foetus
T
Enzootic bovine leucosis only infects cattle
F
Enzootic bovine leukosis occurs only in Holstein-Frisian cattle, other cattle races are resistant
F
Enzootic bovine leukosis has low resistance; it cannot retain its infectivity for a long time in
environment
T
The most severe clinical signs of ovine pulmonary adenomatosis can be seen in lambs
younger than 6 months.
F
Antibodies of animals infected with ovine pulmonary adenomatosis virus can be detected
with ELISA.
F
Adenocarcinoma can be seen postmortem in the case of ovine pulmonary adenomatosis
T
Ovine pulmonary adenomatosis virus is transmitted with tracheal discharge
T
Ovine pulmonary adenomatosis virus can be transmitted with contaminated objects to other farms
F
Ovine pulmonary adenomatosis virus can infect sheep, goats, and cattle
F
The most severe clinical signs of ovine pulmonary adenomatosis can be seen in lambs
younger than 6 months
F
Shedding large amount of nasal discharge is a typical clinical sign of ovine pulmonary
adenomatosis
T
Ovine pulmonary adenomatosis virus replicates in lymphoid cells and causes viraemia
F
Metastasis are rare in the case of Ovine Pulmonary Adenomatosis
T
Ovine pulmonary adenomatosis occurs only in South Africa
F
Ovine pulmonary adenomatosis virus has no onc-gen
T
Ovine pulmonary adenomatosis is prevented with inactivated vaccines
F
Ovine pulmonary adenomatosis spreads with nasal discharge
T
The primary replication site of OPA is in the mucosal cells of the intestines.
F
Metastasis are frequently seen in parenchymal in the case of OPA
F
Ovine pulmonary adenomatosis virus is found in 2-4 months old lambs.
F
Ovine pulmonary adenomatosis virus is replicating in the epithelium of the airways.
T
Tumours can frequently be seen in the liver and the spleen in the case of ovine pulmonary
adenomatosis
F
Ovine pulmonary adenomatosis can be complicated by Pasteurella and Mannheimia strains.
T
In the case of ovine pulmonary adenomatosis lesions are common in the liver
F
Ovine pulmonary andenomatosis can be diagnosed by detecting antibodies with ELISA
F
Ovine pulmonary adenomatosis virus causes interstitial pneumonia
F
Lung adenomatosis causes usually dry cough
F
Lung adenomatosis causes a lot of metastasis.
F
Metastasis are rare in the case of ovine pulmonary adenomatosis
T
Ovine pulmonary adenomatosis has no antibody production
T
Ovine pulmonary adenomatosis virus results in malignant transformation of macrophages
F
Europe is free from ovine pulmonary adenomatosis
F
No antibodies to ovine pulmonary adenomatosis virus can be detected in infected animals
T
Faces of infected animals contain large amount of ovine pulmonary adenomatosis virus
F
Tumour transformation of the epithelial cells happens in the case of ovine pulmonary
adenomatosis
T
Jaagsiekte affects lambs of 3-6 months
F
Jaagsiekte virus can transform human cells.
F
Jaagsiekte is only present in Africa
F
Jaagsiekte causes metastatic abscess formation all over the body
F
Feline leukosis virus will be shed lifelong by infected cats
F
There are no vaccines for the prevention of feline leukosis
F
FOCMA antigen is a typical surface antigen of feline leukosis viruses.
T
Feline leukosis virus can only be transmitted with saliva
F
Cats remain infected with feline leukosis virus lifelong
F
Feline leukosis is maintained by persistently infected cats
T
Feline leukosis virus can be transmitted by direct contact.
T
Feline leukosis virus can cause horizontal and vertical infection
T
Vaccination of only seronegative cats is responsible against feline leukosis
T
Immunotolerant kittens can be born in the case of feline leukosis
T
Feline Leukosis can be eliminated in some cats
T
There are several subgroups of feline leukosis virus
T
Feline leukosis virus can cause immune tolerance
T
Feline sarcomatosis virus is a recombinant virus from feline leukosis virus and host DNA
T
Feline leukosis virus is uniform
F
In the saliva of cats is a high-titer of FeLV
T
FeLV spreads horizontally and vertically
T
Persistent infected cats maintain the infection
T
Feline leukosis virus can cause protective immunity.
T
In Feline leukosis, anaemia is an important sign
T
Cat leukosis virus can be diagnosed with PCR
T
There is no vaccine against Feline leukosis virus
F
Feline leukosis can infect dogs and cats
F
Asymptomatic infection cannot happen in the case of Feline leukosis
F
Feline leukosis virus is immunosuppressive
T
Feline leukosis virus is frequently spread with saliva
T
Feline leukosis virus can infect dogs, cats and wild living carnivorous animals
F
Feline leukosis is a very rare disease
F
Feline sarcomatosis is a defect virus
T
Feline leukosis can cross the placenta
T
FeLV is a uniform virus
F
Infection with feline leukosis virus always appears in clinical signs
F
Feline leukosis virus is spreading by discharge of the infected animal
T
Persistently infected cats can shed the feline leukosis virus in high titres
T
Saliva of the animal contains large amount of the feline leukosis virus
T
Feline leucosis spreads by direct contact
T
Feline immunodeficiency virus causes persistent infection
T
Feline immunodeficiency virus is widespread
T
Feline immunodeficiency virus in cat could be asymptomatic
T
Feline immunodeficiency virus is spread by excretes
T
Feline immunodeficiency virus develops in 3 phases
T
Inactivated vaccines are used for the prevention of avian leukosis
F
Attenuated vaccines are used for the prevention of avian leukosis
F
Avian leukosis viruses have several subgroups
T
Tumours in the liver can be seen in the case of avian leukosis
T
Avian leukosis viruses cause horizontal infection.
T
J subtype of avian leukosis virus is more virulent than the other ones
T
Avian leukosis can be diagnosed by detecting COFAL antigen
T
Lymphoid leukosis is the most frequent clinical form of avian leukosis
T
Avian leukosis viruses cause germinative infection
T
All avian leukosis viruses are oncogenic
T
Avian leukosis viruses have several subgroups
T
Avian leukosis viruses a resistant, they can survive in the bedding for several weeks
F
Avian leukosis causes the malignant transformation of B lymphocytes
T
Avian leukosis virus occurs only in tropical and subtropical countries
F
Avian leuKosis virus can cause only lymphoid leukosis
F
Avian leukosis viruses can cause malignant transformation in different tissues.
T
Germinative infection is an important way of transmission of avian leukosis virus
T
Clinical signs of avian leukosis can be seen typically in broiler chicken
F
Osteopetrosis can be a clinical form of avian leukosis.
T
Avian Leukosis virus is uniform
F
Every avian leukosis viruses is oncogenic
T
Avian leukosis virus cannot infect by germinative way
F
Avian leukosis virus infects B lymphocytes
T
Infection of poultry herds with avian leukosis virus is widespread
T
Clinical signs of avian leukosis generally appear in day old chicken
F
Lymphoid leukosis is the most frequent form of avian leukosis.
T
The main way of prevention of avian leukosis is vaccination using attenuated strains
F
Avian leukosis viruses are shed in the faeces.
T
There is no germinative infection in the case of avian leukosis viruses.
F
The target cells of the avian leukosis viruses are the B lymphocytes
T
There are several subgroups of avian leukosis viruses.
T
All avian leukosis viruses cause malignant transformation of the host cells
T
In a flock infected with avian leukosis virus generally 50-60% of the animals have tumours
F
Detection of COFAL antigen is a frequent way of diagnosis of avian leukosis
T
Avian leukosis is seen during the first week of life in chicken
F
There are resistant lines to avian leukosis
T
Proportion of the animals with tumours is low, 1-4% in the case of avian leukosis
T
Inactivated vaccines are widely used in order to prevent avian leukosis
F
Tumours can be seen in different parenchymal organs in the case of avian leukosis.
T
T-lymphocytes are the target cell of the avian leukosis virus.
F
Avian leucosis and sarcoma infections are very common
T
Avian leucosis can be caused by different retroviruses
T
Congenital transmission of avian leucosis results in immune tolerance
T
Reticuloendotheliosis is caused by J type of avian leukosis virus.
F
Germinative infection can happen in the case of Reticuloendotheliosis
T
Reticuloendotheliosis virus is shed in the faces
T
Reticuloendotheliosis virus can cause germinative infection
T
Stunted growth is a clinical sign of reticuloendotheliosis
T
Reticuloendotheliosis is prevented by vaccination of the parent animals.
F
Immunosuppression is common in the case of Reticuloendotheliosis
T
Retardation is a clinical sign of Reticuloendotheliosis
T
Wide vaccination is used to prevent Reticuloendotheliosis
F
In the case of reticuloendotheliosis immunotolerant chicken can be hatched.
T
Pneumonia is a typical lesion of reticuloendotheliosis
F
In the case of reticuloendotheliosis tumors can be found in the parenchymal organs
T
Avian reticuloendotheliosis may be similar in appearance to Marek ́s disease.
T
Clinical signs of maedi visna are more severe in young animals than in adults
F
Heavy nasal discharge is a clinical sign of maedi
F
The maedi virus and the visna virus are related but they can be differentiated with PCR
F
Interstitial pneumonia is the main postmortem lesion of visna
F
Interstitial pneumonia is the main postmortem lesion of Maedi
T
Maedi and visna are caused by the same virus.
T
Maedi-visna virus is shed in tracheal discharge and milk
T
Maedi-visna is maintained by persistently infected sheep
T
Weakness of the hinder legs is a clinical sign of visna
T
Inactivated and attenuated vaccines are widely used for the prevention of maedi-visna
F
Clinical signs of maedi can be seen in sheep above 3-4 years of age
T
Maedi-visna can occur in sheep, goats, and cattle
F
Europe is already free from maedi-visna
F
Maedi/visna is spreading slowly in the flock.
T
Maedi/visna virus is shed in the milk.
T
Maedi is seen in 3-4 years old sheep
T
Large amount of mucoid nasal discharge is typical in the case of maedi.
F
Maedi/visna spreads from sheep to other animals
T
Maedi/visna virus is shed in nasal discharge, respiratory secretions and milk.
T
Clinical sign of maedi/visna appear from the age of 6-8 months
F
Meadi/visna most important clinical sign is profuse diarrhoea
F
Maedi/visna virus is shed only in tracheal discharge
F
Clinical signs of maedi are mainly seen in lambs below half a year of age
F
Maedi/visna virus causes interstitial pneumonia in sheep
T
Clinical signs of the central nervous system can be seen in the case of visna
T
Maedi/visna virus causes viraemia
T
Wet cough and intensive nasal discharge are typical signs of maedi.
F
De-myelinization is the reason for the clinical signs of visna
T
Attenuated vaccines are widely used to prevent maedi/visn
F
Maedi appears in Hungary
T
Maedi is spreading fast
F
In order to eradicate maedi/visna infected ewes have to be culled with their lambs
F
Clinical sign of maedi/visna appear from the age of 6 months
F
Maedi/visna is spreading fast in the flock
F
Maedi/visna virus is shed only in the tracheal discharge
F
Clinical signs of maedi are generally seen above 3-4 years of age
T
Caprine arthritis-encephalitis virus can cause persistent infection
T
Sheep are resistant against caprine arthritis encephalitis virus
F
Arthritis caused by caprine arthritis encephalitis virus is mainly seen in lambs
F
Encephalitis caused by caprine arthritis encephalitis virus is generally seen in 2-4 month old
kids
T
Caprine arthritis encephalitis virus can be transmitted by milk
T
There is intensive vaccination against Caprine arthritis encephalitis in endemic countries
F
Caprine arthritis encephalitis virus is more frequent in dairy goats than in rural breeds
T
Caprine arthritis encephalitis virus is shed in the milk
T
In the case of caprine arthritis encephalitis the signs of encephalitis can be seen in 2-4
months old kids
T
In the case of caprine arthritis encephalitis, arthritis is less frequent than encephalitis.
F
Kids are recommended to be isolated in a herd where caprine arthritis encephalitis is
present
T
Kids can be infected with caprine arthritis encephalitis virus through the milk
T
Arthritis caused by caprine arthritis-encephalitis virus is typically seen in kids below half a
year of age
F
Caprine arthritis encephalitis is characterized by CNS signs in young goats
T
Caprine arthritis encephalitis virus replicates in the intestinal tract
F
Equine infectious anaemia virus is transmitted with blood of the infected animals
T
Blood sucking arthropods can transmit Equine infectious anaemia virus
T
Mosquitoes are the main vectors of equine infectious anaemia virus; the virus can replicate
in them
F
Agar gel diffusion test is used to detect antibodies against equine infectious anaemia
T
Equine infectious anaemia is an acute disease; it does not have a chronic form
F
Iatrogenic transmission of Equine infectious anaemia can happen
T
Equine infectious anaemia virus can damage the bone marrow
T
There are no vaccines for the prevention of equine infectious anaemia
T
Equine infectious anaemia virus is more resistant than other retroviruses.
T
Equine infectious anaemia virus disappears from animals after the viraemia
F
Fever is a major clinical sign of equine infectious anaemia
T
Equine infectious anaemia virus is resistant, it can survive several months in the environment
T
Only Equidae are susceptible to equine infectious anaemia virus
T
Ticks are vectors of equine infectious anaemia virus
F
Febrile waves can be seen in equine infectious anaemias
T
Equine infectious anaemia is a vector borne disease
T
Equine infectious anaemia virus causes persistent infection.
T
There is no immune reaction in the case of equine infectious anaemia
F
Equine infectious anaemia is zoonotic
F
Equine infectious anaemia is caused by a lentivirus
T
Blood sucking arthropods are mechanical vectors of equine infectious anaemia virus
T
There is no immune reaction in horses against equine infectious anaemia virus
F
Agar gel precipitation test can be used to the detection of antibodies against equine
infectious anaemia virus
T
Equine infectious anaemia can damage the medulla of the bone.
T
Equine infectious anaemia has a weak resistance
F
You cannot diagnose Equine infectious anaemia with serology
F
The resistance of equine infectious anaemia is very low
F
Horses and cattle are susceptible to equine infectious anaemia virus
F
In the case of equine infectious anaemia, haemorrhages cannot be seen
F
Animals infected with equine infectious anaemia virus are lifelong carriers
T
Equine infectious anaemia virus is mainly transmitted with tracheal discharge
F
Attenuated vaccines are used for the prevention of equine infectious anaemia
F
Equine infectious anaemia can be asymptomatic
T
Equine infectious anaemia may cause recurrent fever in horses.
T
Horseflies are mechanical vectors equine anaemia virus.
T
Equine anaemia is a notifiable disease
T
