Virology — MCQs

Virology Indian Medical PG Practice Questions and MCQs

Question 371: Which type of Human Immunodeficiency Virus (HIV) is considered more dangerous?

A. HIV-1 (Correct Answer)
B. HIV-2
C. Both are the same
D. It depends on host factors

Explanation: **Explanation:** **HIV-1** is considered more dangerous than HIV-2 due to its higher **virulence, infectivity, and rapid disease progression.** 1. **Why HIV-1 is the Correct Answer:** * **Viral Load & Transmission:** HIV-1 is associated with significantly higher plasma viral loads compared to HIV-2. This makes it more easily transmissible (both sexually and vertically). * **Disease Progression:** HIV-1 has a shorter incubation period. Without treatment, it leads to a rapid decline in CD4+ T-cell counts, progressing to AIDS much faster than HIV-2. * **Global Prevalence:** HIV-1 is the predominant strain worldwide (pandemic), whereas HIV-2 is largely restricted to West Africa. 2. **Why Other Options are Incorrect:** * **HIV-2:** While it also causes AIDS, it is characterized by a lower viral set point, slower clinical progression, and lower rates of transmission. Notably, HIV-2 is **intrinsically resistant** to Non-Nucleoside Reverse Transcriptase Inhibitors (NNRTIs) like Efavirenz. * **Both are the same:** This is incorrect as they differ genetically (only ~40-50% homology), epidemiologically, and in their clinical course. * **Host Factors:** While host immunity (e.g., CCR5-Δ32 mutation) influences the course of infection, the inherent pathogenic potential of HIV-1 is fundamentally higher than HIV-2. **High-Yield Clinical Pearls for NEET-PG:** * **Origin:** HIV-1 originated from Central African chimpanzees (*SIVcpz*); HIV-2 originated from West African Sooty Mangabeys (*SIVsm*). * **Diagnosis:** Screening is done via **ELISA** (4th Gen tests detect p24 antigen + antibodies). Differentiation between HIV-1 and HIV-2 is crucial for selecting ART regimens. * **Resistance:** HIV-2 is naturally resistant to **NNRTIs** and **Enfuvirtide**. * **Most Common Subtype:** HIV-1 **Group M, Subtype C** is the most common strain in India.

Question 372: What is the most common complication of mumps?

A. Orchitis and oophoritis (Correct Answer)
B. Encephalitis
C. Pneumonia
D. Myocarditis

Explanation: **Explanation:** Mumps is an acute viral infection caused by the **Rubulavirus** (Paramyxoviridae family), primarily characterized by the painful swelling of the parotid glands. **Why Orchitis and Oophoritis are correct:** Epididymo-orchitis is the **most common extra-salivary complication** of mumps in post-pubertal males, occurring in approximately 20-30% of cases. It is usually unilateral and can lead to testicular atrophy, though permanent sterility is rare. Oophoritis (inflammation of the ovaries) occurs in about 5% of post-pubertal females. The virus has a predilection for glandular tissue and the central nervous system. **Analysis of Incorrect Options:** * **B. Encephalitis:** While CNS involvement is common (often presenting as asymptomatic pleocytosis or viral meningitis), true encephalitis is a rare but severe complication (<1% of cases). * **C. Pneumonia:** Unlike other paramyxoviruses like Measles or RSV, mumps rarely involves the lower respiratory tract. * **D. Myocarditis:** This is an extremely rare complication of mumps, usually presenting with transient ECG changes rather than clinical heart failure. **High-Yield Clinical Pearls for NEET-PG:** * **Most common complication in children:** Aseptic meningitis. * **Most common cause of acute pancreatitis in children:** Mumps virus. * **Neurological sequelae:** Mumps is a classic cause of **sudden onset sensorineural deafness** (usually unilateral). * **Diagnosis:** Elevated **Serum Amylase** is a key biochemical marker due to parotid and pancreatic involvement. * **Prevention:** Live attenuated vaccine (Jeryl Lynn strain) as part of the MMR vaccine.

Question 373: A 29-year-old male is found to be HBsAg positive with highly increased SGOT levels but HBeAg negative. Which of the following is true about the patient's status?

A. Precore mutant (Correct Answer)
B. Core-promoter mutant
C. Wild type
D. Surface mutant

Explanation: ### **Explanation** The clinical presentation of an **HBsAg-positive** patient with **elevated transaminases (SGOT/SGPT)** but **negative HBeAg** is a classic indicator of a **Precore Mutant** of the Hepatitis B Virus (HBV). **1. Why Precore Mutant is Correct:** In the wild-type HBV, the *precore* region of the genome codes for the HBeAg (Hepatitis B e-antigen), which serves as a marker for active viral replication and high infectivity. In a **Precore Mutant**, a point mutation (most commonly a **G-to-A mutation at nucleotide 1896**) creates a premature stop codon. This prevents the synthesis of HBeAg. However, the virus continues to replicate actively, leading to liver damage (elevated SGOT/SGPT) and high HBV DNA levels, despite the absence of HBeAg. **2. Why the Other Options are Incorrect:** * **B. Core-promoter mutant:** While these also result in reduced HBeAg production, the classic NEET-PG scenario for "HBeAg negative but active disease" specifically points toward the precore stop codon mutation. * **C. Wild type:** In a wild-type infection with high viral replication and elevated enzymes, the patient would typically be **HBeAg positive**. * **D. Surface mutant:** These mutations occur in the *S gene* (e.g., the "a" determinant). This results in "diagnostic escape" where HBsAg may be undetectable by standard assays, but it does not primarily explain the absence of HBeAg during active hepatitis. ### **Clinical Pearls for NEET-PG:** * **The Mutation:** The most common precore mutation is **G1896A**. * **Serology:** HBsAg (+), Anti-HBe (+), HBeAg (-), but **HBV DNA is high**. * **Clinical Significance:** Precore mutants are associated with a higher risk of severe liver disease, fulminant hepatitis, and progression to cirrhosis compared to the wild type. * **Treatment:** These patients require treatment even though they are HBeAg negative because the liver enzymes are elevated, indicating active necroinflammation.

Question 374: Which of the following is NOT associated with Epstein-Barr virus (EBV)?

A. Infectious mononucleosis
B. Kaposi's sarcoma (Correct Answer)
C. Oral hairy leukoplakia
D. Non-Hodgkin lymphoma (NHL)

Explanation: **Explanation:** **1. Why Kaposi’s Sarcoma is the Correct Answer:** Kaposi’s sarcoma is caused by **Human Herpesvirus 8 (HHV-8)**, also known as Kaposi’s sarcoma-associated herpesvirus (KSHV). While both EBV and HHV-8 belong to the *Gammaherpesvirinae* subfamily and are oncogenic, they are distinct viruses. HHV-8 primarily infects endothelial cells, leading to the characteristic vascular tumors seen in HIV/AIDS patients. **2. Analysis of Incorrect Options (EBV-Associated Conditions):** * **Infectious Mononucleosis (IM):** EBV is the primary causative agent. It is characterized by the triad of fever, pharyngitis, and lymphadenopathy, with a positive Monospot test (heterophile antibodies). * **Oral Hairy Leukoplakia:** This is a non-malignant white lesion on the lateral aspect of the tongue, seen almost exclusively in immunocompromised (HIV) patients. It is caused by EBV replication in squamous epithelial cells. * **Non-Hodgkin Lymphoma (NHL):** EBV is strongly associated with several B-cell lymphomas, including **Burkitt lymphoma** (starry-sky appearance), **Diffuse Large B-cell Lymphoma (DLBCL)**, and Primary CNS lymphoma. **3. NEET-PG High-Yield Clinical Pearls:** * **EBV Receptor:** It binds to the **CD21** receptor (CR2) on B-cells and nasopharyngeal epithelial cells. * **Atypical Lymphocytes:** In IM, the "Downey cells" seen on peripheral smear are actually **activated T-cells (CD8+)** reacting against infected B-cells. * **Other EBV Associations:** Nasopharyngeal carcinoma, Hodgkin Lymphoma (Mixed cellularity subtype), and Duncan’s syndrome (X-linked lymphoproliferative disease). * **Diagnostic Tip:** If a patient with IM is mistakenly given **Ampicillin**, they often develop a characteristic maculopapular rash.

Question 375: Which of the following are features of Parvovirus infection?

A. Arthralgia
B. Pure red cell aplasia
C. Lymphadenopathy
D. All of the above (Correct Answer)

Explanation: **Explanation:** Parvovirus B19 is a small, non-enveloped DNA virus that specifically targets **erythroid progenitor cells** by binding to the **P-antigen** (globoside) on their surface. This tropism and the resulting immune response explain its diverse clinical manifestations. 1. **Arthralgia (Option A):** In adults (especially women), Parvovirus B19 often presents as acute, symmetrical polyarthritis involving small joints of the hands, wrists, and knees. This is an immune-complex mediated (Type III hypersensitivity) reaction. 2. **Pure Red Cell Aplasia (Option B):** Because the virus replicates in and destroys proerythroblasts, it causes a temporary cessation of erythropoiesis. While healthy individuals tolerate this, patients with high red cell turnover (e.g., Sickle Cell Anemia, Hereditary Spherocytosis) develop **Aplastic Crisis**. In immunocompromised patients, the inability to clear the virus leads to chronic **Pure Red Cell Aplasia**. 3. **Lymphadenopathy (Option C):** Though less common than the classic rash, lymphadenopathy is a recognized feature during the initial viremic phase of the infection as the body mounts a systemic immune response. Since all three features are associated with Parvovirus B19 infection, **Option D (All of the above)** is the correct answer. **High-Yield Clinical Pearls for NEET-PG:** * **Erythema Infectiosum (Fifth Disease):** Characterized by the classic **"Slapped Cheek"** appearance in children. * **Hydrops Fetalis:** If a pregnant woman is infected, the virus can cross the placenta, causing severe fetal anemia, high-output heart failure, and generalized edema. * **Diagnosis:** Detection of **IgM antibodies** (acute) or PCR for viral DNA (in immunocompromised/aplastic crisis). * **Receptor:** P-antigen (Globoside). Individuals lacking P-antigen are naturally resistant to infection.

Question 376: Which of the following is NOT an HIV gene?

A. HIV-1 gag gene (encodes structural proteins like p24 and matrix proteins)
B. HIV-1 pol gene (encodes reverse transcriptase, integrase, and protease)
C. HIV-1 env gene (encodes envelope glycoproteins like gp120 and gp41)
D. All of the above are HIV genes (Correct Answer)

Explanation: **Explanation:** The Human Immunodeficiency Virus (HIV) is a complex retrovirus containing three essential structural genes—**gag, pol, and env**—which are required for the viral life cycle and replication. 1. **gag (Group-specific Antigen):** This gene encodes the internal structural proteins. It is translated into a precursor protein (p55) which is later cleaved into the **capsid (p24)**, matrix (p17), and nucleocapsid (p7) proteins. 2. **pol (Polymerase):** This gene encodes the vital enzymes required for replication: **Reverse Transcriptase** (converts RNA to DNA), **Integrase** (incorporates viral DNA into the host genome), and **Protease** (cleaves precursor proteins into functional units). 3. **env (Envelope):** This gene encodes the precursor gp160, which is cleaved by host cell proteases into **gp120** (surface glycoprotein for attachment to CD4) and **gp41** (transmembrane protein for fusion). Since all three options (A, B, and C) represent the core structural genes of HIV, the correct answer is **D**. **Clinical Pearls for NEET-PG:** * **p24 Antigen:** This is the earliest serological marker of HIV infection (detected by ELISA) and is used to diagnose infection during the "window period." * **gp120:** Responsible for tropism; it binds to the **CD4 receptor** and co-receptors (CCR5 or CXCR4). * **Regulatory Genes:** Apart from these three, HIV has regulatory genes like **tat** (transactivation) and **rev**, and accessory genes like **nef, vif, vpu, and vpr**. * **Western Blot:** Traditionally used for confirmation, it detects antibodies against specific proteins: p24 (gag), p31/p66 (pol), and gp41/gp120/gp160 (env).

Question 377: What is the most predominant type of poliovirus?

A. Type I (Correct Answer)
B. Type II
C. Type III
D. Combined infection of II & III

Explanation: **Explanation:** Poliovirus is a member of the *Picornaviridae* family (genus Enterovirus) and exists in three distinct serotypes: 1, 2, and 3. **1. Why Type I is correct:** * **Type I (Brunhilde)** is the most common and predominant serotype globally. It is the most frequent cause of paralytic poliomyelitis and is responsible for the majority of epidemics. It is also the most difficult to eradicate and remains the only wild poliovirus (WPV) type still circulating (WPV1). **2. Why the other options are incorrect:** * **Type II (Lansing):** This type was the most antigenic and easiest to eradicate. The Global Commission for the Certification of Poliomyelitis Eradication declared Wild Poliovirus Type 2 eradicated in 2015. Most current Type 2 cases are vaccine-derived (VDPV). * **Type III (Leon):** This type is less common than Type I. It was officially declared eradicated worldwide in 2019. * **Combined infection:** While concurrent infections can occur, they do not represent the "predominant type" of the virus in epidemiological terms. **High-Yield NEET-PG Pearls:** * **Route of Transmission:** Fecal-oral (most common in developing countries) and droplet (in areas with high hygiene). * **Specimen of Choice:** Stool is the best sample for viral isolation (highest viral load). * **Vaccine Strains:** The Sabin vaccine (OPV) contains live attenuated strains. Type 2 was removed from the trivalent OPV to create the **bivalent OPV (Types 1 & 3)** to reduce the risk of Vaccine-Associated Paralytic Polio (VAPP). * **Immunity:** Infection with one type does not provide cross-immunity against the other two types.

Question 378: The 'owl eye' appearance of an infected cell is caused by which of the following viruses?

A. Variola virus
B. Rabies virus
C. Poliovirus
D. Cytomegalovirus (Correct Answer)

Explanation: **Explanation:** The correct answer is **Cytomegalovirus (CMV)**. The "owl’s eye" appearance is a classic histopathological hallmark of CMV infection. **1. Why Cytomegalovirus is correct:** CMV is a member of the *Betaherpesvirinae* subfamily. When it infects a cell, it causes significant enlargement of both the cell and its nucleus (cytomegaly). It produces a large, central, basophilic **intranuclear inclusion body** surrounded by a clear halo, extending toward the nuclear membrane. This specific morphology resembles the eye of an owl. **2. Why the other options are incorrect:** * **Variola virus (Smallpox):** Characterized by **Guarnieri bodies**, which are eosinophilic *intracytoplasmic* inclusion bodies. * **Rabies virus:** Characterized by **Negri bodies**, which are eosinophilic *intracytoplasmic* inclusions typically found in Purkinje cells of the cerebellum and pyramidal cells of the hippocampus. * **Poliovirus:** An Enterovirus that causes cell lysis but does not produce a characteristic "owl’s eye" inclusion. **3. High-Yield Clinical Pearls for NEET-PG:** * **Inclusion Type:** CMV produces both **intranuclear** (owl's eye) and **intracytoplasmic** inclusions. * **Congenital CMV:** The most common viral cause of congenital sensorineural hearing loss and mental retardation. Look for "periventricular calcifications" in clinical stems. * **Transplant/HIV Patients:** CMV is a major pathogen causing retinitis (pizza-pie appearance), esophagitis (linear ulcers), and pneumonia. * **Culture:** CMV is traditionally grown on **Human Fibroblast cell lines**, showing a "shell vial culture" positive for p72 antigen.

Question 379: Which of the following is false regarding poliomyelitis?

A. Descending paralysis
B. Bilateral symmetrical paralysis (Correct Answer)
C. Non-progressive paralysis
D. Lower motor neuron type paralysis

Explanation: Poliomyelitis is an acute viral infection caused by the Poliovirus (an Enterovirus), which selectively destroys the **anterior horn cells** of the spinal cord. ### **Why Option B is the Correct Answer (False Statement)** The hallmark of paralytic polio is **asymmetrical** paralysis. The virus affects motor neurons in a random, patchy distribution. Therefore, it typically presents as **unilateral** involvement or involvement of different muscle groups on both sides with varying degrees of severity. Symmetrical paralysis is more characteristic of conditions like Guillain-Barré Syndrome (GBS). ### **Analysis of Other Options** * **A. Descending paralysis:** This is a characteristic feature of polio. The paralysis often starts proximally (e.g., hip/shoulder) and moves distally (e.g., feet/hands). * **C. Non-progressive paralysis:** Once the acute febrile phase ends and the temperature returns to normal, the paralysis does not progress further. This is known as "morning paralysis." * **D. Lower motor neuron (LMN) type:** Since the virus destroys the anterior horn cells (the final common pathway for motor signals), it results in LMN signs: flaccid paralysis, loss of deep tendon reflexes (areflexia), and muscle atrophy. ### **High-Yield Clinical Pearls for NEET-PG** * **Most common presentation:** Inapparent/Asymptomatic infection (>90% of cases). * **Specimen of choice:** Stool (virus is excreted for weeks). * **Post-Polio Syndrome:** Occurs decades after recovery due to the gradual failure of overworked remaining motor neurons. * **Differential Diagnosis:** Unlike Polio, **GBS** presents with *ascending*, *symmetrical* paralysis and *sensory* involvement. * **Vaccines:** Salk (IPV - Killed) and Sabin (OPV - Live attenuated). Sabin can rarely cause VAPP (Vaccine-Associated Paralytic Polio).

Question 380: What is the relationship between viremia and the presence of rubella virus in the throat of infected persons, and the onset of the rash?

A. Viremia and rubella virus in the throat precede the rash by 5 to 7 days. (Correct Answer)
B. Viremia and rubella virus in the throat precede the rash by 1 to 2 days.
C. Viremia and rubella virus in the throat occur coincidentally with the rash.
D. Viremia and rubella virus in the throat occur 1 to 2 days after the rash.

Explanation: **Explanation:** The correct answer is **A**. Rubella (German Measles) follows a specific pathogenetic timeline. After initial replication in the respiratory epithelium and cervical lymph nodes, the virus enters the bloodstream (**viremia**) and spreads to various organs, including the skin. 1. **Why Option A is Correct:** The incubation period of Rubella is typically 14–21 days. Viremia and viral shedding in the throat (nasopharyngeal secretions) begin approximately **7 days before the onset of the rash**. This is a critical period because the patient is highly infectious *before* clinical symptoms appear. The rash itself is an immunologic response (antigen-antibody complexes) rather than a direct viral effect on the skin. 2. **Why Options B, C, and D are Incorrect:** These options underestimate the timeline of viral dissemination. By the time the rash appears (Option C), viremia is usually resolving because circulating antibodies are beginning to neutralize the virus. Viral shedding in the throat can persist for a few days after the rash starts, but it begins much earlier than 1–2 days prior (Option B) or after (Option D). **High-Yield Clinical Pearls for NEET-PG:** * **Infectivity Period:** Patients are most infectious from 7 days before to 7 days after the appearance of the rash. * **Forchheimer Spots:** Small, red petechiae on the soft palate seen during the prodromal phase (not pathognomonic). * **Lymphadenopathy:** Post-auricular and suboccipital lymphadenopathy is the most characteristic clinical feature, often preceding the rash. * **Congenital Rubella Syndrome (CRS):** The greatest risk to the fetus is when maternal viremia occurs during the first trimester (highest risk in the first 8 weeks).

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