Virology — MCQs

Virology Indian Medical PG Practice Questions and MCQs

Question 501: Dengue hemorrhagic fever is caused by which of the following?

A. Type I dengue virus
B. Reinfection with the same serotype of dengue virus
C. Reinfection with a different serotype of dengue virus (Correct Answer)
D. Infection in an immunocompromised host

Explanation: **Explanation:** The correct answer is **C. Reinfection with a different serotype of dengue virus.** The pathogenesis of Dengue Hemorrhagic Fever (DHF) and Dengue Shock Syndrome (DSS) is primarily explained by the phenomenon of **Antibody-Dependent Enhancement (ADE)**. There are four distinct serotypes of Dengue virus (DEN-1 to DEN-4). A primary infection provides lifelong immunity to that specific serotype but only temporary, partial cross-protection against others. When a person is reinfected with a **different serotype** (secondary infection), the pre-existing non-neutralizing antibodies from the first infection bind to the new virus. Instead of neutralizing it, these antibodies facilitate the entry of the virus into macrophages via Fc receptors. This leads to increased viral replication, a massive release of cytokines ("cytokine storm"), and complement activation, resulting in increased vascular permeability, plasma leakage, and thrombocytopenia—the hallmarks of DHF. **Analysis of Incorrect Options:** * **Option A:** A primary infection with any single serotype (like Type I) typically causes classic Dengue Fever (Breakbone fever), which is usually self-limiting and rarely progresses to DHF. * **Option B:** Reinfection with the same serotype is impossible due to lifelong homologous immunity provided by neutralizing antibodies. * **Option C:** While immunocompromised states increase the risk of severe disease in many infections, DHF is specifically an **immunopathological** reaction; it occurs in immunocompetent individuals because it requires a robust (though maladaptive) immune response. **High-Yield Clinical Pearls for NEET-PG:** * **Vector:** *Aedes aegypti* (Day biter; breeds in artificial collections of clean water). * **Tourniquet Test:** A positive test (≥10-20 petechiae per square inch) is a clinical indicator of capillary fragility in DHF. * **Lab Findings:** Hemoconcentration (rising Hematocrit >20%) is a key sign of plasma leakage. * **Serology:** NS1 antigen is the marker of choice for early diagnosis (Day 1-5). IgM appears later (after Day 5).

Question 502: Epstein-Barr virus (EBV) is responsible for all of the following conditions except?

A. Nasopharyngeal carcinoma
B. Burkitt's lymphoma
C. Hepatoma (Correct Answer)
D. Infectious mononucleosis

Explanation: **Explanation:** The **Epstein-Barr Virus (EBV)**, also known as Human Herpesvirus 4 (HHV-4), is a potent oncogenic virus with a strong tropism for B-lymphocytes and epithelial cells. **Why Hepatoma is the correct answer:** Hepatoma (Hepatocellular Carcinoma) is primarily associated with chronic infections of **Hepatitis B Virus (HBV)** and **Hepatitis C Virus (HCV)**, as well as cirrhosis and aflatoxin exposure. EBV does not play a role in the pathogenesis of primary liver cancer. While EBV can cause transient hepatitis during acute infection (Infectious Mononucleosis), it does not lead to chronic liver malignancy. **Analysis of other options:** * **Nasopharyngeal Carcinoma:** EBV is strongly linked to the undifferentiated type of this tumor, particularly in Southern China and Southeast Asia. It involves the clonal expansion of EBV-infected epithelial cells. * **Burkitt's Lymphoma:** This is a B-cell malignancy highly associated with EBV, especially the "Endemic" (African) form. It characteristically involves the **t(8;14)** translocation of the *c-myc* oncogene. * **Infectious Mononucleosis (Glandular Fever):** This is the primary acute clinical manifestation of EBV, characterized by the triad of fever, pharyngitis, and lymphadenopathy, with the presence of **Atypical Lymphocytes (Downey cells)** in the peripheral smear. **High-Yield Clinical Pearls for NEET-PG:** * **Receptor:** EBV binds to the **CD21** receptor (CR2) on B-cells. * **Diagnosis:** The **Paul-Bunnell Test** (detecting heterophile antibodies) is the classic screening test. * **Other EBV Associations:** Oral Hairy Leukoplakia (in HIV patients), Hodgkin’s Lymphoma (Mixed cellularity type), and Gastric Carcinoma. * **Atypical Lymphocytes:** These are actually activated **CD8+ T-cells** reacting against the infected B-cells.

Question 503: All of the following statements are true regarding human T cell leukemia virus 1 except?

A. It causes adult T cell lymphoma/leukemia
B. It has tropism for CD8+ T cells (Correct Answer)
C. It has a long latent period of about 40 to 60 years
D. Leukemia develops in only 3 to 5% of infected individuals

Explanation: **Explanation:** Human T-cell Lymphotropic Virus type 1 (HTLV-1) is a complex retrovirus. The correct answer is **Option B** because HTLV-1 primarily exhibits tropism for **CD4+ T cells**, not CD8+ T cells. It uses the GLUT-1 receptor to enter cells, leading to the malignant transformation of helper T cells. **Analysis of Options:** * **Option A (True):** HTLV-1 is the causative agent of **Adult T-cell Leukemia/Lymphoma (ATLL)**. It is also associated with HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP). * **Option C (True):** The virus is known for an exceptionally **long latent period**. Most patients are infected during infancy (via breast milk), but clinical leukemia typically manifests 40 to 60 years later. * **Option D (True):** HTLV-1 has low oncogenic penetrance; only **3–5%** of lifelong carriers eventually develop ATLL. The majority of infected individuals remain asymptomatic carriers. **High-Yield Clinical Pearls for NEET-PG:** * **Oncogenesis:** Unlike other retroviruses, HTLV-1 does not carry a host-derived oncogene. Instead, it uses the **Tax gene**, which activates host cell transcription factors (like NF-κB) to promote proliferation and inhibit apoptosis. * **Morphology:** A characteristic finding in the peripheral blood smear of ATLL patients is the presence of **"Flower cells"** (lymphocytes with polylobated nuclei). * **Transmission:** Similar to HIV—via blood transfusion, sexual contact, and vertically (primarily through prolonged breastfeeding). * **Diagnosis:** Screening is done via ELISA; confirmation is via Western Blot or PCR.

Question 504: Which one of the following viruses is considered a human tumor virus?

A. Epstein-Barr virus (EBV)
B. Human Immunodeficiency Virus (HIV)
C. Papillomavirus (Correct Answer)
D. Varicella-zoster virus (VZV)

Explanation: **Explanation:** The correct answer is **Papillomavirus (HPV)**. Human tumor viruses, or oncogenic viruses, are those capable of inducing neoplastic transformation in host cells. **1. Why Papillomavirus is correct:** High-risk strains of Human Papillomavirus (primarily **HPV 16 and 18**) are strongly associated with cervical, anogenital, and oropharyngeal cancers. The oncogenic potential lies in the viral proteins **E6 and E7**, which inhibit the host’s tumor suppressor proteins **p53 and Rb**, respectively. This leads to uncontrolled cell cycle progression and genomic instability. **2. Why the other options are incorrect:** * **Epstein-Barr virus (EBV):** While EBV is indeed an oncogenic virus (associated with Burkitt lymphoma and Nasopharyngeal carcinoma), in the context of standard multiple-choice questions where only one "best" answer is sought, HPV is often the classic prototype for "human tumor viruses" due to its direct causal link to major epithelial cancers. *Note: If this were a multiple-select question, EBV would also be correct.* * **HIV:** HIV is a lentivirus that causes immunodeficiency. While it increases the risk of cancers (like Kaposi sarcoma) by suppressing the immune system, it is not considered a direct "tumor virus" because it does not transform cells via oncogenes. * **Varicella-zoster virus (VZV):** VZV causes chickenpox and shingles; it has no known oncogenic potential. **High-Yield NEET-PG Pearls:** * **DNA Oncogenic Viruses:** HPV, EBV, Hepatitis B (HBV), Human Herpesvirus 8 (HHV-8), and Merkel Cell Polyomavirus. * **RNA Oncogenic Viruses:** Hepatitis C (HCV) and Human T-cell Lymphotropic Virus-1 (HTLV-1). * **Mechanism Tip:** Remember **"6-53, 7-Rb"** (E6 acts on p53; E7 acts on Rb) to quickly recall HPV pathogenesis.

Question 505: Inclusion bodies are not seen in which of the following viral infections?

A. Cytomegalovirus (CMV)
B. Epstein-Barr virus (EBV) (Correct Answer)
C. Herpes simplex virus (HSV)
D. Rabies virus

Explanation: Inclusion bodies are aggregates of viral proteins or nucleic acids within a cell that are visible under a light microscope. While most members of the *Herpesviridae* family produce characteristic inclusions, **Epstein-Barr Virus (EBV)** is a notable exception. ### **Why EBV is the Correct Answer** EBV primarily infects B-lymphocytes and epithelial cells. Unlike other herpesviruses, EBV does not typically produce visible intracellular inclusion bodies during its replicative cycle. Instead, the hallmark of EBV infection (Infectious Mononucleosis) is the presence of **Atypical Lymphocytes (Downey cells)**—which are activated T-cells reacting to the infected B-cells, not viral inclusions themselves. ### **Analysis of Incorrect Options** * **Cytomegalovirus (CMV):** Characterized by large, basophilic intranuclear inclusions surrounded by a clear halo, giving the classic **"Owl’s eye" appearance**. * **Herpes Simplex Virus (HSV):** Produces eosinophilic intranuclear inclusions known as **Cowdry Type A bodies** (also seen in Varicella-Zoster). * **Rabies Virus:** A classic example of intracytoplasmic inclusions called **Negri bodies**, typically found in the Purkinje cells of the cerebellum and pyramidal cells of the hippocampus. ### **High-Yield Clinical Pearls for NEET-PG** * **Intranuclear Inclusions:** DNA viruses (except Poxvirus). Examples: Cowdry A (HSV), Cowdry B (Polio), Owl's eye (CMV). * **Intracytoplasmic Inclusions:** RNA viruses (except Influenza and Measles). Examples: Negri bodies (Rabies), Guarnieri bodies (Smallpox), Henderson-Patterson bodies (Molluscum contagiosum). * **Both Intranuclear & Intracytoplasmic:** Measles (Warthin-Finkeldey cells). * **Mnemonic:** EBV is "Empty" of inclusions but "Extra" (Atypical) lymphocytes.

Question 506: Which of the following influenza virus types is NOT currently circulating in the world?

A. H1N1
B. H3N2
C. H5N1 (Correct Answer)
D. Influenza B virus

Explanation: ### Explanation The correct answer is **C. H5N1**. **1. Why H5N1 is the correct answer:** In the context of human epidemiology, "circulating" refers to viruses that undergo regular, sustained human-to-human transmission (seasonal flu). **H5N1** is an **Avian Influenza (Bird Flu)** virus. While it causes sporadic, severe infections in humans through direct contact with infected poultry, it has **not** yet acquired the ability for sustained human-to-human transmission. Therefore, it is not considered a "circulating" human influenza subtype. **2. Analysis of Incorrect Options:** * **A. H1N1:** This is a subtype of Influenza A. The **A(H1N1)pdm09** strain has been circulating globally since the 2009 pandemic and is a standard component of the seasonal trivalent/quadrivalent vaccines. * **B. H3N2:** This is the other major subtype of Influenza A currently circulating in humans. It often causes more severe seasonal outbreaks in the elderly compared to H1N1. * **C. Influenza B:** Unlike Influenza A, Type B is almost exclusively a human pathogen and does not have subtypes (only lineages like Victoria and Yamagata). It circulates globally every year. **3. High-Yield Clinical Pearls for NEET-PG:** * **Antigenic Shift:** Major genetic changes (reassortment) leading to **Pandemics**. Only occurs in **Influenza A**. * **Antigenic Drift:** Minor point mutations leading to **Epidemics**. Occurs in both **Influenza A and B**. * **Nomenclature:** Hemagglutinin (H) is for attachment; Neuraminidase (N) is for viral release. * **Drug of Choice:** **Oseltamivir** (Neuraminidase inhibitor) is the preferred treatment for both circulating and avian strains. * **Current Human Circulation:** Currently, only **Influenza A (H1N1 and H3N2)** and **Influenza B** circulate regularly among humans.

Question 507: SSPE is a rare complication of which disease?

A. Mumps
B. Measles (Correct Answer)
C. Rubella
D. Influenza

Explanation: **Explanation:** **Subacute Sclerosing Panencephalitis (SSPE)**, also known as Dawson disease, is a progressive, fatal neurodegenerative condition caused by a persistent infection with a **defective Measles virus**. **1. Why Measles is Correct:** SSPE occurs years (typically 7–10 years) after an initial measles infection, usually in children who contracted the virus before age two. The underlying mechanism involves a **mutated measles virus** (lacking the 'M' or matrix protein) that cannot bud from host cells. Instead, it spreads directly from cell to cell via syncytia formation, leading to chronic inflammation, demyelination, and neuronal death in the CNS. **2. Why Other Options are Incorrect:** * **Mumps:** While mumps can cause acute viral meningitis or encephalitis, it is not associated with a chronic, progressive sclerosing panencephalitis like SSPE. * **Rubella:** Rubella is associated with **Progressive Rubella Panencephalitis (PRP)**, which clinically mimics SSPE but is etiologically distinct and much rarer. * **Influenza:** Influenza is linked to acute complications like Reye’s syndrome (if aspirin is used) or acute encephalopathy, but not a delayed-onset chronic panencephalitis. **3. High-Yield Clinical Pearls for NEET-PG:** * **Clinical Stages:** Characterized by behavioral changes, followed by **myoclonic jerks**, and eventually dementia/coma. * **Diagnosis:** * **EEG:** Shows characteristic **periodic complexes** (high-voltage slow waves). * **CSF:** Shows significantly **elevated Anti-Measles antibody titers** and oligoclonal bands. * **Prevention:** The incidence of SSPE has drastically reduced due to the **MMR vaccine**. * **Pathology:** Presence of **Cowdry type A** intranuclear inclusion bodies in neurons and glial cells.

Question 508: Which serological marker indicates Hepatitis B infectivity?

A. Anti-HBsAg
B. HBsAg + HBeAg (Correct Answer)
C. Anti-HBsAg - Anti-HBc
D. Anti-HBeAg + Anti-HBs Ag

Explanation: ### Explanation **Correct Answer: B. HBsAg + HBeAg** In Hepatitis B serology, the presence of **HBsAg (Hepatitis B surface Antigen)** is the hallmark of infection, indicating that the virus is present in the body. However, **HBeAg (Hepatitis B e-Antigen)** is the specific marker for **active viral replication and high infectivity**. When both are positive, it signifies that the patient is highly contagious and has a high viral load in the blood and body fluids. #### Analysis of Incorrect Options: * **Option A (Anti-HBsAg):** This antibody indicates **immunity** (either from vaccination or recovery). It is a neutralizing antibody and signifies that the person is no longer infectious. * **Option C (Anti-HBsAg - Anti-HBc):** This profile is seen in individuals who have **recovered from a natural infection**. They are immune and non-infectious. * **Option D (Anti-HBeAg + Anti-HBsAg):** The presence of Anti-HBe indicates that viral replication has slowed down (seroconversion), and Anti-HBs indicates immunity. This person is in the recovery phase and has low to no infectivity. #### NEET-PG High-Yield Pearls: * **HBsAg:** First marker to appear in blood; indicates infection (acute or chronic). * **HBeAg:** Best indicator of **infectivity** and viral replication. * **Anti-HBc (Total):** Indicates exposure to the actual virus (not seen in vaccinated individuals). * **IgM anti-HBc:** The only marker positive during the **"Window Period"** (the gap between HBsAg disappearing and Anti-HBs appearing). * **HBV DNA:** The most sensitive quantitative marker for viral load and monitoring treatment response.

Question 509: Meningitis is characterized by the acute onset of fever and stiff neck. Aseptic meningitis may be caused by a variety of microbial agents. During the initial 24 hours of the course of aseptic meningitis, what is the characteristic finding in an affected person's cerebrospinal fluid?

A. Decreased protein content
B. Elevated glucose concentration
C. Lymphocytosis
D. Polymorphonuclear leukocytosis (Correct Answer)

Explanation: **Explanation:** The term **aseptic meningitis** refers to a clinical syndrome of meningeal inflammation where routine bacterial cultures are negative, most commonly caused by viruses (e.g., Enteroviruses). **Why Option D is Correct:** While viral meningitis is classically associated with **lymphocytosis**, the "early phase" (initial 24–48 hours) is a high-yield exception. During this hyperacute period, the inflammatory response often begins with a transient **Polymorphonuclear (PMN) leukocytosis**. This "neutrophilic shift" can mimic bacterial meningitis, making early diagnosis challenging. As the infection progresses beyond 24–48 hours, the cellular profile typically shifts to the characteristic lymphocytic predominance. **Why the other options are incorrect:** * **A & B:** In viral meningitis, the **glucose concentration is typically normal** (unlike bacterial meningitis where it is low), and the **protein content is normal to mildly elevated** (never decreased). * **C:** Lymphocytosis is the hallmark of viral meningitis in the *subacute* phase, but it is not the characteristic finding during the *initial 24 hours* described in the question. **NEET-PG High-Yield Pearls:** * **Most common cause of aseptic meningitis:** Enteroviruses (Coxsackievirus, Echovirus). * **CSF Profile in Viral Meningitis:** Normal glucose, normal/slightly high protein, and lymphocytic pleocytosis (after the first 24 hours). * **Mollaret Meningitis:** Recurrent aseptic meningitis often associated with HSV-2. * **Diagnostic Gold Standard:** PCR of the CSF is more sensitive than viral culture for identifying the causative agent.

Question 510: Negri bodies are characteristic inclusions seen in which viral infection?

A. Cytomegalovirus (CMV)
B. Rabies (Correct Answer)
C. Herpes simplex virus
D. Epstein-Barr virus (EBV)

Explanation: **Explanation:** **Negri bodies** are the pathognomonic histopathological hallmark of **Rabies virus** infection. These are sharply outlined, eosinophilic (pinkish), round or oval **intracytoplasmic inclusion bodies** found in the cytoplasm of neurons. They are most commonly found in the **Purkinje cells of the cerebellum** and the **pyramidal cells of the hippocampus (Ammon’s horn)**. They represent sites of viral replication and consist of ribonuclear proteins. **Analysis of Incorrect Options:** * **A. Cytomegalovirus (CMV):** Characterized by large, basophilic **intranuclear** inclusions surrounded by a clear halo, giving an **"Owl’s eye" appearance**. * **C. Herpes simplex virus (HSV):** Characterized by **Cowdry Type A** inclusions, which are eosinophilic intranuclear bodies. HSV also shows multinucleated giant cells on a Tzanck smear. * **D. Epstein-Barr virus (EBV):** Does not typically produce classic inclusion bodies; instead, it is associated with **atypical lymphocytes (Downey cells)** in the peripheral blood. **High-Yield Clinical Pearls for NEET-PG:** * **Nature of Inclusions:** Most DNA viruses produce intranuclear inclusions (except Poxvirus), while most RNA viruses produce intracytoplasmic inclusions (except Measles, which produces both). * **Rabies Virus:** A bullet-shaped, negative-sense ssRNA virus (Rhabdoviridae). * **Diagnosis:** While Negri bodies are specific, they are only present in about 70-80% of cases. The **Direct Fluorescent Antibody (DFA)** test on brain tissue or skin biopsy (from the nape of the neck) is the current gold standard for diagnosis. * **Guarnieri bodies:** Intracytoplasmic inclusions seen in Variola (Smallpox) and Vaccinia.

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