Virology Practice Questions

Q: Subacute sclerosing panencephalitis (SSPE) is not diagnosed by which of the following?

Electroencephalogram (EEG). **Explanation:** Subacute Sclerosing Panencephalitis (SSPE) is a progressive, fatal neurodegenerative disease caused by a persistent infection with a mutant strain of the **Measles virus**. The diagnosis relies on demonstrating high titers of measles antibodies and viral presence in the CNS. **Why Option A is the Correct Answer:** While an **Electroencephalogram (EEG)** is a vital supportive tool in the clinical workup of SSPE—characteristically showing **periodic, high-voltage slow-wave complexes** (Radermecker complexes)—it is **not diagnostic** on its own. EEG findings are suggestive but non-specific, as similar patterns can occur in other encephalopathies. Definitive diagnosis requires microbiological or pathological evidence of the virus. **Analysis of Incorrect Options:** * **Option B & C:** A hallmark of SSPE is the presence of **intrathecal synthesis** of measles antibodies. Diagnosis requires demonstrating high titers of anti-measles IgG in both the **blood (serum)** and **CSF**. A CSF-to-serum antibody ratio is often used to confirm the diagnosis. * **Option D:** Demonstration of **Measles virus antigen** or viral RNA in brain tissue via biopsy (or autopsy) using immunohistochemistry or PCR is a definitive diagnostic method. Histology typically shows **Cowdry type A inclusion bodies**. **High-Yield Clinical Pearls for NEET-PG:** * **Latency:** SSPE typically occurs 5–10 years after an initial measles infection. * **Pathogenesis:** Caused by a "defective" measles virus (mutations in the **M (Matrix) protein** prevent normal viral budding). * **CSF Findings:** Raised gamma globulins (oligoclonal bands) but **normal** glucose and cell count. * **Clinical Stages:** Characterized by behavioral changes, followed by **myoclonic jerks**, and eventually dementia/coma.

Q: Which of the following is a true finding regarding Hepatitis C virus?

Antibody to HCV may not be detected in the acute stage. **Explanation:** **Hepatitis C Virus (HCV)**, a member of the *Flaviviridae* family, is characterized by a significant "window period." In the acute stage of infection, anti-HCV antibodies may take **6 to 12 weeks** (or longer) to develop. Therefore, a patient may be viremic and symptomatic while testing negative for antibodies. The definitive diagnosis during this early phase is made by detecting **HCV RNA** using PCR. **Analysis of Options:** * **Option A (Incorrect):** HCV is primarily transmitted via **parenteral routes** (blood transfusions, IV drug use). Hepatitis A and E are the primary viruses spread via the fecal-oral route. * **Option C (Incorrect):** HCV is notorious for its high chronicity rate. Approximately **75%–85%** of infected individuals develop chronic hepatitis, which can lead to cirrhosis and hepatocellular carcinoma (HCC). * **Option D (Incorrect):** While historically difficult to grow, HCV **can be cultured** in vitro using specific cell lines (e.g., Huh7 human hepatoma cells). This was a breakthrough that allowed for the development of Direct-Acting Antivirals (DAAs). **High-Yield Clinical Pearls for NEET-PG:** * **Most common cause** of post-transfusion hepatitis (historically). * **HCV RNA** is the first marker to appear (as early as 1–2 weeks post-exposure). * **Genotype 3** is the most common genotype found in India. * Unlike Hepatitis B, there is **no vaccine** available for HCV due to the high antigenic variation in its E2 envelope glycoprotein (hypervariable regions).

Q: Trachoma is caused by which serotype of Chlamydia trachomatis?

A, B, C. **Explanation:** *Chlamydia trachomatis* is an obligate intracellular bacterium classified into several serovars (serotypes) based on differences in its major outer membrane protein (MOMP). These serovars exhibit distinct tissue tropisms and clinical manifestations: 1. **Serotypes A, B, Ba, and C (Correct Answer):** These are the causative agents of **Endemic Trachoma**, a chronic keratoconjunctivitis. It is the leading infectious cause of preventable blindness worldwide. Transmission occurs via eye-to-eye contact, fomites, or eye-seeking flies (*Musca sorbens*). 2. **Serotypes D to K (Incorrect):** These serotypes primarily infect the urogenital tract. They cause **Inclusion Conjunctivitis** (in neonates and adults), non-gonococcal urethritis (NGU), cervicitis, and pelvic inflammatory disease (PID). Unlike Trachoma, these are sexually transmitted. 3. **Serotypes L1, L2, and L3 (Incorrect):** These are more invasive strains that cause **Lymphogranuloma Venereum (LGV)**, a systemic sexually transmitted infection characterized by genital ulcers and painful inguinal lymphadenopathy (Buboes). **High-Yield Clinical Pearls for NEET-PG:** * **SAFE Strategy for Trachoma:** **S**urgery (for trichiasis), **A**ntibiotics (Azithromycin), **F**acial cleanliness, and **E**nvironmental improvement. * **Diagnosis:** Giemsa stain shows **Halberstaedter-Prowazek (HP) inclusion bodies** (intracytoplasmic) near the nucleus. * **Drug of Choice:** Oral **Azithromycin** (single dose) is the preferred treatment for Trachoma control programs. * **Morphology:** Chlamydia exists in two forms: the **Elementary Body** (infectious, extracellular) and the **Reticulate Body** (reproductive, intracellular).

Q: What is true about prions?

Associated with misfolding of protein. **Explanation:** Prions (Proteinaceous Infectious Particles) are unique pathogens that lack nucleic acids (DNA/RNA). The fundamental mechanism of prion disease involves the **misfolding of a normal host protein**, known as PrPc (cellular prion protein), into an abnormal, protease-resistant isoform called **PrPsc** (scrapie prion protein). This misfolded protein acts as a template, inducing other normal proteins to misfold, leading to neurodegeneration. **Analysis of Options:** * **A. Encoded by viral genome:** Incorrect. Prions are not viruses; they are encoded by the host's own **PRNP gene** located on chromosome 20. * **C. Non-infectious:** Incorrect. Prions are highly infectious and can be transmitted via contaminated neurosurgical instruments, corneal transplants, or ingestion of infected tissue (e.g., Kuru). * **D. Immunogenic:** Incorrect. Because prions are derived from host proteins, the immune system does not recognize them as foreign. Therefore, they **do not elicit an inflammatory or immune response** (no fever, no antibody production). **High-Yield Clinical Pearls for NEET-PG:** * **Resistance:** Prions are notoriously resistant to standard sterilization methods (autoclaving, UV light, and formalin). They require specific protocols like **1N NaOH for 1 hour** or gravity displacement autoclaving at **134°C**. * **Histopathology:** Characterized by **spongiform degeneration** (vacuolation of neurons), neuronal loss, and amyloid plaques without inflammation. * **Key Diseases:** Creutzfeldt-Jakob Disease (CJD), Kuru, Fatal Familial Insomnia (FFI) in humans; Bovine Spongiform Encephalopathy (Mad Cow Disease) in cattle. * **Diagnosis:** Detection of **14-3-3 protein** in CSF is a significant diagnostic marker.

Q: An HIV-infected patient presents with oral lesions. What is the most likely causative organism?

Candida. **Explanation:** **Why Candida is the correct answer:** Oropharyngeal Candidiasis (Oral Thrush) is the **most common opportunistic infection** in HIV-infected individuals. It typically occurs when the CD4 count falls below **200-500 cells/mm³**. Clinically, it presents as creamy white, curd-like patches on the tongue or buccal mucosa that can be scraped off, leaving an erythematous base. It is often the first clinical sign of HIV progression. **Analysis of Incorrect Options:** * **A. Epstein-Barr virus (EBV):** While EBV causes **Oral Hairy Leukoplakia** in HIV patients (white, corrugated lesions on the lateral borders of the tongue), it is less common than Candidiasis. Crucially, these lesions *cannot* be scraped off. * **C. Cytomegalovirus (CMV):** CMV typically causes painful, deep **oral ulcers** or esophagitis in severely immunocompromised patients (CD4 < 50 cells/mm³), but it is not the most frequent cause of oral lesions. * **D. Pneumocystis carinii (jirovecii):** This is the most common opportunistic *respiratory* infection (Pneumonia) in HIV patients. While it can rarely present extrapulmonary, it is not a primary cause of oral lesions. **High-Yield Clinical Pearls for NEET-PG:** * **Most common oral manifestation of HIV:** Candidiasis. * **Treatment of choice:** Topical Nystatin or Clotrimazole for mild cases; Oral Fluconazole for moderate to severe cases. * **Oral Hairy Leukoplakia (EBV):** A key diagnostic marker for HIV progression; does not require specific treatment unless symptomatic. * **Kaposi Sarcoma (HHV-8):** Presents as painless, purple/red nodules on the hard palate; it is the most common oral malignancy in HIV.

Q: Which is the longest DNA segment of the hepatitis B virus genome?

P gene. **Explanation:** The Hepatitis B Virus (HBV) is a unique, partially double-stranded circular DNA virus (Hepadnaviridae). Its compact genome consists of approximately 3,200 nucleotides and contains four overlapping open reading frames (ORFs). **1. Why P gene is correct:** The **P gene** is the largest ORF, encompassing nearly **80% of the entire HBV genome**. It encodes the viral **DNA polymerase**, a multifunctional enzyme that possesses reverse transcriptase, DNA-dependent DNA polymerase, and RNase H activities. It is essential for viral replication and is the primary target for antiviral drugs like Tenofovir and Entecavir. **2. Why other options are incorrect:** * **S gene:** Encodes the surface proteins (HBsAg). While clinically significant for diagnosis, it is much shorter than the P gene. * **C gene:** Encodes the core protein (HBcAg) and the precore protein (HBeAg). It is significantly smaller than the P gene. * **X gene:** This is the **smallest ORF** in the HBV genome. It encodes the HBx protein, which acts as a transcriptional transactivator and is implicated in the development of hepatocellular carcinoma (HCC). **High-Yield Clinical Pearls for NEET-PG:** * **Genome Structure:** HBV has a "relaxed circular DNA" (rcDNA) which is converted into **cccDNA** (covalently closed circular DNA) in the host nucleus—the template for all viral transcripts. * **Replication:** HBV is the only DNA virus that replicates via an **RNA intermediate** using reverse transcriptase. * **Dane Particle:** The complete infectious virion is a 42 nm spherical particle. * **Smallest Gene:** X gene (associated with oncogenesis). * **Largest Gene:** P gene (encodes Polymerase).

Q: All of the following are true about HIV infection except?

Increased release of acid labile interferon. **Explanation:** The correct answer is **C (Increased release of acid-labile interferon)** because HIV infection is actually associated with the production of **acid-labile Interferon-alpha (IFN-α)**, not its increased release as a protective mechanism. In HIV patients, the presence of acid-labile IFN-α is a marker of disease progression and is often found in the serum of those with AIDS or symptomatic HIV, rather than being a standard physiological response to the virus. **Analysis of Options:** * **Option A (Enveloped RNA virus):** This is **true**. HIV is a member of the *Lentivirus* genus within the *Retroviridae* family. It possesses a lipid envelope derived from the host cell membrane and contains two copies of single-stranded positive-sense RNA. * **Option B (Rate of killing vs. T4 molecules):** This is **true**. The HIV gp120 envelope glycoprotein binds specifically to the **CD4 (T4) molecule**. Cells with higher densities of CD4 receptors on their surface are more susceptible to viral entry and subsequent cytopathic destruction. * **Option D (Decreased delayed hypersensitivity):** This is **true**. HIV causes a profound depletion of CD4+ T cells, leading to a defect in cell-mediated immunity. This results in **anergy**, manifested as a decreased or absent delayed-type hypersensitivity (DTH) skin test response (e.g., to Tuberculin). **High-Yield Clinical Pearls for NEET-PG:** * **Primary Receptor:** CD4 molecule. * **Co-receptors:** **CCR5** (macrophages/early infection) and **CXCR4** (T-cells/late infection). Individuals with a homozygous **CCR5-Δ32 mutation** are resistant to HIV-1 infection. * **Hallmark Immunological Defect:** Inversion of the CD4:CD8 ratio (normal is ~2:1; in AIDS it is <1:1). * **Acid-labile IFN-α:** Its presence in HIV is unusual because IFN-α is typically acid-stable; its appearance in HIV/SLE is a specific diagnostic nuance.

Q: Owl eye inclusion bodies are seen in which of the following viral infections?

Cytomegalovirus (CMV). **Explanation:** The correct answer is **Cytomegalovirus (CMV)**. **1. Why CMV is correct:** Cytomegalovirus belongs to the Beta-herpesvirinae subfamily. It is characterized by causing massive cell enlargement (cytomegaly). The hallmark histopathological finding is the presence of **large, eosinophilic intranuclear inclusion bodies** surrounded by a clear halo, which gives the nucleus an **"Owl’s Eye" appearance**. These inclusions represent sites of viral replication. CMV can also produce smaller, basophilic cytoplasmic inclusions. **2. Why the other options are incorrect:** * **Herpes Simplex Virus (HSV):** HSV produces **Cowdry Type A** inclusion bodies (eosinophilic intranuclear bodies) and multinucleated giant cells (seen on Tzanck smear), but they do not typically exhibit the "Owl’s Eye" morphology. * **Epstein-Barr Virus (EBV):** EBV is associated with atypical lymphocytes (Downey cells) in the peripheral blood, but it does not typically produce characteristic inclusion bodies in tissue sections. * **Hepatitis B Virus (HBV):** Chronic HBV infection is characterized by **"Ground-glass hepatocytes,"** which result from the accumulation of HBsAg in the endoplasmic reticulum, not "Owl's Eye" inclusions. **3. NEET-PG High-Yield Pearls:** * **"Owl’s Eye" Nucleus (Histology):** Also seen in **Reed-Sternberg cells** (Hodgkin Lymphoma), but in virology, it specifically refers to CMV. * **CMV Diagnosis:** In immunocompromised patients (HIV/Transplant), CMV causes retinitis, esophagitis, and pneumonia. * **Congenital CMV:** The most common viral cause of congenital sensorineural hearing loss and mental retardation; look for periventricular calcifications. * **Ganciclovir** is the drug of choice for CMV infections.

Q: Which of the following conditions is caused by HHV-8?

Kaposi sarcoma. **Explanation:** **Human Herpesvirus 8 (HHV-8)**, also known as **Kaposi Sarcoma-associated Herpesvirus (KSHV)**, is a gamma-herpesvirus that primarily infects vascular endothelial cells. It carries oncogenes (like viral cyclin and v-FLIP) that promote cell proliferation and inhibit apoptosis. In immunocompromised states, particularly HIV/AIDS, HHV-8 leads to the development of **Kaposi Sarcoma**, a multicentric vascular tumor characterized by spindle cells and slit-like neovascular spaces. **Analysis of Incorrect Options:** * **A & B (Burkitt's Lymphoma & Nasopharyngeal Carcinoma):** Both are strongly associated with **Epstein-Barr Virus (EBV)**, also known as HHV-4. EBV is a gamma-herpesvirus that infects B-cells and epithelial cells. * **D (Hepatic Carcinoma):** Hepatocellular carcinoma is primarily linked to chronic infections with **Hepatitis B Virus (HBV)** and **Hepatitis C Virus (HCV)**, as well as aflatoxin exposure. **High-Yield Clinical Pearls for NEET-PG:** * **HHV-8 Spectrum:** Besides Kaposi Sarcoma, HHV-8 is also the causative agent of **Primary Effusion Lymphoma (PEL)** and **Multicentric Castleman Disease**. * **Transmission:** HHV-8 is most commonly transmitted through saliva and sexual contact. * **Histopathology:** Look for "spindle-shaped cells" and "extravasated RBCs" in biopsy descriptions of Kaposi Sarcoma. * **Classification:** Remember the "Rule of 8"—HHV-8 causes Kaposi Sarcoma (the 8th virus causes the sarcoma starting with 'K', the 11th letter, but often associated with AIDS/Advanced stages).

Q: Progressive multifocal leukoencephalopathy is due to which of the following viruses?

JC virus. ### Explanation **Correct Answer: A. JC virus** **1. Why JC Virus is Correct:** Progressive Multifocal Leukoencephalopathy (PML) is a demyelinating disease of the Central Nervous System caused by the **JC virus** (John Cunningham virus). It is a member of the *Polyomaviridae* family. The virus infects and destroys **oligodendrocytes** (the cells responsible for producing myelin in the CNS), leading to multifocal areas of demyelination. PML occurs almost exclusively in **immunocompromised individuals**, particularly those with HIV/AIDS (CD4 count <200 cells/mm³), hematological malignancies, or those on monoclonal antibodies like Natalizumab. **2. Why Other Options are Incorrect:** * **B. Papova virus:** This is an obsolete taxonomic name. Previously, *Papovaviridae* included Papillomaviruses and Polyomaviruses. While JC virus was once under this umbrella, "JC virus" is the specific etiologic agent required for this question. * **C. Measles:** Measles virus is associated with **Subacute Sclerosing Panencephalitis (SSPE)**, a late-onset chronic neurological complication, not PML. * **D. Japanese encephalitis:** This is an acute viral encephalitis caused by a Flavivirus, transmitted by *Culex* mosquitoes, presenting with acute fever and altered sensorium, rather than chronic demyelination. **3. High-Yield Clinical Pearls for NEET-PG:** * **MRI Findings:** PML typically shows "classic" multiple, non-enhancing, subcortical white matter lesions without mass effect (often in the parieto-occipital region). * **Diagnosis:** Gold standard is PCR for JC virus DNA in the Cerebrospinal Fluid (CSF). * **Histology:** Look for "ground-glass" viral intranuclear inclusions in oligodendrocytes and enlarged, atypical astrocytes. * **BK Virus:** A "cousin" of the JC virus, also a Polyomavirus, primarily causes **hemorrhagic cystitis** and nephropathy in transplant patients.

Question 1

Subacute sclerosing panencephalitis (SSPE) is not diagnosed by which of the following?

Accepted Answer

Electroencephalogram (EEG)

Answer

Antibodies to measles in cerebrospinal fluid (CSF)

Answer

Antibodies to measles in blood

Answer

Measles antigen in brain biopsy

Question 2

Which of the following is a true finding regarding Hepatitis C virus?

Accepted Answer

Antibody to HCV may not be detected in the acute stage

Answer

Spreads via the fecal-oral route

Answer

Does not cause chronic hepatitis

Answer

Cannot be cultured in vitro

Question 3

Trachoma is caused by which serotype of Chlamydia trachomatis?

Accepted Answer

A, B, C

Answer

D to K

Answer

L1, L2, L3

Answer

All of the above

Question 4

What is true about prions?

Accepted Answer

Associated with misfolding of protein

Answer

Encoded by viral genome

Answer

Non-infectious

Answer

Immunogenic

Question 5

An HIV-infected patient presents with oral lesions. What is the most likely causative organism?

Accepted Answer

Candida

Answer

Epstein-Barr virus (EBV)

Answer

Cytomegalovirus (CMV)

Answer

Pneumocystis carinii

Question 6

Which is the longest DNA segment of the hepatitis B virus genome?

Accepted Answer

P gene

Answer

X gene

Answer

S gene

Answer

C gene

Question 7

All of the following are true about HIV infection except?

Accepted Answer

Increased release of acid labile interferon

Answer

Caused by an enveloped RNA virus

Answer

Rate of killing is directly proportional to T4 molecules on the cell surface

Answer

Decreased delayed hypersensitivity activity reaction

Question 8

Owl eye inclusion bodies are seen in which of the following viral infections?

Accepted Answer

Cytomegalovirus (CMV)

Answer

Herpes Simplex Virus (HSV)

Answer

Epstein-Barr Virus (EBV)

Answer

Hepatitis B Virus (HBV)

Question 9

Which of the following conditions is caused by HHV-8?

Accepted Answer

Kaposi sarcoma

Answer

Burkitt's lymphoma

Answer

Nasopharyngeal carcinoma

Answer

Hepatic carcinoma

Question 10

Progressive multifocal leukoencephalopathy is due to which of the following viruses?

Accepted Answer

JC virus

Answer

Papova virus

Answer

Measles

Answer

Japanese encephalitis

Virology — MCQs

Virology — MCQs

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