Podcast
Questions and Answers
What is the defining genomic feature of retroviruses that fundamentally dictates their replication strategy and interaction with the host cell?
What is the defining genomic feature of retroviruses that fundamentally dictates their replication strategy and interaction with the host cell?
- A single-stranded positive-sense RNA genome that is directly translated into viral proteins.
- A segmented double-stranded RNA genome that undergoes reassortment during replication.
- A single-stranded positive-sense RNA genome that is reverse transcribed into DNA for integration into the host cell’s genome. (correct)
- A double-stranded DNA genome that integrates directly into the host cell’s DNA.
Which enzymatic activity is essential for retroviruses to establish a persistent infection in a host cell?
Which enzymatic activity is essential for retroviruses to establish a persistent infection in a host cell?
- Reverse transcriptase, for converting viral RNA into DNA.
- Integrase, for incorporating the viral DNA into the host genome. (correct)
- RNA polymerase, for transcribing viral RNA.
- Protease, for maturation of viral proteins.
Which of the following is a characteristic shared by both persistent infections and oncogenic potential in retroviruses?
Which of the following is a characteristic shared by both persistent infections and oncogenic potential in retroviruses?
- The requirement for a highly lytic replication cycle that rapidly destroys host cells.
- The production of a potent toxin that directly induces cellular damage and disease.
- The integration of the provirus into the host cell genome, leading to long-term presence or potential cellular transformation. (correct)
- The ability to evade the host's immune response through frequent antigenic variation.
How does the integration of a retroviral provirus lead to oncogenesis?
How does the integration of a retroviral provirus lead to oncogenesis?
What is the primary genetic difference between transducing and cis-activating retroviruses concerning oncogenesis?
What is the primary genetic difference between transducing and cis-activating retroviruses concerning oncogenesis?
Given that retroviruses integrate their genetic material into the host cell's genome, which mechanism of oncogenesis would least likely involve direct alteration of the host cell's DNA sequence?
Given that retroviruses integrate their genetic material into the host cell's genome, which mechanism of oncogenesis would least likely involve direct alteration of the host cell's DNA sequence?
In the context of retroviral oncogenesis, how do cis-activating and trans-activating mechanisms differ in their immediate effect on the host cell's gene expression?
In the context of retroviral oncogenesis, how do cis-activating and trans-activating mechanisms differ in their immediate effect on the host cell's gene expression?
Considering the three mechanisms of retrovirus-induced cell transformation, in which mechanism would the timeline for the development of clinical disease most likely be the longest?
Considering the three mechanisms of retrovirus-induced cell transformation, in which mechanism would the timeline for the development of clinical disease most likely be the longest?
How does the genome organization of Flaviviruses differ from that of Retroviruses, influencing their respective replication strategies and potential for integration into the host genome?
How does the genome organization of Flaviviruses differ from that of Retroviruses, influencing their respective replication strategies and potential for integration into the host genome?
A key difference between Flaviviruses and Retroviruses lies in their mechanism of replication and integration. What is the most significant implication of this difference in terms of the host cell?
A key difference between Flaviviruses and Retroviruses lies in their mechanism of replication and integration. What is the most significant implication of this difference in terms of the host cell?
How does the strategy of transmission generally differ between Flaviviruses and Retroviruses?
How does the strategy of transmission generally differ between Flaviviruses and Retroviruses?
How does the non-cytopathic nature of some Flavivirus strains complicate disease management and control?
How does the non-cytopathic nature of some Flavivirus strains complicate disease management and control?
Given Bovine Viral Diarrhea Virus (BVDV) can cause either transient or persistent infections in cattle, what is a critical determinant that differentiates the outcome of these two types of infections?
Given Bovine Viral Diarrhea Virus (BVDV) can cause either transient or persistent infections in cattle, what is a critical determinant that differentiates the outcome of these two types of infections?
What is the most significant implication of persistent BVDV infections in cattle populations?
What is the most significant implication of persistent BVDV infections in cattle populations?
How can mucosal disease arise in persistently infected calves with BVDV, and what is its significance in terms of disease pathogenesis?
How can mucosal disease arise in persistently infected calves with BVDV, and what is its significance in terms of disease pathogenesis?
What is the primary difference in genome organization that accounts for the tissue tropism switch seen in feline enteric coronavirus (FECV) leading to feline infectious peritonitis (FIP)?
What is the primary difference in genome organization that accounts for the tissue tropism switch seen in feline enteric coronavirus (FECV) leading to feline infectious peritonitis (FIP)?
How does antibody-dependent enhancement (ADE) contribute to the unique pathogenesis observed in feline infectious peritonitis (FIP)?
How does antibody-dependent enhancement (ADE) contribute to the unique pathogenesis observed in feline infectious peritonitis (FIP)?
What is the molecular basis for the tissue tropism switch observed in the transition from feline enteric coronavirus (FECV) to feline infectious peritonitis virus (FIPV)?
What is the molecular basis for the tissue tropism switch observed in the transition from feline enteric coronavirus (FECV) to feline infectious peritonitis virus (FIPV)?
What is the most accurate description of the role of antibody-dependent enhancement (ADE) in the pathogenesis of Feline Infectious Peritonitis (FIP)?
What is the most accurate description of the role of antibody-dependent enhancement (ADE) in the pathogenesis of Feline Infectious Peritonitis (FIP)?
Considering that Feline Infectious Peritonitis (FIP) results from a mutation of Feline Enteric Coronavirus (FECV), what is the primary reason that an antibody response, initially intended to neutralize the virus, paradoxically worsens the disease?
Considering that Feline Infectious Peritonitis (FIP) results from a mutation of Feline Enteric Coronavirus (FECV), what is the primary reason that an antibody response, initially intended to neutralize the virus, paradoxically worsens the disease?
Given the role of both tissue tropism and antibody-dependent enhancement (ADE) in the pathogenesis of Feline Infectious Peritonitis (FIP), which of the following scenarios would likely lead to the most severe FIP outcome?
Given the role of both tissue tropism and antibody-dependent enhancement (ADE) in the pathogenesis of Feline Infectious Peritonitis (FIP), which of the following scenarios would likely lead to the most severe FIP outcome?
Which of the following strategies leverages the unique replication mechanism of retroviruses to achieve targeted gene editing in eukaryotic cells?
Which of the following strategies leverages the unique replication mechanism of retroviruses to achieve targeted gene editing in eukaryotic cells?
Which aspect of retroviral reverse transcription poses the greatest challenge for maintaining the genetic stability of retroviral vectors used in gene therapy?
Which aspect of retroviral reverse transcription poses the greatest challenge for maintaining the genetic stability of retroviral vectors used in gene therapy?
What is a primary safety concern associated with the use of retroviral vectors in gene therapy, considering their mechanism of integration into the host cell genome?
What is a primary safety concern associated with the use of retroviral vectors in gene therapy, considering their mechanism of integration into the host cell genome?
What strategy has been employed to reduce or eliminate the risk of insertional mutagenesis in retroviral vector-mediated gene therapy?
What strategy has been employed to reduce or eliminate the risk of insertional mutagenesis in retroviral vector-mediated gene therapy?
Why do persistent infections with non-cytopathic BVDV strains complicate disease eradication efforts more than transient infections?
Why do persistent infections with non-cytopathic BVDV strains complicate disease eradication efforts more than transient infections?
Given the role of macrophages in the pathogenesis of FIP, which therapeutic approach would most directly target disease progression?
Given the role of macrophages in the pathogenesis of FIP, which therapeutic approach would most directly target disease progression?
What is the MOST critical factor that determines whether a calf infected with BVDV will develop a persistent infection?
What is the MOST critical factor that determines whether a calf infected with BVDV will develop a persistent infection?
How does antigenic variation (mutations in viral protein structure) affect the long-term control of flavivirus infections, such as those caused by Bovine Viral Diarrhea Virus (BVDV)?
How does antigenic variation (mutations in viral protein structure) affect the long-term control of flavivirus infections, such as those caused by Bovine Viral Diarrhea Virus (BVDV)?
Considering the persistent nature of retroviral infections, what is the MOST significant challenge in developing curative therapies for retrovirus-associated diseases, such as those caused by HIV?
Considering the persistent nature of retroviral infections, what is the MOST significant challenge in developing curative therapies for retrovirus-associated diseases, such as those caused by HIV?
You're working in a veterinary diagnostic lab and receive a sample from a calf suspected of having Bovine Viral Diarrhea Virus (BVDV). Which diagnostic technique would be MOST appropriate for identifying a persistently infected (PI) animal, given that PI animals may not show obvious clinical signs?
You're working in a veterinary diagnostic lab and receive a sample from a calf suspected of having Bovine Viral Diarrhea Virus (BVDV). Which diagnostic technique would be MOST appropriate for identifying a persistently infected (PI) animal, given that PI animals may not show obvious clinical signs?
Which feature of retroviruses is the basis for the development of diagnostic tools to detect specific pathogens in molecular diagnostics?
Which feature of retroviruses is the basis for the development of diagnostic tools to detect specific pathogens in molecular diagnostics?
Given the differences in genomic structure, what might be the main rationale for why there is not a live attenuated vaccine for Retroviruses, while there are for Flaviviruses?
Given the differences in genomic structure, what might be the main rationale for why there is not a live attenuated vaccine for Retroviruses, while there are for Flaviviruses?
Following a diagnosis of Feline Infectious Peritonitis (FIP) in a multi-cat household, what strategy is LEAST useful as an intervention to protect the other cats?
Following a diagnosis of Feline Infectious Peritonitis (FIP) in a multi-cat household, what strategy is LEAST useful as an intervention to protect the other cats?
Knowing that Bovine Viral Diarrhea Virus (BVDV) can cause both transient and persistent infections, what is the MOST effective long-term strategy for controlling BVDV in a cattle herd?
Knowing that Bovine Viral Diarrhea Virus (BVDV) can cause both transient and persistent infections, what is the MOST effective long-term strategy for controlling BVDV in a cattle herd?
Why are persistent infections with BVDV more challenging to control than transient infections within a cattle population?
Why are persistent infections with BVDV more challenging to control than transient infections within a cattle population?
Flashcards
Retroviridae
Retroviridae
Family of viruses with ss(+)RNA genome and DNA intermediate in replication.
Reverse Transcriptase
Reverse Transcriptase
An enzyme unique to retroviruses that synthesizes DNA from an RNA template, crucial for viral replication.
Provirus
Provirus
Viral DNA integrated into the host cell genome.
Retroviral Infections
Retroviral Infections
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Proto-oncogene
Proto-oncogene
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Oncogene
Oncogene
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Oncogene Capture (transducing)
Oncogene Capture (transducing)
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Insertional Activation (cis-activating)
Insertional Activation (cis-activating)
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Transactivation (trans-activating)
Transactivation (trans-activating)
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Flaviviridae
Flaviviridae
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Viral Transmission
Viral Transmission
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BVDV
BVDV
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Persistent Viral infections
Persistent Viral infections
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"Plain Jane" BVDV infection
"Plain Jane" BVDV infection
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Mucosal Disease
Mucosal Disease
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Teratogenic effects
Teratogenic effects
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Coronaviridae
Coronaviridae
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Tissue tropism switch
Tissue tropism switch
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FECV
FECV
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FIPV
FIPV
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Antibody-Dependent Enhancement (ADE)
Antibody-Dependent Enhancement (ADE)
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Study Notes
Lecture 6: RNA Viruses I
Retroviridae Family Properties
- Possesses single-stranded positive-sense RNA, with a DNA intermediate.
- It is an enveloped virus containing a helical nucleocapsid.
- Uses reverse transcriptase.
- Integrates provirus into the host cell genome.
- Causes persistent, pathogenic infections.
- Diseases include immune deficiency and oncogenesis in the host.
- There are 2 subfamilies, 7 genera, and multiple unique species.
Retroviridae Taxonomy
- Alpharetrovirus includes Avian leukosis virus, Avian sarcoma virus, Avian myeloblastosis virus, and Rous sarcoma virus.
- Betaretrovirus includes Mouse mammary tumour virus and Jaagsiekte sheep retrovirus.
- Gammaretrovirus includes Feline leukemia virus, Feline sarcoma virus and Reticuloendotheliosis virus.
- Deltaretrovirus includes Bovine leukemia virus and Human T-lymphotropic viruses 1 and 2.
- Epsilonretrovirus includes Walleyed dermal sarcoma virus.
- Lentivirus includes Human and Simian immunodeficiency viruses, Maedi/visna virus, Caprine arthritis-encephalitis virus, Equine infectious anemia virus, Feline and Bovine immunodeficiency virus.
- Spumaretrovirinae includes Spumavirus, causing foamy cytopathology in cell culture and not associated with clinical disease.
- Can cause oncogenic (+/- immune suppression) or immunodeficiency/immune-mediated (+/- neoplasia secondary to immunodeficiency) diseases.
Retrovirus-Induced Oncogenesis
- A proto-oncogene refers to a gene encoding for proteins that regulate cell growth and differentiation that can become an oncogene potentially causing cancer.
- Proto-oncogenes control cell growth and are highly regulated.
Mechanisms of Cell Transformation by Retroviruses
- There are 3 primary mechanisms of cell transformation by retroviruses.
- Oncogene capture where (c-onc -> v-onc) is transducing results in the rapid induction of clinical disease.
- Insertional mutations cause activation of adjacent c-onc causing cis-activation and resulting in intermediate timeline of clinical disease.
- Oncogenesis mediated by essential retroviral proteins leads to trans-activation resulting in a slow timeline of disease.
Flaviviridae Properties
- Contains a single-stranded negative-sense RNA genome.
- Enveloped with icosahedral symmetry (spherical).
- Causes persistent (asymptomatic) infections.
- Exhibits vertical vs. horizontal transmission patterns.
- May have non-cytopathic vs. cytopathic strains.
- Can have different disease syndromes.
- The family consists of four genera and many species.
Flaviviridae Taxonomy
- Orthoflavivirus includes Yellow fever, Japanese encephalitis, Dengue and Zika viruses, West Nile virus, Tickborne encephalitis and Kyasanur Forest disease viruses, as well as Powassan virus.
- Pestivirus includes Bovine viral diarrhea virus (BVDV), Classical swine fever virus and Border disease virus.
- Includes the Hepacivirus and Pegivirus genera.
Persistent Infection with Bovine Viral Diarrhea Virus (BVDV)
- Results in subclinical disease.
- "Plain Jane BVDV infection" can cause pyrexia and oral ulcerations, inappetence, depression, decreased milk production, excessive nasal/ocular secretions or diarrhea.
- Can cause BVDV infection and immunosuppression.
- Additionally, causes Bovine respiratory disease and pneumonia.
- May result in Hemorrhagic syndrome (Severe BVDV infection).
Coronaviridae Family Properties
- Has single-stranded positive-sense RNA.
- Enveloped and has a helical nucleocapsid.
- Undergoes tissue tropism switch, where it can change from intestinal epithelium to macrophages.
- Causes antibody-dependent enhancement of disease.
- The Feline enteric coronavirus (FECV) can transform to Feline infectious peritonitis virus (FIPV).
Tissue Tropism in Coronaviridae
- Low virulent biotype: mild diarrhea
- The tissue tropism of Feline enteric coronavirus occurs in the intestinal epithelium resulting in an enterotropic effect.
- The tissue tropism of Feline infectious peritonitis has an affinity for macrophages, resulting in a pantropic (systemic) effect that is highly virulent and associated with severe systemic disease.
Antibody-Dependent Enhancement of Disease in FIP
- Results in a diminished ability of immune cells to clear the virus.
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