Virology — MCQs

Virology Indian Medical PG Practice Questions and MCQs

Question 1101: Tzank smear is used for the diagnosis of which of the following?

A. Herpes Simplex Virus (HSV) (Correct Answer)
B. Psittacosis
C. Cryptococcus
D. Rickettsia

Explanation: **Explanation:** The **Tzanck smear** is a rapid bedside diagnostic test used primarily for the presumptive diagnosis of infections caused by the **Herpesviridae** family, specifically **Herpes Simplex Virus (HSV-1, HSV-2)** and **Varicella-Zoster Virus (VZV)**. **Why the correct answer is right:** The procedure involves scraping the base of a fresh vesicular lesion and staining it with Giemsa, Wright, or Leishman stain. The hallmark finding is the presence of **multinucleated giant cells** (formed by the fusion of infected keratinocytes) and **Acantholysis** (loss of intercellular connections). It may also show eosinophilic intranuclear inclusion bodies known as **Cowdry Type A bodies**. **Analysis of Incorrect Options:** * **B. Psittacosis:** Caused by *Chlamydia psittaci*. Diagnosis is typically made via serology (CFT) or PCR. Microscopic examination would show **LCL bodies** (Levinthal-Cole-Lillie), not Tzanck cells. * **C. Cryptococcus:** This is a fungus diagnosed using **India Ink** preparation (to see the capsule) or Mucicarmine stain. * **D. Rickettsia:** These are obligate intracellular bacteria diagnosed via the **Weil-Felix reaction** (serology) or Gimenez stain. **High-Yield Clinical Pearls for NEET-PG:** * **Limitation:** Tzanck smear **cannot distinguish** between HSV-1, HSV-2, and VZV. For definitive differentiation, viral culture or PCR is required. * **Other uses:** Apart from Herpes, Tzanck smear is used in dermatology to diagnose **Pemphigus Vulgaris** (shows Tzanck cells/acantholytic cells) and **Cytomegalovirus (CMV)**. * **Don't confuse:** Cowdry Type A (Herpes) vs. Cowdry Type B (Polio/Adenovirus).

Question 1102: Human papilloma virus is a:

A. RNA virus
B. DNA virus (Correct Answer)
C. Both
D. None

Explanation: **Explanation:** **Human Papillomavirus (HPV)** is a member of the **Papillomaviridae** family. It is characterized as a small, non-enveloped virus containing a **double-stranded, circular DNA genome**. 1. **Why Option B is Correct:** HPV belongs to the group of DNA viruses. Its replication occurs within the nucleus of host squamous epithelial cells (keratinocytes). The viral DNA integrates into the host genome in malignant lesions, particularly through the expression of oncoproteins **E6 and E7**, which inhibit tumor suppressor proteins p53 and pRb, respectively. 2. **Why Other Options are Incorrect:** * **Option A:** HPV does not possess an RNA genome. Common RNA viruses include HIV, Hepatitis C, and Influenza. * **Option C & D:** Viruses are strictly classified by their primary nucleic acid type (either DNA or RNA); they do not contain both as their primary genetic material. **High-Yield Clinical Pearls for NEET-PG:** * **Morphology:** Icosahedral symmetry, non-enveloped (ether resistant). * **Oncogenic Strains:** Types **16 and 18** are high-risk and most commonly associated with **Cervical Cancer**, oropharyngeal cancer, and anal cancer. * **Benign Strains:** Types **6 and 11** cause **Condyloma acuminatum** (genital warts) and laryngeal papillomatosis. * **Diagnosis:** Characterized by **Koilocytes** (cells with perinuclear halo and wrinkled nuclei) on a Pap smear. * **Vaccination:** The Quadrivalent vaccine (Gardasil) targets types 6, 11, 16, and 18.

Question 1103: What is true about prions?

A. Are virus-coded
B. Cause misfolding of protein (Correct Answer)
C. Cleave protein
D. Are defective in protein synthesis

Explanation: **Explanation:** Prions (Proteinaceous Infectious Particles) are unique pathogens because they lack nucleic acids (DNA or RNA). The fundamental mechanism of prion disease is the **conformational change** of a normal host protein into a pathological isoform. 1. **Why the correct answer is right:** The normal cellular prion protein (**PrPc**), which is rich in alpha-helices, undergoes a post-translational conformational change to become the infectious **PrPsc** (scrapie form), which is rich in **beta-pleated sheets**. This PrPsc acts as a template, inducing other normal PrPc molecules to misfold. These misfolded proteins are resistant to proteases, leading to their accumulation in the brain, resulting in neuronal death and the characteristic "spongiform" appearance. 2. **Why the incorrect options are wrong:** * **A. Are virus-coded:** Prions are not viruses. They are encoded by the host's own genome (specifically the *PRNP* gene on chromosome 20). * **C. Cleave protein:** Prions do not possess enzymatic or proteolytic activity; they cause structural rearrangement through protein-protein interaction. * **D. Are defective in protein synthesis:** Prion diseases are disorders of **protein folding**, not protein synthesis (translation). **High-Yield Clinical Pearls for NEET-PG:** * **Resistance:** Prions are highly resistant to standard sterilization methods (autoclaving, UV light, and boiling). They are inactivated by **1N NaOH for 1 hour** or **porous load autoclaving at 134°C**. * **Human Diseases:** Kuru (associated with cannibalism), Creutzfeldt-Jakob Disease (CJD), and Fatal Familial Insomnia. * **Histology:** Characterized by spongiform degeneration, neuronal loss, and astrocytosis **without** an inflammatory response (no pleocytosis in CSF).

Question 1104: What is the primary reservoir of Herpes Simplex Virus (HSV)?

A. Humans (Correct Answer)
B. Monkeys
C. Both humans and monkeys
D. Neither humans nor monkeys

Explanation: **Explanation:** **1. Why Humans are the Correct Answer:** Herpes Simplex Virus (HSV-1 and HSV-2) is an obligate human pathogen. **Humans are the only natural reservoir** for these viruses. The virus maintains itself in the human population through a cycle of primary infection, latency in sensory nerve ganglia (Trigeminal for HSV-1, Sacral for HSV-2), and periodic reactivation (shedding). Because there is no animal reservoir or environmental source, transmission occurs exclusively through direct contact with infected secretions or mucosal surfaces. **2. Why Other Options are Incorrect:** * **B & C (Monkeys):** While some herpesviruses are zoonotic (e.g., *B virus* or *Herpesvirus simiae* from Macaque monkeys can cause fatal encephalitis in humans), HSV-1 and HSV-2 do not naturally circulate in monkeys or other animals. * **D (Neither):** This is incorrect as the virus requires a biological host to survive and replicate; it cannot persist indefinitely in the environment. **3. NEET-PG High-Yield Clinical Pearls:** * **Site of Latency:** HSV-1 typically remains latent in the **Trigeminal ganglion**, while HSV-2 remains latent in the **Sacral ganglia (S2-S3)**. * **Gold Standard Diagnosis:** While PCR is the most sensitive test (especially for CNS infections), the **Tzanck Smear** is a classic exam favorite showing **multinucleated giant cells** with **Cowdry Type A** intranuclear inclusion bodies. * **Encephalitis:** HSV-1 is the most common cause of sporadic fatal viral encephalitis, typically involving the **temporal lobes**. * **Neonatal Herpes:** Usually caused by HSV-2 acquired during passage through the birth canal.

Question 1105: Which viral infection is NOT transmitted by blood transfusion?

A. Parvovirus B-19
B. Dengue virus (Correct Answer)
C. Cytomegalovirus
D. Hepatitis G virus

Explanation: **Explanation:** The correct answer is **Dengue virus**. While many viruses can cause viremia, the standard criteria for a virus to be considered "transmissible by blood transfusion" (TTIs) include a prolonged asymptomatic viremic phase and stability in stored blood components. 1. **Why Dengue is the correct answer:** Dengue virus is primarily an **Arbovirus** transmitted via the bite of the *Aedes aegypti* mosquito. While rare case reports of transfusion-transmitted Dengue exist during massive outbreaks, it is **not** classified as a standard transfusion-transmitted infection (TTI) because the viremic phase is very short-lived and typically coincides with high fever (symptomatic), meaning infected donors are usually deferred during screening. 2. **Analysis of incorrect options:** * **Parvovirus B-19:** This is a small, non-enveloped DNA virus that is highly resistant to inactivation. It causes significant viremia and is a well-known risk in blood transfusions, particularly for patients with hemolytic anemias (risk of aplastic crisis). * **Cytomegalovirus (CMV):** CMV remains latent within **leukocytes** (monocytes and neutrophils). It is a major TTI, which is why "leukoreduction" of blood bags is practiced to prevent CMV transmission to immunocompromised recipients. * **Hepatitis G virus (HGV/GBV-C):** HGV is a blood-borne Flavivirus. Although its clinical pathogenicity is low, it is frequently transmitted via blood products and co-infects patients with HIV or HCV. **High-Yield Clinical Pearls for NEET-PG:** * **Most common TTI globally:** Hepatitis B Virus (HBV). * **Window period:** The time between infection and detection. Nucleic Acid Testing (NAT) has significantly reduced this for HIV, HBV, and HCV. * **Bacterial contamination:** More common in **Platelets** (stored at room temperature) than RBCs (stored at 4°C). *Yersinia enterocolitica* is the most common contaminant of refrigerated RBCs.

Question 1106: What is the most common cause of death in Epstein-Barr virus (EBV) infection?

A. Splenic abscess
B. Meningo-encephalitis (Correct Answer)
C. Fulminant hepatitis
D. Auto-immune hemolytic anemia

Explanation: **Explanation:** Epstein-Barr Virus (EBV), the primary cause of Infectious Mononucleosis (IM), is generally a self-limiting condition. However, when fatalities occur, they are most frequently attributed to neurological complications. **1. Why Meningo-encephalitis is correct:** Neurological complications occur in approximately 1–5% of patients with IM. Among these, **meningo-encephalitis** and Guillain-Barré syndrome are the most severe. Encephalitis leads to cerebral edema and increased intracranial pressure, making it the leading cause of EBV-related mortality. **2. Analysis of Incorrect Options:** * **Splenic Abscess:** While **Splenic Rupture** is a classic, high-yield complication of EBV (occurring in 0.1% of cases), splenic *abscess* is not a characteristic feature. Rupture is the second most common cause of death, but it is less frequent than neurological fatalities. * **Fulminant Hepatitis:** EBV commonly causes a mild, transient elevation of liver enzymes (transaminitis). While jaundice may occur, progression to fulminant hepatic failure is extremely rare in immunocompetent hosts. * **Auto-immune Hemolytic Anemia (AIHA):** EBV is associated with "Cold Agglutinin Disease" (IgM antibodies against i-antigen on RBCs). While this causes transient hemolysis in about 2% of cases, it is rarely fatal. **Clinical Pearls for NEET-PG:** * **Triad of IM:** Fever, Pharyngitis, and Lymphadenopathy (typically posterior cervical). * **Diagnostic Hallmark:** Atypical lymphocytes (Downey cells) on peripheral smear (CD8+ T-cells). * **The "Ampicillin Rash":** Administration of Ampicillin or Amoxicillin in a patient with EBV leads to a characteristic maculopapular rash. * **Cancers associated with EBV:** Burkitt Lymphoma, Nasopharyngeal Carcinoma, and Hodgkin Lymphoma (Mixed cellularity type).

Question 1107: Which of the following statements is true about interferons?

A. Host protein (Correct Answer)
B. Viral protein
C. Inactivated by nuclease
D. Virus specific

Explanation: **Explanation:** Interferons (IFNs) are low-molecular-weight **host-encoded proteins** (specifically glycoproteins) produced by cells in response to viral infections or other stimuli. They are a critical component of the innate immune system. * **Why Option A is Correct:** Interferons are synthesized by the host cell's ribosomes using host genetic templates. When a cell is infected by a virus, it produces IFNs to signal neighboring cells to enter an "antiviral state." * **Why Option B is Incorrect:** They are not encoded by the viral genome. They are the host's defensive response to the presence of viral double-stranded RNA or other pathogen-associated molecular patterns (PAMPs). * **Why Option C is Incorrect:** Interferons are proteins, not nucleic acids. Therefore, they are **resistant to nucleases** (RNase and DNase) but are inactivated by proteolytic enzymes (proteases). * **Why Option D is Incorrect:** Interferons are **species-specific but NOT virus-specific**. This means human interferon will work against many different types of viruses (Influenza, Hepatitis, etc.) in human cells, but human interferon will not be effective in mouse cells. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** IFNs do not act directly on the virus. They induce the synthesis of host enzymes like **2',5'-oligoadenylate synthetase** and **protein kinase R (PKR)**, which inhibit viral protein synthesis and degrade viral mRNA. * **Classification:** * **Type I (IFN-α, IFN-β):** Produced by leucocytes and fibroblasts; primarily antiviral. * **Type II (IFN-γ):** Produced by T-cells and NK cells; primarily immunomodulatory (activates macrophages). * **Clinical Use:** Recombinant IFNs are used in treating Hepatitis B, Hepatitis C, Kaposi Sarcoma, and Multiple Sclerosis (IFN-β).

Question 1108: Progressive multifocal leukoencephalopathy is caused by which virus?

A. Epstein-Barr virus
B. Varicella-zoster virus
C. Cytomegalovirus
D. JC polyomavirus (Correct Answer)

Explanation: **Explanation:** **Progressive Multifocal Leukoencephalopathy (PML)** is a rare, demyelinating disease of the Central Nervous System (CNS) caused by the **JC virus (JCV)**, a member of the *Polyomaviridae* family. The virus typically causes a latent infection in the kidneys and lymphoid tissues of healthy individuals. However, in states of severe **immunosuppression** (most commonly AIDS, but also in patients on monoclonal antibodies like Natalizumab), the virus reactivates. It crosses the blood-brain barrier and infects **oligodendrocytes**, the cells responsible for producing myelin in the CNS. This leads to widespread demyelination, presenting clinically with rapidly progressive focal neurological deficits, cognitive decline, and visual disturbances. **Analysis of Incorrect Options:** * **A. Epstein-Barr virus (EBV):** Primarily associated with infectious mononucleosis, Burkitt lymphoma, and Primary CNS Lymphoma in HIV patients, but not demyelinating disease. * **B. Varicella-zoster virus (VZV):** Causes chickenpox and shingles. Neurological complications include encephalitis or vasculopathy, but not PML. * **C. Cytomegalovirus (CMV):** In immunocompromised patients, it typically causes retinitis, esophagitis, or CMV encephalitis (characterized by periventricular calcifications), not multifocal demyelination. **High-Yield Clinical Pearls for NEET-PG:** * **MRI Findings:** PML shows multiple, non-enhancing, subcortical white matter lesions without mass effect (classically in the parieto-occipital region). * **Histopathology:** Look for the triad of **demyelination**, **giant atypical astrocytes**, and **oligodendrocyte nuclei with "ground-glass" viral inclusions**. * **Diagnosis:** Gold standard is PCR for JC virus DNA in the Cerebrospinal Fluid (CSF). * **Mnemonic:** **J**unction **C**onnection (JC virus) destroys the "connections" (myelin) in the brain.

Question 1109: Which of the following is true regarding Parvovirus infection?

A. Erythroid progenitors are affected (Correct Answer)
B. Myeloid precursors are affected
C. Individuals with P antigen are resistant to infection
D. The majority of infections are chronic

Explanation: **Explanation:** **Parvovirus B19** is a small, non-enveloped single-stranded DNA virus with a specific tropism for rapidly dividing cells, particularly the **erythroid progenitor cells** in the bone marrow. 1. **Why Option A is Correct:** Parvovirus B19 targets the **P antigen** (globoside) on the surface of erythroid precursor cells (proerythroblasts and normoblasts). Once inside, the virus replicates and causes cell lysis, leading to a temporary cessation of red blood cell production. In healthy individuals, this is clinically insignificant, but in patients with high RBC turnover (e.g., Sickle Cell Anemia), it can trigger an **Aplastic Crisis**. 2. **Why Other Options are Incorrect:** * **Option B:** The virus specifically targets the erythroid lineage; it does **not** typically affect myeloid (white blood cell) precursors. * **Option C:** The **P antigen** is the essential cellular receptor for the virus. Therefore, individuals who lack the P antigen (the rare $p$ phenotype) are actually **resistant** to Parvovirus B19 infection, not susceptible. * **Option D:** The majority of Parvovirus B19 infections are **acute and self-limiting**. Chronic infections are rare and typically occur only in severely immunocompromised individuals who cannot mount an antibody response. **High-Yield Clinical Pearls for NEET-PG:** * **Erythema Infectiosum (Fifth Disease):** Characterized by the classic **"Slapped Cheek" appearance** and a lace-like reticular rash on the trunk. * **Hydrops Fetalis:** If a pregnant woman is infected, the virus can cross the placenta, attack fetal erythroid cells, and cause severe fetal anemia and high-output heart failure. * **Arthropathy:** Common in adults, presenting as symmetrical small joint arthritis (mimicking Rheumatoid Arthritis). * **Diagnosis:** Detection of **IgM antibodies** (acute) or PCR for viral DNA. On bone marrow biopsy, look for **Giant Pronormoblasts** with intranuclear inclusions.

Question 1110: The presence of Negri inclusion bodies in host cells is characteristic of which viral infection?

A. Mumps
B. Infectious mononucleosis
C. Rabies (Correct Answer)
D. Congenital rubella

Explanation: **Explanation:** The correct answer is **Rabies**. Negri bodies are the pathognomonic histopathological hallmark of Rabies virus infection. **1. Why Rabies is Correct:** Negri bodies are **intracytoplasmic, eosinophilic, round-to-oval inclusion bodies** found in the cytoplasm of neurons. They represent sites of viral replication (nucleocapsid accumulation). They are most commonly found in the **Purkinje cells of the cerebellum** and the **pyramidal cells of the hippocampus (Ammon’s horn)**. Their presence is 100% specific for a Rabies diagnosis, though they are absent in about 20% of cases. **2. Why Other Options are Incorrect:** * **Mumps:** Characterized by parotitis and orchitis; it does not produce Negri bodies. * **Infectious Mononucleosis (EBV):** Characterized by **Atypical lymphocytes (Downey cells)** in the peripheral blood smear, not intracellular inclusion bodies. * **Congenital Rubella:** Associated with the "classic triad" (cataracts, sensorineural deafness, and PDA) and "blueberry muffin" spots, but lacks specific diagnostic inclusion bodies like Negri bodies. **3. NEET-PG High-Yield Pearls:** * **Stain used:** Sellers’ stain (basic fuchsin and methylene blue) is traditionally used to visualize Negri bodies. * **Viral Structure:** Rabies is a Rhabdovirus, characterized by a **bullet-shaped** morphology and a negative-sense ssRNA genome. * **Other Inclusion Bodies for Comparison:** * **Guarnieri bodies:** Smallpox (intracytoplasmic). * **Cowdry Type A:** Herpes Simplex and Varicella Zoster (intranuclear). * **Owl’s Eye appearance:** Cytomegalovirus (intranuclear). * **Henderson-Peterson bodies:** Molluscum contagiosum (intracytoplasmic).

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