Block 10 Oncovirus Of Wbc MCQ's

1. Inclusion bodies are:

Accumulations of viral proteins in stained, infected cells

Induced by the action of interferon

Found in non-permissive infections of cells

Viral organelles of respiration

Inclusion bodies are accumulations of viral proteins in stained, infected cells. These bodies are formed as a result of viral replication within the host cell. When a cell is infected by a virus, it starts producing viral proteins as part of the replication process. These proteins can aggregate and form inclusion bodies, which can be visualized using staining techniques. Inclusion bodies are commonly observed in viral infections and can help in the diagnosis of viral diseases. They are not induced by interferon or found in viral organelles of respiration.

Explanation

Inclusion bodies are accumulations of viral proteins in stained, infected cells. These bodies are formed as a result of viral replication within the host cell. When a cell is infected by a virus, it starts producing viral proteins as part of the replication process. These proteins can aggregate and form inclusion bodies, which can be visualized using staining techniques. Inclusion bodies are commonly observed in viral infections and can help in the diagnosis of viral diseases. They are not induced by interferon or found in viral organelles of respiration.

2. 30-year-old woman is worked up for an abnormal Pap smear. Colposcopy shows lesions in the cervix indicative of a malignancy caused by Papillomavirus infection. Which of the following is the most likely process of transformation?

Creating a hotspot for v-Src integration near a c-oncogene, thereby increasing cell growth and proliferation

Permanently activating the Pkr pathway involved in cell growth and proliferation

Binding protein E7 to Rb and bypassing cell cycle control

Permanently activating the p53 pathway involved in cell growth and proliferation

Permanently activating cell signalling pathways involved in cell growth and proliferation

The most likely process of transformation in this case is the binding of protein E7 to Rb and bypassing cell cycle control. This is because the question states that the lesions in the cervix are indicative of a malignancy caused by Papillomavirus infection, and one of the key mechanisms by which Papillomavirus causes cancer is through the binding of its E7 protein to the Rb protein. This binding disrupts the normal cell cycle control and allows for uncontrolled cell growth and proliferation, leading to the development of malignancy.

Explanation

The most likely process of transformation in this case is the binding of protein E7 to Rb and bypassing cell cycle control. This is because the question states that the lesions in the cervix are indicative of a malignancy caused by Papillomavirus infection, and one of the key mechanisms by which Papillomavirus causes cancer is through the binding of its E7 protein to the Rb protein. This binding disrupts the normal cell cycle control and allows for uncontrolled cell growth and proliferation, leading to the development of malignancy.

3. The HPV E7 protein leads the infected cell into the S phase of the cell cycle by

Activating the mitogen activated protein kinase signaling cascade through PP2A phosphatase inhibition

Targeting the proapoptotic protein p53 for ubiquitin-dependent proteasomal degradation

Uncoupling the retinoblastoma restriction point protein pRb from the E2F family of transcription factors

Complexing with and activating the cyclin D/CDK4 kinase complex

The HPV E7 protein is responsible for uncoupling the retinoblastoma restriction point protein pRb from the E2F family of transcription factors. This uncoupling allows the cell to progress into the S phase of the cell cycle.

Explanation

The HPV E7 protein is responsible for uncoupling the retinoblastoma restriction point protein pRb from the E2F family of transcription factors. This uncoupling allows the cell to progress into the S phase of the cell cycle.

4. Which of the following oncogenic double–stranded DNA viruses binds to C3d/CD21?

Adenovirus

Poxvirus

Human T-Leukemia Virus

Kaposi's-associated Herpes Virus

Epstein-Barr virus

Epstein-Barr virus is the correct answer because it is known to bind to C3d/CD21. C3d is a complement protein that is involved in the immune response, and CD21 is a receptor found on B cells. Epstein-Barr virus is a double-stranded DNA virus that primarily infects B cells and is associated with various cancers, including Burkitt's lymphoma and nasopharyngeal carcinoma. By binding to C3d/CD21, the virus is able to enter and infect B cells, leading to its oncogenic effects.

Explanation

Epstein-Barr virus is the correct answer because it is known to bind to C3d/CD21. C3d is a complement protein that is involved in the immune response, and CD21 is a receptor found on B cells. Epstein-Barr virus is a double-stranded DNA virus that primarily infects B cells and is associated with various cancers, including Burkitt's lymphoma and nasopharyngeal carcinoma. By binding to C3d/CD21, the virus is able to enter and infect B cells, leading to its oncogenic effects.

5. What are the characteristics of Cytomegalovirus?

Naked ds DNA virus causing two different types of inclusions

Enveloped ds DNA virus with no know oncogenic potential

Naked ss positive RNA virus transmitted by the fecal oral route

Enveloped ss negative RNA virus

Naked ss negative virus replicating in the nucleus

Cytomegalovirus is an enveloped ds DNA virus, meaning it has a double-stranded DNA genome surrounded by an envelope. It is known for causing two different types of inclusions in infected cells. The virus does not have any known oncogenic potential, meaning it does not have the ability to cause cancer. Therefore, the correct answer is that cytomegalovirus is an enveloped ds DNA virus with no known oncogenic potential.

Explanation

Cytomegalovirus is an enveloped ds DNA virus, meaning it has a double-stranded DNA genome surrounded by an envelope. It is known for causing two different types of inclusions in infected cells. The virus does not have any known oncogenic potential, meaning it does not have the ability to cause cancer. Therefore, the correct answer is that cytomegalovirus is an enveloped ds DNA virus with no known oncogenic potential.

6. Cell transformation can be induced by:

Virally-encoded phosphatases that target the Erk1/Erk2 signalling pathway

Virally-encoded permanently activated Src homolog signalling molecules

Virally-encoded Ras homologs that constitutively hydrolyse GTP

Virally-encoded myc inhibitors

Virally-encoded scaffolding proteins that inactivate the SH2 domain of Src-homology signalling molecules

Virally-encoded permanently activated Src homolog signalling molecules can induce cell transformation. These molecules, when introduced into the cell by a virus, are constantly active and can initiate signaling pathways that promote cell growth and division. This uncontrolled activation of cell signaling can lead to the transformation of normal cells into cancerous cells.

Explanation

Virally-encoded permanently activated Src homolog signalling molecules can induce cell transformation. These molecules, when introduced into the cell by a virus, are constantly active and can initiate signaling pathways that promote cell growth and division. This uncontrolled activation of cell signaling can lead to the transformation of normal cells into cancerous cells.

7. Which of the following statements is false?

Virally-encoded proteins that mimic signalling molecules can contribute to cell transformation

Virally-encoded functional cyclin homologs can contribute to cell transformation

Virally-encoded proteins that inactivate cyclin-dependent kinase inhibitors can contribute to cell transformation.

Virally-encoded proteins that activate cyclin-dependent kinase inhibitors can contribute to cell transformation

Virally-encoded proteins that maintain signalling molecules in an activated state can contribute to cell transformation

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Explanation

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8. Viral cell transformation can result from (1) the insertion of viral oncogenes into host cell genomes, (2) the integration of proviruses into host cell genomes near proto-oncogene regulatory sequences, (3) the permanent activation by viruses of host cell signalling pathways, and (4) the alteration of host cell cycling regulation by viruses. Which viruses are responsible for cell transformation due to integration of proviruses in the vicinity of proto-oncogenes (nontransducing viruses)?

Adenoviruses

Hepadnaviruses (Hepatitis B Virus)

Papillomaviruses

Herpesviruses

Retroviruses

Transforming Oncogenic Retroviruses.
Introduction of a new transforming gene into the cell (direct-acting): Retroviruses containing oncogenic, cell-derived sequences in their genomes carry these sequences to each newly infected cell. They are highly oncogenic No human example is currently known.
Indirect-acting: The virus alters the expression of preexisting cellular genes through inserting the provirus. Proto-oncogenes might be activated by this insertional activation: Promoter insertion. Such a promoter might be contained in the LTR of inserted retroviruses. Integration close to a proto-oncogene may activate the expression of the gene: Enhancer Insertion. The enhancer is a DNA sequence increasing the rate of transcription by binding regulatory proteins (Meisenberg/Simmons, 2006).

Explanation

Transforming Oncogenic Retroviruses.
Introduction of a new transforming gene into the cell (direct-acting): Retroviruses containing oncogenic, cell-derived sequences in their genomes carry these sequences to each newly infected cell. They are highly oncogenic No human example is currently known.
Indirect-acting: The virus alters the expression of preexisting cellular genes through inserting the provirus. Proto-oncogenes might be activated by this insertional activation: Promoter insertion. Such a promoter might be contained in the LTR of inserted retroviruses. Integration close to a proto-oncogene may activate the expression of the gene: Enhancer Insertion. The enhancer is a DNA sequence increasing the rate of transcription by binding regulatory proteins (Meisenberg/Simmons, 2006).

9. Virus shedding during acute EBV infection can be diminished by using acyclovir, a nucleoside analogue. Which of the following polymerases would be involved in this process?

RNA-dependent RNA polymerase

RNA-dependent DNA polymerase

DNA-dependent RNA polymerase

DNA-dependent DNA polymerase

Reverse transcriptase

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Explanation

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10. Your patient is a college student who presents with mononucleosis like disease. What characteristic of Epstein-Barr virus is responsible for both the rash that is sometimes seen in EBV infectious mononucleosis and the presence of antibody which will agglutinate sheep red blood cells?

EBNA

Latency

Triggering of the Downey type II cells

Replication and assembly in the nucleus of the cells

Poly B cell expansion

Poly B cell expansion is the characteristic of Epstein-Barr virus that is responsible for both the rash seen in EBV infectious mononucleosis and the presence of antibody which will agglutinate sheep red blood cells. This expansion of B cells leads to an increase in the production of antibodies, including those that can agglutinate sheep red blood cells. Additionally, the expansion of B cells can also cause a rash as part of the immune response to the virus.

Explanation

Poly B cell expansion is the characteristic of Epstein-Barr virus that is responsible for both the rash seen in EBV infectious mononucleosis and the presence of antibody which will agglutinate sheep red blood cells. This expansion of B cells leads to an increase in the production of antibodies, including those that can agglutinate sheep red blood cells. Additionally, the expansion of B cells can also cause a rash as part of the immune response to the virus.