Virology Practice Questions

Q: Which of the following types of viruses is MOST likely to undergo an abrupt major antigenic shift, permitting reinfection in a previously exposed individual?

Orthomyxo viruses. **Explanation:** The correct answer is **Orthomyxo viruses** (specifically Influenza A). The underlying medical concept is **Antigenic Shift**, which occurs due to the **segmented genome** of the virus. 1. **Why Orthomyxo viruses are correct:** Influenza A viruses have a genome consisting of 8 distinct RNA segments. When two different strains infect the same host cell (e.g., in a pig or bird), these segments can undergo **reassortment**. This results in a major, abrupt change in the surface glycoproteins (Hemagglutinin and Neuraminidase), creating a novel subtype. Because the population has no pre-existing immunity to this new subtype, it frequently leads to **pandemics**. 2. **Why other options are incorrect:** * **Coxsackie viruses (Picornaviridae):** These are non-enveloped, positive-sense single-stranded RNA viruses. They lack a segmented genome and do not undergo reassortment/antigenic shift. * **Hepadna viruses (Hepatitis B):** These are DNA viruses that replicate via reverse transcription. While they have various genotypes, they do not exhibit abrupt major antigenic shifts. * **Herpes viruses:** These are large, double-stranded DNA viruses. They are known for **latency** rather than antigenic shift. Their surface antigens remain relatively stable over time. **High-Yield Clinical Pearls for NEET-PG:** * **Antigenic Shift:** Major change (Reassortment) $\rightarrow$ Segmented genome $\rightarrow$ Causes **Pandemics** (Only Influenza A). * **Antigenic Drift:** Minor change (Point mutations) $\rightarrow$ Occurs in both Influenza A and B $\rightarrow$ Causes **Epidemics** and necessitates annual vaccine updates. * **Segmented Viruses Mnemonic (BOAR):** **B**unyaviridae, **O**rthomyxoviridae, **A**renaviridae, **R**eoviridae. These are the viruses capable of reassortment.

Q: Which of the following statements is FALSE regarding Hepatitis C Virus?

Hepatocellular injury is caused by viral replication.. **Explanation:** The correct answer is **C**. In Hepatitis C Virus (HCV) infection, hepatocellular injury is primarily **immune-mediated** rather than a direct cytopathic effect of viral replication. The damage to hepatocytes is caused by the host’s cytotoxic T-lymphocytes (CD8+ T cells) and inflammatory cytokines attempting to clear the infected cells. This chronic inflammatory state leads to fibrosis, cirrhosis, and eventually malignancy. **Analysis of other options:** * **Option A:** HCV is a member of the *Flaviviridae* family. It is an enveloped, **positive-sense, single-stranded RNA** virus. * **Option B:** HCV is a major risk factor for **Hepatocellular Carcinoma (HCC)**. Unlike HBV, HCV does not integrate into the host genome; instead, it promotes carcinogenesis through chronic inflammation and the action of non-structural proteins (like NS5A). * **Option D:** The primary screening tool for HCV is the **anti-HCV antibody test** (ELISA). A positive result is then confirmed by HCV RNA PCR to distinguish between active infection and prior cleared infection. **High-Yield Clinical Pearls for NEET-PG:** * **"The Silent Epidemic":** HCV has the highest rate of chronicity (75–85%) among hepatitis viruses. * **Extrahepatic Manifestations:** Strongly associated with **Mixed Cryoglobulinemia**, Membranoproliferative Glomerulonephritis (MPGN), and Porphyria Cutanea Tarda. * **Treatment:** The goal is "Sustained Virologic Response" (SVR), now highly achievable with Direct-Acting Antivirals (DAAs) like Sofosbuvir. * **Vaccine:** There is **no vaccine** for HCV due to the high antigenic variation of its envelope glycoproteins (E1/E2) and the lack of proofreading by its RNA polymerase.

Q: 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?

Precore mutant. ### **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.

Q: Which of the following is false regarding poliomyelitis?

Bilateral symmetrical paralysis. 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).

Q: Antemortem diagnosis of rabies is commonly made by?

Skin biopsy. **Explanation:** The antemortem diagnosis of rabies is challenging and requires high sensitivity. The **Skin Biopsy** (taken from the nuchal skin at the hairline) is considered the most reliable antemortem method. **1. Why Skin Biopsy is correct:** Rabies virus is highly neurotropic. After replicating in muscle cells, it travels via retrograde axonal transport to the CNS and subsequently spreads to highly innervated organs. The skin at the **nape of the neck** contains a high density of nerve plexuses surrounding hair follicles. A full-thickness skin biopsy allows for the detection of rabies antigen using **Direct Fluorescent Antibody (DFA)** testing or viral RNA via RT-PCR within these cutaneous nerves. **2. Analysis of Incorrect Options:** * **Corneal Scraping (A):** While historically used, it has low sensitivity and is technically difficult to perform without causing trauma. It is no longer the preferred method. * **Brain Biopsy (B):** This is the "Gold Standard" for diagnosis (looking for **Negri bodies**), but it is almost exclusively performed **post-mortem**. It is too invasive for routine antemortem diagnosis. * **Saliva (D):** Saliva can be used for RT-PCR or viral isolation, but viral shedding is intermittent. Therefore, a single negative saliva test cannot rule out rabies; multiple samples are required, making it less definitive than a skin biopsy. **High-Yield Pearls for NEET-PG:** * **Gold Standard (Post-mortem):** DFA on brain tissue (Hippocampus/Cerebellum). * **Pathognomonic sign:** Negri bodies (intracytoplasmic eosinophilic inclusions). * **Incubation period:** Usually 1–3 months (rarely 1 year). * **Hydrophobia:** Occurs due to forceful spasms of the diaphragm and accessory respiratory muscles when attempting to swallow.

Q: All of the following are clinical manifestations of Epstein Barr virus (EBV), EXCEPT:

Slow virus disease. **Explanation:** **1. Why "Slow virus disease" is the correct answer:** Slow virus diseases are characterized by a very long incubation period (months to years) and a progressive, usually fatal, clinical course. Classic examples include **Subacute Sclerosing Panencephalitis (SSPE)** caused by Measles, **Progressive Multifocal Leukoencephalopathy (PML)** caused by the JC virus, and Prion diseases (like Kuru or CJD). Epstein-Barr Virus (EBV), a member of the *Gammaherpesvirinae* subfamily, causes acute, latent, or neoplastic infections, but it is not classified as a "slow virus." **2. Analysis of incorrect options:** * **Infectious Mononucleosis (IM):** This is the most common acute clinical manifestation of EBV ("Glandular fever"). It presents with the classic triad of fever, pharyngitis, and lymphadenopathy, often accompanied by atypical lymphocytosis (Downey cells). * **Lymphoma:** EBV is highly oncogenic. It is strongly associated with **Burkitt lymphoma** (starry-sky appearance), Hodgkin lymphoma, and B-cell lymphomas in immunocompromised patients. * **Bell’s Palsy:** EBV is a recognized viral trigger for facial nerve paralysis (Bell’s palsy). It is often listed alongside HSV-1 and VZV as a potential causative agent for cranial nerve mononeuropathy. **3. NEET-PG High-Yield Pearls:** * **Receptor:** EBV binds to the **CD21** receptor (CR2) on B-cells and nasopharyngeal epithelial cells. * **Diagnosis:** The **Paul-Bunnell Test** (detecting heterophile antibodies) is the classic screening test. * **Other Malignancies:** EBV is also linked to **Nasopharyngeal Carcinoma** and Oral Hairy Leukoplakia (in HIV patients). * **Atypical Lymphocytes:** These are actually activated **T-cells (CD8+)** responding to the infected B-cells.

Q: Hepatitis B surface antigen in a patient's serum indicates that the patient is:

Potentially infectious. **Explanation:** The presence of **Hepatitis B surface antigen (HBsAg)** in a patient's serum is the hallmark of an active Hepatitis B virus (HBV) infection. It is the first serological marker to appear after infection (appearing before the onset of symptoms or elevation of ALT) and its presence signifies that the virus is actively replicating or present in the liver. Therefore, any individual who is HBsAg-positive must be considered **potentially infectious** via blood, semen, or other body fluids. **Analysis of Options:** * **Option A (Recovered):** Recovery is characterized by the disappearance of HBsAg and the appearance of **Anti-HBs** (protective antibodies). * **Option C (Acceptable blood donor):** Any person testing positive for HBsAg is permanently deferred from blood donation to prevent transfusion-transmitted HBV. * **Option D (Immune to exacerbations):** Persistence of HBsAg beyond 6 months indicates **chronic infection**. Chronic carriers are at risk for acute exacerbations (flares), cirrhosis, and hepatocellular carcinoma; they are not immune to the disease's progression. **NEET-PG High-Yield Pearls:** * **HBsAg:** The first marker to appear; if it persists >6 months, the patient is a chronic carrier. * **Anti-HBs:** Indicates immunity (either via recovery or vaccination). * **HBeAg:** An indicator of high viral replication and **high infectivity**. * **Window Period:** The interval where HBsAg disappears but Anti-HBs hasn't appeared yet. The only marker present is **Anti-HBc IgM**. * **Screening:** HBsAg is the primary tool for screening blood donors and pregnant women.

Q: Which of the following viruses does not produce viral esophagitis?

Adenovirus. **Explanation:** Viral esophagitis is a common opportunistic infection, primarily occurring in immunocompromised individuals (e.g., HIV/AIDS, transplant recipients, or those on chemotherapy). **Why Adenovirus is the correct answer:** While **Adenovirus** is a common cause of respiratory infections, conjunctivitis (pink eye), and hemorrhagic cystitis, it is **not** a recognized cause of viral esophagitis. It typically affects the respiratory and gastrointestinal tracts (causing diarrhea), but esophageal involvement is clinically negligible or non-existent. **Analysis of incorrect options:** * **Herpes Simplex Virus (HSV):** HSV-1 is the most common cause of viral esophagitis. It typically presents with "punched-out" ulcers and characteristic **Cowdry Type A** intranuclear inclusion bodies. * **Cytomegalovirus (CMV):** CMV is the second most common cause. Unlike HSV, it produces large, shallow, linear ulcerations. Histology shows "Owl’s eye" inclusion bodies (both intranuclear and intracytoplasmic). * **Varicella-Zoster Virus (VZV):** Though rarer than HSV or CMV, VZV can cause esophagitis, usually in children with chickenpox or immunocompromised adults with disseminated shingles. It presents with vesicular lesions similar to its cutaneous manifestation. **NEET-PG High-Yield Pearls:** 1. **HSV Esophagitis:** Multiple, small, deep ulcers. Biopsy shows multinucleated giant cells with Tzanck smear positivity. 2. **CMV Esophagitis:** Large, solitary, shallow/linear ulcers. It is a common AIDS-defining illness (CD4 < 50 cells/mm³). 3. **Treatment:** Acyclovir is the drug of choice for HSV/VZV; Ganciclovir is used for CMV. 4. **Candida albicans:** The most common overall cause of infectious esophagitis (presents with white plaques/pseudomembranes).

Q: Which marker is positive in a patient who is a supercarrier of Hepatitis B?

HBeAg. In Hepatitis B serology, the term **"Supercarrier"** refers to an individual who is not only chronically infected but also highly infectious to others. ### 1. Why HBeAg is the Correct Answer **HBeAg (Hepatitis B e-Antigen)** is the hallmark of **active viral replication**. When HBeAg is present in the blood, it indicates a high viral load and high infectivity. A "supercarrier" is defined by the presence of HBeAg, as these patients have a significantly higher risk of transmitting the virus via needle-stick injuries or vertical transmission (mother-to-child) compared to HBeAg-negative carriers. ### 2. Analysis of Incorrect Options * **HBsAg (Hepatitis B Surface Antigen):** While HBsAg is the first marker to appear and its persistence for >6 months defines a **chronic carrier**, it does not distinguish between low and high infectivity. All supercarriers are HBsAg positive, but not all HBsAg positive patients are supercarriers. * **Anti-HBc IgG:** This antibody indicates a past or chronic infection. It persists for life after exposure but does not correlate with the level of viral replication or infectivity. * **All of the above:** While a supercarrier will technically be positive for HBsAg and Anti-HBc IgG, **HBeAg** is the specific diagnostic marker that defines the "supercarrier" status (high infectivity state). ### 3. High-Yield Clinical Pearls for NEET-PG * **Best indicator of infectivity:** HBeAg (or HBV-DNA levels). * **First marker to appear:** HBsAg. * **Marker of "Window Period":** Anti-HBc IgM (HBsAg and Anti-HBs are both negative). * **Marker of Immunity:** Anti-HBs (indicates recovery or vaccination). * **Vertical Transmission:** If a mother is HBeAg positive, the risk of transmitting HBV to the newborn is ~90%.

Question 1

Which of the following types of viruses is MOST likely to undergo an abrupt major antigenic shift, permitting reinfection in a previously exposed individual?

Accepted Answer

Orthomyxo viruses

Answer

Coxsackie viruses

Answer

Hepadna viruses

Answer

Herpes viruses

Question 2

Which of the following statements is FALSE regarding Hepatitis C Virus?

Accepted Answer

Hepatocellular injury is caused by viral replication.

Answer

It has single-stranded RNA.

Answer

It is associated with hepatocellular carcinoma.

Answer

Serologic testing detects antibody to HCV.

Question 3

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?

Accepted Answer

Precore mutant

Answer

Core-promoter mutant

Answer

Wild type

Answer

Surface mutant

Question 4

Which of the following is false regarding poliomyelitis?

Accepted Answer

Bilateral symmetrical paralysis

Answer

Descending paralysis

Answer

Non-progressive paralysis

Answer

Lower motor neuron type paralysis

Question 5

Antemortem diagnosis of rabies is commonly made by?

Accepted Answer

Skin biopsy

Answer

Corneal scraping

Answer

Brain biopsy

Answer

Saliva

Question 6

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

Accepted Answer

Viremia and rubella virus in the throat precede the rash by 5 to 7 days.

Answer

Viremia and rubella virus in the throat precede the rash by 1 to 2 days.

Answer

Viremia and rubella virus in the throat occur coincidentally with the rash.

Answer

Viremia and rubella virus in the throat occur 1 to 2 days after the rash.

Question 7

All of the following are clinical manifestations of Epstein Barr virus (EBV), EXCEPT:

Accepted Answer

Slow virus disease

Answer

Bell's palsy

Answer

Infectious mononucleosis

Answer

Lymphoma

Question 8

Hepatitis B surface antigen in a patient's serum indicates that the patient is:

Accepted Answer

Potentially infectious

Answer

Recovered

Answer

An acceptable blood donor

Answer

Immune to subsequent exacerbations of the disease

Question 9

Which of the following viruses does not produce viral esophagitis?

Accepted Answer

Adenovirus

Answer

Herpes simplex

Answer

Varicella

Answer

Cytomegalovirus

Question 10

Which marker is positive in a patient who is a supercarrier of Hepatitis B?

Accepted Answer

HBeAg

Answer

HBsAg

Answer

Anti-HBc IgG

Answer

All of the above

Virology — MCQs

Virology — MCQs

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