Pathogenesis of Viral Infections — MCQs
What is a potential outcome of the integration of a viral genome into a host cell chromosome?
Which of the following is not a component of innate immunity?
Assertion: VZV vaccine is live attenuated. Reason: It cannot be given to immunocompromised patients.
Which of the following is an RNA oncogenic virus?
All of the following are RNA viruses except
What is the mechanism behind the increased risk of HIV acquisition in individuals with genital herpes?
Which of the following is true about anti-CMV IgG antibodies?
Histopathological feature of HIV encephalitis is/are-
Which of the following diseases is caused by the virus shown below?
Binding of gp120 causes:
Pathogenesis of Viral Infections Indian Medical PG Practice Questions and MCQs
Question 1: What is a potential outcome of the integration of a viral genome into a host cell chromosome?
- A. Altered growth
- B. Malignancy
- C. Latency
- D. All of the options (Correct Answer)
Explanation: ***All of the options*** - The insertion of a viral genome, known as a **provirus**, into the host chromosome can lead to a variety of sustained and complex interactions. - This integration can cause **long-term changes** in cell behavior, including altered gene expression and cell cycle regulation, which may manifest as any of the specified outcomes. *Malignancy* - Viral integration can interrupt or activate host genes, such as **oncogenes** or **tumor suppressor genes**, leading to uncontrolled cell proliferation and potential tumor formation. - An example is **human papillomavirus (HPV)** integrating into host cells, increasing the risk of cervical cancer. *Altered growth* - Integration can change the cell's normal growth patterns, either by promoting excessive division or by causing cell cycle arrest, impacting tissue development and function. - This can be due to the insertion of viral promoters or enhancers near growth-regulating genes. *Latency* - The integrated viral genome can remain dormant within the host chromosome without producing new viral particles for extended periods, a state known as **latency**. - During latency, the virus can be reactivated later to cause a productive infection, as seen with **herpesviruses**.
Question 2: Which of the following is not a component of innate immunity?
- A. Epithelial barriers
- B. NK cells
- C. Dendritic cells
- D. Helper T lymphocytes (Correct Answer)
Explanation: ***Helper T lymphocyte*** - Helper T lymphocytes are a crucial part of **adaptive immunity** [4], facilitating responses against pathogens. - They specifically activate B cells and cytotoxic T cells [2], unlike components of innate immunity, which respond nonspecifically. *NK cells* - Natural Killer (NK) cells are integral to **innate immunity** [1], targeting infected or tumor cells without prior sensitization. - They play a role in the initial response to viral infections and can produce **cytokines** [2]. *Epithelial barriers* - Epithelial barriers act as the first line of defense in **innate immunity** [1], preventing pathogen entry. - They include physical and chemical barriers like skin and mucous membranes [3]. *Dendritic cells* - Dendritic cells are key antigen-presenting cells involved in **innate immunity** [1] and link to adaptive immunity. - They capture and present antigens [2], activating T cells to mount an immune response. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 194-196. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 207-208. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 152-153. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 196-198.
Question 3: Assertion: VZV vaccine is live attenuated. Reason: It cannot be given to immunocompromised patients.
- A. Both true, reason doesn't explain assertion
- B. Assertion true, reason false
- C. Assertion false, reason true
- D. Both true, reason explains assertion (Correct Answer)
Explanation: ***Both true, reason explains assertion*** - The **VZV (varicella-zoster virus) vaccine** is indeed a **live attenuated vaccine** containing weakened virus - the assertion is **TRUE** - It **cannot be given to immunocompromised patients** due to risk of vaccine-strain disease - the reason is **TRUE** - The reason **directly explains the assertion**: BECAUSE the vaccine is live attenuated, it poses infection risk and therefore cannot be used in immunocompromised individuals - The **causal relationship** is clear: live attenuated nature → contraindication in immunocompromised patients *Both true, reason doesn't explain assertion* - While both statements are factually true, this option would only be correct if the reason was unrelated to the assertion - However, the reason **directly explains WHY** the live attenuated nature is clinically significant - The contraindication is a **direct consequence** of the vaccine being live attenuated, so the reason does explain the assertion *Assertion true, reason false* - The assertion is true (VZV vaccine is live attenuated) - However, the reason is also **TRUE** - live attenuated vaccines are indeed contraindicated in immunocompromised patients due to risk of disseminated vaccine-strain infection - Since both statements are true, this option is incorrect *Assertion false, reason true* - The assertion is **TRUE**, not false - VZV vaccine (Varivax, Zostavax) is a **live attenuated vaccine** containing the Oka strain - This option incorrectly claims the assertion is false - Since the assertion is factually correct, this option cannot be right
Question 4: Which of the following is an RNA oncogenic virus?
- A. Cytomegalovirus (CMV)
- B. Hepatitis B Virus (HBV)
- C. Human T-lymphotropic Virus (HTLV) (Correct Answer)
- D. Human Immunodeficiency Virus (HIV)
Explanation: ***Human T-lymphotropic Virus (HTLV)*** - **HTLV-1** is a well-established **RNA oncogenic virus** that causes Adult T-cell Leukemia/Lymphoma (ATLL). - It utilizes **reverse transcriptase** to convert its RNA genome into DNA, which then integrates into the host cell's genome, leading to malignant transformation. *Cytomegalovirus (CMV)* - CMV is a **DNA virus** and belongs to the Herpesviridae family. - While it can cause disease, it is not primarily classified as an **oncogenic virus**, although some studies suggest associations with certain cancers. *Hepatitis B Virus (HBV)* - HBV is a **DNA virus** that primarily causes acute and chronic hepatitis. - It is a major risk factor for **hepatocellular carcinoma (HCC)**, but it itself is a DNA virus, not an RNA virus. *Human Immunodeficiency Virus (HIV)* - HIV is an **RNA retrovirus**, but it is generally considered **non-oncogenic** in the direct sense. - While HIV-infected individuals have an increased risk of certain cancers (e.g., Kaposi's sarcoma, non-Hodgkin lymphoma), these are usually due to **immunosuppression** allowing co-infecting oncogenic viruses (like HHV-8 or EBV) to proliferate, rather than direct oncogenic action of HIV itself.
Question 5: All of the following are RNA viruses except
- A. Influenza virus
- B. Parainfluenza virus
- C. Mumps virus
- D. Herpes virus (Correct Answer)
Explanation: ***Herpes virus*** - **Herpesviruses** are a large family of **DNA viruses** that cause diseases in animals, including humans. - They are characterized by their ability to establish **latent infections** and periodically reactivate. *Influenza virus* - The **influenza virus** is an **RNA virus** belonging to the family **Orthomyxoviridae**. - It is known for causing the seasonal **flu** and respiratory infections. *Parainfluenza virus* - **Parainfluenza viruses** are a group of **RNA viruses** in the family **Paramyxoviridae**. - They are a common cause of **respiratory tract infections**, especially in children, leading to conditions like **croup**. *Mumps virus* - The **mumps virus** is an **RNA virus** that is part of the **Paramyxoviridae** family. - It is well-known for causing **mumps**, which is characterized by the swelling of the **parotid glands**.
Question 6: What is the mechanism behind the increased risk of HIV acquisition in individuals with genital herpes?
- A. HSV glycoproteins enhance HIV binding to target cells
- B. HSV inhibits local innate immune responses
- C. HSV increases HIV viral load through transactivation
- D. HSV disrupts epithelial barrier and recruits CD4+ cells (Correct Answer)
Explanation: ***HSV disrupts epithelial barrier and recruits CD4+ cells*** - Genital herpes causes **lesions and ulcerations** in the genital mucosa, which disrupt the integrity of the epithelial barrier, creating portals of entry for HIV. - The inflammatory response to HSV infection leads to the recruitment of **CD4+ T cells** and other HIV target cells to the genital tract, making them readily available for HIV infection. *HSV glycoproteins enhance HIV binding to target cells* - While HSV modifies cellular surfaces, its glycoproteins are not directly known to **enhance HIV binding** to its primary receptors (CD4 and co-receptors) on target cells. - This mechanism is not considered a primary driver of the increased HIV acquisition risk in the context of HSV. *HSV inhibits local innate immune responses* - HSV does have mechanisms to evade host immunity, but its primary impact on HIV acquisition is not through a generalized **inhibition of overall innate immune responses** that would directly increase HIV entry. - Instead, the physical disruption and cellular recruitment are more significant factors. *HSV increases HIV viral load through transactivation* - This mechanism refers more to the potential interaction of HSV with established HIV infection to **replicate more HIV**, not primarily to the initial acquisition of HIV. - While co-infection *can* impact HIV viral replication, it's not the main reason for increased susceptibility to *acquiring* HIV.
Question 7: Which of the following is true about anti-CMV IgG antibodies?
- A. IgG avidity assay helps in differentiating past and primary infection (Correct Answer)
- B. Denotes latent CMV infection
- C. Denotes chronic CMV infection with immunity to other serotypes
- D. Indicates acute CMV infection
Explanation: ***IgG avidity assay helps in differentiating past and primary infection*** - **IgG avidity** measures the binding strength of IgG antibodies to their antigen. In a **primary infection**, IgG antibodies have low avidity. - As the immune response matures over several months, the avidity of IgG antibodies increases, indicating a **past infection**. *Denotes latent CMV infection* - While the presence of IgG antibodies indicates a past exposure and often a latent infection, it doesn't solely *denote* latency, as primary infection also involves IgG production. - **Latent CMV infection** specifically refers to the persistence of the virus in cells without active replication, which is usually confirmed by the presence of IgG antibodies but needs further contextual information like negative IgM and viral load. *Denotes chronic CMV infection with immunity to other serotypes* - CMV typically exists as one serotype, and IgG antibodies confer protection against *re-activation* of that specific virus, not immunity to "other serotypes." - **Chronic infection** usually implies ongoing active replication or persistent symptoms, which a positive IgG alone does not confirm. *Indicates acute CMV infection* - **Acute CMV infection** is primarily indicated by the presence of **IgM antibodies**, which appear early in the infection. - While IgG antibodies also rise during acute infection, their presence alone is not specific for an **acute phase** as they persist after the infection resolves.
Question 8: Histopathological feature of HIV encephalitis is/are-
- A. Microglial nodules (Correct Answer)
- B. Lewy body
- C. Fibrillary plaque
- D. Negri body
Explanation: ***Microglial nodules*** - **Microglial nodules** are a hallmark histopathological feature of **HIV encephalitis**, representing clusters of activated microglia and macrophages in the brain parenchyma [2]. - These nodules often contain **multinucleated giant cells**, which are believed to be formed by the fusion of HIV-infected macrophages and are pathognomonic for HIV encephalitis [1]. *Lewy body* - **Lewy bodies** are abnormal aggregates of protein (primarily **alpha-synuclein**) that develop inside nerve cells, primarily associated with **Parkinson's disease** and **Lewy body dementia**. - They are not characteristic of HIV encephalitis or other viral infections of the brain. *Fibrillary plaque* - **Fibrillary plaques**, specifically **amyloid plaques**, are extracellular deposits of aggregated **beta-amyloid protein** found in the brains of individuals with **Alzheimer's disease**. - These are a key feature of neurodegenerative conditions but are not seen in HIV encephalitis. *Negri body* - **Negri bodies** are eosinophilic, sharply demarcated neuronal cytoplasmic inclusions found in the pyramidal cells of the hippocampus and Purkinje cells of the cerebellum in individuals with **rabies**. - They are specific to rabies infection and are not associated with HIV encephalitis. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Manifestations Of Central And Peripheral Nervous System Disease, pp. 711-712. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Peripheral Nerves and Skeletal Muscles, pp. 1255-1256.
Question 9: Which of the following diseases is caused by the virus shown below?
- A. Neurodegenerative disorder
- B. Swimming pool conjunctivitis (Correct Answer)
- C. Solid organ graft infection
- D. Solid organ graft rejection
Explanation: ***Swimming pool conjunctivitis*** - The image displays an **adenovirus**, characterized by its **icosahedral shape** and distinct **fiber proteins** projecting from the vertices. - Adenoviruses are a common cause of **pharyngoconjunctival fever**, often referred to as "swimming pool conjunctivitis" due to its spread in **inadequately chlorinated swimming pools**. - This is the **most characteristic disease** associated with adenovirus infection, particularly serotypes **3, 4, and 7**. *Neurodegenerative disorder* - Adenoviruses are **not associated** with neurodegenerative disorders. - Neurodegenerative conditions are typically linked to **prions, misfolded proteins**, or other viral agents like **JC virus** (progressive multifocal leukoencephalopathy). - Adenoviruses cause **acute infections**, not chronic neurodegeneration. *Solid organ graft infection* - While adenoviruses can cause severe infections in **immunocompromised patients**, including transplant recipients, this is not their most characteristic presentation. - In transplant patients, adenovirus may cause **colitis, hepatitis, or nephritis**, but these are **opportunistic infections** rather than the typical disease association. - The characteristic disease remains **conjunctivitis and respiratory infections** in immunocompetent hosts. *Solid organ graft rejection* - **Graft rejection** is an **immunological process** where the recipient's immune system attacks the transplanted organ, not a viral infection. - Adenovirus does not directly cause the mechanism of graft rejection. - While viral infections may complicate graft outcomes, rejection itself is **immune-mediated**, not infectious.
Question 10: Binding of gp120 causes:
- A. Infection of target cell
- B. Facilitation of co-receptor binding (Correct Answer)
- C. Fusing of virus and target cell
- D. None of the options
Explanation: ***Facilitation of co-receptor*** - **gp120** binding to the **CD4 receptor** on target cells induces a conformational change in gp120, which then exposes or creates a binding site for a **chemokine co-receptor** (CCR5 or CXCR4). - This interaction is crucial for the subsequent steps of viral entry, as it allows the virus to make further contact with the cell surface. *Infection of target cell* - While binding of gp120 is the *first step* in infection, it does not directly cause the infection itself. - Infection occurs after a series of events including co-receptor binding, membrane fusion, and reverse transcription. *Fusing of virus and target cell* - **Fusion** of the viral and cellular membranes is primarily mediated by **gp41**, which is part of the gp160 envelope glycoprotein complex alongside gp120. - This fusion event *follows* the binding of gp120 to CD4 and the co-receptor, as gp120 binding initiates the conformational changes that expose and activate gp41. *None of the options* - One of the provided options accurately describes a direct consequence of gp120 binding, making this option incorrect.
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