Virology L7 & 1/2 8 Flashcards
FOR RNA VIRUSES dont memorize the polarity “only know if they are ss or ds”
Retroviridae
Characteristics
§ Linear (+)sense ? or ds? RNA
§ shape? capsid
§ Envelope with ?-proteins
§ Release by ?
Transmission
§ ?-to-cell
§ ?
§ ? (e.g. Jaagsiekte)
** Pseudodiploid ? = 2 identical shape? (+)sense ss RNA strands **
Retro = reverse/backward
§ RNA is ?-transcribed to DNA-intermediates via ? (RT)
§ Retrovirus DNA is inserted in host genome as ?
FOR RNA VIRUSES dont memorize the polarity “only know if they are ss or ds”
Retroviridae
Characteristics
§ Linear (+)sense ss RNA
§ icosahderal capsid
§ Envelope with gag-proteins
§ Release by budding
Transmission
§ cell-to-cell
§ fluid
§ airborne (e.g. Jaagsiekte)
** Pseudodiploid genome = 2 identical linear (+)sense ss RNA strands ** (note: the strands aren’t connected to each other so they aren’t considered a double stranded virus)
Retro = reverse/backward
§ RNA is reverse-transcribed to DNA-intermediates via reverse transcriptase (RT)
§ Retrovirus DNA is inserted in the host genome as provirus
below IMP to understand:
PICTURE:
ENTRY: “entry” occurs through membrane fusion and then the uncoating step - release from capsid and then RNA virus moves to nucleus and will have replication of their genome following actions of the reverse transcriptase which makes the double-stranded intermediate
the double-stranded piece are integrated with the help of another enzyme called “integrase” which cut open the host genome literally and inserts viral genome into it
EXIT: during stress, RNA release occurs where RNA pol II (helps in proteolytic cleavage during virion maturation), another enzyme that helps in releasing that provirus
and then we have transcription and splicing thus, back to single-stranded RNA strands (until this happens in the nucleus)
then outside the nucleus, the virus is built and replication occurs and then proteins are made (such as Gag proteins and envelope proteins as seen in pic), and then all are assembled and released.
IMP SLIDE! ! !
Retroviridae
Three important viral enzymes
§ ?
§ ?: integration of viral DNA into host’s genome
§ ?: proteolytic cleavage during virion maturation
§ ? cells are required for building in the genetic material
-> EXCEPT genus ?: can integrate in non-dividing host cells
§ Retroviridae infect a wide range of animals including humans
§ Associated with ? syndromes and cancer
§ Oncovirus = any virus with ? or ? genome causing ?
§ Proto-oncogene = gene that encodes for proteins regulating cell ? and differentiation and that can become an ? (gene potentially causing cancer)
IMP SLIDE! ! !
Retroviridae
Three important viral enzymes
§ reverse transcriptase
§ Integrase: integration of viral DNA into host’s genome
§ RNA pol II: proteolytic cleavage during virion maturation
§ active cells are required for building in the genetic material
-> EXCEPT genus Lentivirus: can integrate in non-dividing host cells
§ Retroviridae infect a wide range of animals including humans
§ Associated with immunodeficiency syndromes and cancer
§ Oncovirus = any virus with DNA or RNA genome causing cancer
§ Proto-oncogene = gene that encodes for proteins regulating cell growth and differentiation and that can become an oncogene (gene potentially causing cancer)
(note: smtms protogene transforms into protooncogene thus producing cancer; WHY we can pinpoint why cancer develops - many diff. rzns also included
altho they belong to the same family have diff. ways of replication strategies (so approach also differs)
IMP SLIDE/pic !!
(GOOGLE: A proto-oncogene is a healthy gene found in the cell. Each proto-oncogene is responsible for making a protein involved in cell growth, division, and other processes)
§ Proto-oncogenes mistakenly incorporated into provirus
§ Disruption of cellular proto-oncogenes (e.g. viral promoter triggers overexpression)
ACUTELY transforming retrovirus:
- faster development of cancer cells
- infection of cells and integration of proto-oncogene
- infection of new host cell
- integration and expression of viral oncogene
(many virions are produced here and can affect many cells thus called acute and so cancer develops faster
the moment they build a provirus, they kind of cut the proto-oncogene into pieces and they take a part of that oncogene in their pro-virus, smtms happens randomly
As a result, you will have virus particles when this cell again releases its provirus (called ONCOGENE) and creates new variants,
you will have new variants that hold a little bit of that proto-oncogene in here
VIRAL ONCOGENE = provirus incorporating natural protooncogene
When these virions (blue ones) infect in a new host cell that will lead to the expression of the viral oncogene and to a transformation of that newly infected cell So the newly infected cell becomes a cancer cell!)
SLOWLY transforming retrovirus:
- just 1 here
- infection with retrovirus carrying promoter gene
- integration of promoter gene adjacent to proto-oncogene
- conversion of proto-oncogene to oncogene
(just 1 virion causing cancer so only 1 cancer cell; sometimes can take years)
(notes: here in slowly tran. retrovirus: virus (blue one) incorporates a promoter gene;
A promoter gene that’s kind of like an extra boost. Gene promotes the translation of certain genes. This is a viral genome that holds already promoter genes, and that is integrated next to the promoter oncogene.
So we have the proto-oncogene present in our genome and the provirus pushes itself next to it. And that provirus holds a promoter gene.
At this point, that promoter gene will induce the conversion of your natural proto-oncogene to an oncogene and that 1 cell becomes an infected cell.)
THEREFORE
SLOWLY TRAN. V. = 1 virus = 1 infected cell
ACUTELY TRAN V. = release of many diff. virions that infect many cells (1st infection ability to more quickly infect cells than slowly transforming virus)
AVIAN LEUKOSIS (look at slides for pics)
genus Alpharetrovirus
** species: Avian ? ? virus (ASLV or ALV) **
host: ?
§ ? leukosis and ? (blood cell tumor from lymphocytes)
AVIAN LEUKOSIS
genus Alpharetrovirus
** species: Avian sarcoma leucosis virus (ASLV or ALV) **
host: poultry
§ Lymphoid leukosis and lymphoma (blood cell tumor from lymphocytes)
Enzootic nasal tumor
§ Genus ?,
species Enzootic ? ? virus (ENTV)
§ Host: sheep, ?
§ Tumors in the ? epithelium
Jaagsiekte (same genus as enzootic nasal tumor)
Genus Betaretrovirus,
species Jaagsiekte ? retrovirus (JSRV)
Host: sheep, ?
Contagious lung cancer or ovine pulmonary adenocarcinoma: ? distress when u chase animals
(massive sputum = characteristic of jaagsiekta (chasing)
Enzootic nasal tumor
§ Genus Betaretrovirus,
species Enzootic nasal tumor virus (ENTV)
§ Host: sheep, goat
§ Tumors in the nasal epithelium
Jaagsiekte
Genus Betaretrovirus,
species Jaagsiekte sheep retrovirus (JSRV)
Host: sheep, goats
Contagious lung cancer or ovine pulmonary adenocarcinoma: respiratory distress when u chase animals
(massive sputum = characteristic of jaagsiekta (chasing)
Bovine leukosis
§ Genus ?retrovirus,
species Bovine ? Virus
§ Host: ?
§ Enlargement of ? nodes (e.g. retro-ocular -> protrusion of ? membrane)
Bovine leukosis
§ Genus Deltaretrovirus,
species Bovine Leukemia Virus
§ Host: cattle
§ Enlargement of lymph nodes (e.g. retro-ocular -> protrusion of conjunctival membrane)
Equine Infectious Anemia, Swamp Fever
§ Genus ?virus,
species Equine ? ? virus
§ Host: ?
§ ?, thrombocytopenia, ?, ? loss, ? of legs
§ Mechanical vectors: stable ?!
Equine Infectious Anemia, Swamp Fever
§ Genus Lentivirus,
species Equine Infectious Anemia virus
§ Host: equidae
§ anemia, thrombocytopenia, fever, weight loss, swelling of legs
§ Mechanical vectors: stable flies!
(anemia - episodes (chronic) so is stable; can developed after several years; over have more and more and then more strong clinical signs
-flies can play a role as mechanical vector; viruses don’t have an active replication cycle inside the fly hence mechanical vector; ZIKA virus (active replication cycle in mosquitoes)
Feline Leukemia (IMP SLIDE!!!)
§ Genus ?retrovirus, species Feline Leukemia Virus (FeLV)
§ Host: ?
§ Transmission: ** close contact with ? or ? secretions **, to a lesser extent through milk & blood
§ Infection in ? possible
§ ? carriers (0.5% of pet cats) -> risk to others!
Feline Leukemia
§ Genus gammaretrovirus, species Feline Leukemia Virus (FeLV)
§ Host: felids
§ Transmission: ** close contact with nasal or saliva secretions **, to a lesser extent through milk & blood
§ Infection in utero possible
§ asymptomatic carriers (0.5% of pet cats) -> risk to others! (can be transmitted vertically (offspring)!!
right pic:
early immune response = ABORTIVE INFECTION: effective immune response, replication halted, rarely diagnosed as infection gets cleared in local lymph nodes (includes going through oropharynx, then tonsils & then clears the infection at local lymph nodes)
late immune response = REGRESSIVE infection: effective immune response, transient viraemia, viral reactivation possible (bone marrow)
- here we see spread of virus in the blood thus “active viraemia”; from blood they can move to bone marrow where they can effect the precursors of your blood cells
- - here they can remain asymptomatic in regressive infection
poor/absent immune response = progressive infection: continuously viraemic, disease development, poor diagnosis
- However, what we do see is that there’s a large chunk of animals that can become more progressive and they will be continuously viraemic. at this point -> high loads of virus particles in the blood, but also secondary infections. And so you will not only have these clinical signs of leukemia, you will have the anemia, look scraggly (epithelial problems susceptible to bacterial infection)
(if a cat has FLV and asymptomatic then can ask the O to not let it be around other cats and monitor it closely and any other health issues to get an idea of which stage of FLV it might be in)
left pic: virus shed in the saliva and other bodily fluids of an infected cat
primarily transmitted from queens to kittens (some risk of transmission from prolonged contact or bite wounds)
- can lead to:
1. abortive infection
- regressive infection
a. may remain asymptomatic for life b. can become progressive with inciting cause - progressive infection -> will develop clinical signs
Feline Leukemia
§ Clinical signs: ?, fever, ?, opportunistic ?, bone ? disorders
§ ? or in final stage ?
§ More progressive than ?
§ Vaccines and more intense testing -> decline of prevalence of ? infections
Feline Leukemia
§ Clinical signs: lethargy, fever, opportunistic infections, stomatitis, bone marrow disorders
§ immunosuppression or in final stage lymphomas
§ More progressive than FIV
§ Vaccines and more intense testing -> decline of prevalence of FeLV infections
Feline immunodeficiency - IMP SLIDE!!!
§ Genus ? (same genus as equine infectious anemia virus),
species Feline ? Virus (FIV)
§ Host: ? (2.2-4.4% infected worldwide), endemic in African lions
§ Transmission: ** ? injuries (saliva) **
§ Virus infects CD4-T cells, CD8-T cells, B cells and macrophages -> depletion of CD4-T cells
§ Clinical signs: attack on ? system -> anemia, low ? blood cell count -> secondary infections, cancer, ? diseases (pic in Q)
Feline immunodeficiency
§ Diagnosis: detection of antibodies -> seropositive
§ Control: ? or ? cats (no need for ? – consensus USA)
Feline immunodeficiency
§ Genus Lentivirus (same genus as equine infectious anemia virus),
species Feline leukomia Virus (FIV)
§ Host: cats (2.2-4.4% infected worldwide), endemic in African lions
§ Transmission: ** BITE injuries (saliva) **
§ Virus infects CD4-T cells, CD8-T cells, B cells and macrophages -> depletion of CD4-T cells
§ Clinical signs: attack on immune system -> anemia, low white blood cell count -> secondary infections, cancer, neurological diseases (pic in Q)
Feline immunodeficiency
§ Diagnosis: detection of antibodies -> seropositive
§ Control: spaying or neutering cats (no need for euthanasia – consensus USA)
note: pics are imp!! go through them!
right pic shows HIV but FIV similar HIV
1. read
in the left pic:
1. virus shed in the saliva of an infected cat (note: in FeLV also in body fluids as well as in saliva)
2. primarily transmitted via a deep wound
3. asymptomatic
4. from asymptomatic -> either remain asymptomatic for life OR progression to clinical disease
Rhabdoviridae
§ Characteristics
§ Linear (-)sense ss or ds RNA ?
§ ** IMP Helical ? **
§ Enveloped or non-enveloped?
§ ** ? -shaped **
§ Release by ?
§ Ribonucleoprotein complex: RNA bound by viral ?
§ ? body: eosinophilic, inclusion bodies found in the ? of infected nerve cells
§ Hosts: (in)vertebrates
§ Cell tropism: neurons -> ? virus
§ Transmission: animal bite -> ? (rabies)
§ Present in all continents except Antarctica and ?
Rhabdoviridae
§ Characteristics
§ Linear (-)sense ss RNA
§ ** IMP Helical nucleocapsid **
§ Enveloped
§ ** BULLET -shaped **
§ Release by budding
§ Ribonucleoprotein complex: RNA bound by viral nucleoprotein
§ NEGRI body: eosinophilic, inclusion bodies found in the cytoplasm of infected nerve cells
§ Hosts: (in)vertebrates
§ Cell tropism: neurons -> neurovirulent virus
§ Transmission: animal bite -> saliva (rabies)
§ Present in all continents except Antarctica and Australia
Rabies
§ Genus ?, species ? Virus
§ Reservoir: dogs, cats, wild ? & ?, bats, ?
§ Animal bite -> initial replication in myocytes -> transport through peripheral nerves -> central nervous sytem -> ** neuronal infection! **
§ ** Virus is shed in ? of infected animals **
§ fast or slow?-moving virus (~ distance bite to brain)
§ Incubation time: 3-8 days or weeks? in dogs
Rabies
§ Genus Lyssavirus, species Rabies Virus
§ Reservoir: dogs, cats, wild canids & fields, bats, mongooses
§ Animal bite -> initial replication in myocytes -> transport through peripheral nerves -> central nervous sytem -> ** neuronal infection! **
§ ** Virus is shed in the saliva of infected animals **
§ slow-moving virus (~ distance bite to brain)
§ Incubation time: 3-8 weeks in dogs
(virus NOT found in blood!! as they are only in myocytes (so distance from origin of replication to CNS) so luckier to be bitten on toe than closer to CNS (can take weeks for it to reach CNS) however if closer to CNS then bad as it will reach CNS faster)
Rabies
§ After the virus reaches brain, three phases are defined:
§ ? Phase (2-3 days): nervousness, anxiety, solitude, different behavior (friendly -> irritable; aggressive -> affectionate). Licking of the ? side is mostly observed.
§ ? Phase (1-7 days): ?, irritable, hyperresponsive to ? and auditory stimuli, roaming, ?.
§ ? Phase: ? (inability to swallow), deep labored breathing, ? facial muscles, ? failure and death
Rabies
- direct fluorescent antibody test: look for presence of rabies virus ? in brain tissue
- not in the ?!!!
Rabies
§ After the virus reaches brain, three phases are defined:
§ prodomal Phase (2-3 days): CHANGE IN BEHAVIOUR; nervousness, anxiety, solitude, different behavior (friendly -> irritable; aggressive -> affectionate). Licking of the bite side is mostly observed.
§ furious Phase (1-7 days): restless, irritable, hyperresponsive to visual and auditory stimuli, roaming, disorientated.
§ paralytic Phase: salivate (inability to swallow), deep labored breathing, paralyzed facial muscles, respiratory failure and death
Rabies
- direct fluorescent antibody test: look for presence of rabies virus antigens in brain tissue
- not in the BLOOD!!!
- ZOONOTIC!!!
IMP SLIDE!!
Orthomyxoviridae
Characteristics
§ Segmented ? (-)sense ss RNA
(remember!! SEGMENTED. - has a big devlopement on how they develop, replicate etc.)
§ Enveloped with ** ? **
§ Release by ?
§ Glycoprotein spikes
§ Neuraminidase = NA = N
§ Haemaglutinin = HA = H
Three genera are defined by antigenic differences in nucleoprotein and matrix protein:
§ Influenza virus A: humans, birds, ? (pandemics!)
§ Influenza virus B: humans, ?
§ Influenza virus C: humans, ?, dogs
International nomenclature of infuenza viruses
IMP SLIDE!!
Orthomyxoviridae
Characteristics
§ Segmented linear (-)sense ss RNA
(remember!! SEGMENTED. - has a big devlopement on how they develop, replicate etc.)
§ Enveloped with ** spikes **
§ Release by budding
§ Glycoprotein spikes
§ Neuraminidase = NA = N
§ Haemaglutinin = HA = H
Three genera are defined by antigenic differences in nucleoprotein and matrix protein:
§ Influenza virus A: humans, birds, mammals (pandemics!) - influenza A most common one
§ Influenza virus B: humans, seals
§ Influenza virus C: humans, pigs, dogs
pic: THGSYS (virus type, host of origin (if humans no host of origin), geographic origin, strain number, year of isolation, virus subtype
Flu epi - & pandemics
- influenza A subtypes are defined by H & N ?
- Multiple strains within a subtype
regular epidemic and pandemic (don’t memorize the years)
- Reassortment = mixing of ? material of species into new ?, resulting in a ? virus
Flu epi - & pandemics
- influenza A subtypes are defined by H & N virus
- Multiple strains within a subtype
regular epidemic and pandemic (don’t memorize the years)
- Reassortment = mixing of the genetic material of species into a new combination, resulting in a reassortment virus (can include different species)
Flu epi- & pandemics IMP SLIDE!!!!
Antigenic ? = small changes in the genes that happen continually over time as the virus replicates (Influenza A, Influenza B)
§ Closely related viruses share ? properties -> ?
§ HOWEVER when accumulation of changes over time -> then immune system does no longer recognize virus (renew influenza vaccines!)
§ Antigenic ? = abrupt, major genetic changes in Influenza A viruses, resulting in new HA and/or new NA proteins -> new Influenza A subtype
Flu epi- & pandemics IMP SLIDE!!!!
Antigenic drift = small changes in the genes that happen continually over time as the virus replicates (Influenza A, Influenza B)
§ Closely related viruses share antigenic properties -> cross-protection
§ HOWEVER when an accumulation of changes over time -> then the immune system does no longer recognize the virus (renew influenza vaccines!)
§ Antigenic shift = abrupt, major genetic changes in Influenza A viruses, resulting in new HA and/or new NA proteins -> new Influenza A subtype
RNA viruses
Coronaviridae
Characteristics
§ Linear (+)sense ss or ds? RNA
§ Enveloped with “ ** ? **” (petal-shaped spikes)
§ Release by ?
§ Hosts: ?, humans
Transmission:
§ ? of small droplets
§ ?-oral route
§ Primary site of infection: ? cells of respiratory or ? tract
§ Epidemiology
§ Feline ? coronavirus (FECV) & Feline ? ? virus (FIPV)
§ Transmissible ? virus swine (TGEV)
RNA viruses
Coronaviridae
Characteristics
§ Linear (+)sense ss RNA
§ Enveloped with “ ** PEPLOMERS **” (petal-shaped spikes)
§ Release by exocytosis
§ Hosts: vertebrates, humans
Transmission:
§ inhalation of small droplets
§ fecal-oral route
§ Primary site of infection: epithelial cells of the respiratory or intestinal tract
Epidemiology
§ Feline enteric coronavirus (FECV) & Feline infectious peritonitis virus (FIPV)
§ Transmissible gastroenteritis virus swine (TGEV)
blue ones are virion particles being released in the pic
IMP SLIDE!!!
FIP
FECV mutates in body and becomes FIPV
- FIPV has tropsim for macrophages (the turning of all or part of an organism in a particular direction in response to an external stimulus).
- asymptomatic carriers shed the virus in faeces
- FIPV is incurable and fatal
(notes:
- v regularly transmitted from cat to cat through the fecal-oral route.
- shed from faeces but can’t see it clinically
- often have asymptomatic carriers of feline enteric coronavirus, so it maintains itself in that cat population.
- problem is smtms the virus undergoes mutation and thus it changes its tropism from intestinal cells to macrophages
- and it is this change in tropism that will lead to a different clinical pattern; unlike feline enetero virus, FIPV can be seen
- one of the most common infectious diseases in v young cats and is in the stage is INCURABLE and fatal.
FIP (1-3%)
- resistant (5-10%)
- transient infection (70%) mild diarrhea
- persistent carrier (5-10%)
(And so a lot of asymptomatic infections or transient infections with your feline, in theory, corona virus, transient infections, self-limiting diarrhea - this is a self-limiting infection - DONT TREAT IT WITH ANTIBOITICS!
so animals will overcome this however persistent carriers, they are a problem because the resistant carriers, they will not show clinical signs, but they will have a continuous excretion of high loads of these virus particles.
So they will be continuously leading to a high infection pressure in the environment.
So if you have a couple of these in the cattery, that’s not good bc then you have a higher chance of an individual developing FIP.
