Virology Practice Questions

Q: A 30-year-old patient presented with a 10-day history of jaundice. Liver function tests showed a bilirubin of 10 mg/dl, SGOT/SGPT of 1100/1450, and serum alkaline phosphatase of 240 IU. The patient was positive for HBsAg. What is the confirmatory test to establish an acute Hepatitis B infection?

IgM anti-HBc antibody. ### Explanation **1. Why IgM anti-HBc is the Correct Answer:** In clinical practice, the presence of **HBsAg** (Hepatitis B surface antigen) indicates that the patient is currently infected with HBV, but it cannot distinguish between an **acute infection** and a **chronic carrier state** (where HBsAg persists for >6 months). The **IgM anti-HBc (Hepatitis B core antibody)** is the definitive marker for **acute infection**. It appears shortly after HBsAg and remains positive for approximately 4–6 months. Crucially, it is the only marker present during the **"Window Period"** (the gap between the disappearance of HBsAg and the appearance of Anti-HBs), making it the gold standard for diagnosing acute HBV. **2. Why the Other Options are Incorrect:** * **HBeAg (Option B):** This is a marker of **active viral replication** and high infectivity. While often present in acute phases, it can also be seen in chronic "wild-type" infections; thus, it is not specific for an acute diagnosis. * **HBV DNA by PCR (Option C):** This is the most sensitive marker for quantifying **viral load** and monitoring treatment response. However, it does not differentiate between acute and chronic phases. * **Anti-HBc antibody (Option D):** This refers to **Total Anti-HBc** (IgM + IgG). Since IgG anti-HBc persists for life, a "Total" test cannot differentiate a new infection from a past or chronic one. **3. NEET-PG High-Yield Pearls:** * **Window Period Marker:** IgM anti-HBc. * **Marker of Recovery/Immunity:** Anti-HBs (Hepatitis B surface antibody). * **Chronic Infection:** Defined by the persistence of HBsAg for **>6 months**. * **Post-Vaccination Profile:** Only Anti-HBs is positive (HBsAg and Anti-HBc are negative). * **Rule of Thumb:** If HBsAg (+) and IgM anti-HBc (+), it is **Acute**. If HBsAg (+) and IgM anti-HBc (–) but IgG anti-HBc (+), it is **Chronic**.

Q: A viral organism was isolated from a painful blister on the lip of a teenage girl. The agent was found to have double-stranded, linear DNA and was enveloped. The patient had a similar sore approximately 2 months ago. Which of the following is the most likely causative organism?

Herpes simplex type 1 virus. ### Explanation **Correct Answer: C. Herpes simplex type 1 virus (HSV-1)** The clinical presentation of a painful blister on the lip (herpes labialis) in a teenager, combined with a history of recurrence, is classic for **Herpes simplex virus type 1 (HSV-1)**. * **Virology:** HSV-1 is a member of the *Herpesviridae* family, characterized by a **double-stranded, linear DNA** genome and a lipid **envelope** derived from the host nuclear membrane. * **Pathogenesis:** After the primary infection, the virus remains **latent** in the sensory nerve ganglia (specifically the **trigeminal ganglion** for oral lesions). Periodic reactivation leads to recurrent sores, often triggered by stress, sunlight, or fever. **Incorrect Options:** * **A. Adenovirus:** While it has dsDNA, it is **non-enveloped**. It typically causes pharyngoconjunctival fever or keratoconjunctivitis, not recurrent vesicular lip sores. * **B. Coxsackie virus:** Part of the *Picornaviridae* family, it has a **ssRNA** genome and is **non-enveloped**. It causes Herpangina or Hand-Foot-Mouth disease, which present as ulcers but do not typically recur in the same site. * **D. Herpes zoster virus (VZV):** Although it is an enveloped dsDNA virus, it typically presents as a **dermatomal** rash (shingles) in older or immunocompromised individuals. Recurrence twice within two months in a teenager is highly atypical for VZV. **High-Yield Clinical Pearls for NEET-PG:** * **Tzanck Smear:** Look for **multinucleated giant cells** and **Cowdry Type A** intranuclear inclusion bodies. * **Latency Site:** HSV-1 (Trigeminal ganglion); HSV-2 (Sacral ganglion); VZV (Dorsal root ganglion). * **Drug of Choice:** Acyclovir (inhibits viral DNA polymerase). * **Enveloping:** Herpesviruses are unique because they acquire their envelope by budding through the **inner nuclear membrane**.

Q: A male patient is HBsAg positive, HBeAg negative, and anti-HBe antibody positive. HBV DNA copies are 100,000/ml, and SGOT and SGPT are elevated to 6 times the upper limit of normal. What is the likely diagnosis?

HBV precore mutant. ### Explanation The correct answer is **HBV precore mutant**. In a typical (wild-type) Hepatitis B infection, the presence of **HBeAg** indicates active viral replication and high infectivity. However, in a **precore mutant** (most commonly a G-to-A mutation at nucleotide 1896), the virus develops a stop codon that prevents the production of HBeAg, even though the virus continues to replicate vigorously. **Why it is the correct diagnosis:** The patient presents with a "discordant" profile: **HBeAg is negative** and **anti-HBe is positive** (suggesting low replication), yet the **HBV DNA is high** (100,000 copies/ml) and **ALT/AST are significantly elevated** (6x normal). This combination of negative HBeAg with high DNA and active liver inflammation is the hallmark of a precore mutant infection. **Why other options are incorrect:** * **HBV surface mutant:** This involves mutations in the 'a' determinant of HBsAg. These patients are typically HBsAg negative but HBV DNA positive (occult infection). * **Wild HBsAg:** In wild-type infection, high viral replication (high DNA) would almost always be accompanied by a **positive HBeAg**. * **Inactive HBV carrier:** While these patients are HBeAg negative and anti-HBe positive, they must have **low/undetectable HBV DNA** ( 2,000 IU/ml and ALT is elevated. * **Serological Gap:** If a patient has high DNA but is HBeAg negative, always suspect a mutant strain.

Q: Hepatitis C virus resembles which of the following virus groups?

Flaviviruses. ### Explanation **Correct Option: D (Flaviviruses)** Hepatitis C Virus (HCV) is classified under the family **Flaviviridae** and the genus *Hepacivirus*. It resembles other Flaviviruses (like Yellow Fever or Dengue virus) because it is an **enveloped, positive-sense single-stranded RNA (+ssRNA)** virus. A key structural characteristic it shares with this group is its genomic organization and the presence of an icosahedral nucleocapsid. **Why other options are incorrect:** * **Picornaviruses (Option A):** While Hepatitis A (HAV) belongs to this family, Picornaviruses are **non-enveloped** RNA viruses. HCV is enveloped. * **Herpesviruses (Option B):** These are large, **enveloped double-stranded DNA (dsDNA)** viruses. Their replication and structure are entirely different from the RNA-based HCV. * **Hepadnaviruses (Option C):** This family includes Hepatitis B Virus (HBV). Hepadnaviruses are **partially double-stranded DNA** viruses that utilize reverse transcriptase, unlike the direct RNA replication of HCV. **High-Yield Clinical Pearls for NEET-PG:** * **Genomic Stability:** HCV lacks 3'-5' exonuclease activity (proofreading), leading to high antigenic variation and the formation of **quasispecies**. This is the primary reason why a vaccine for HCV has not yet been developed. * **Transmission:** Primarily parenteral (blood-borne). It has the highest rate of progression to **chronic infection** (~80%) among all hepatitis viruses. * **Diagnosis:** Screening is done via Anti-HCV antibodies (ELISA); confirmation and viral load are assessed via **HCV-RNA (PCR)**. * **Association:** Strongly linked to Cryoglobulinemia and Hepatocellular Carcinoma (HCC).

Q: Which influenza strain has caused a pandemic?

H1N1. **Explanation:** Influenza pandemics occur due to **Antigenic Shift**, a process where a major change in the surface glycoproteins (Hemagglutinin and Neuraminidase) occurs, usually through genetic reassortment between human and animal viruses. This results in a novel virus to which the global population has little to no immunity. **Why H1N1 is correct:** **H1N1** is the most significant pandemic strain in history. It was responsible for the **1918 Spanish Flu** (the deadliest pandemic) and the **2009 Swine Flu** pandemic. Because it successfully adapted for efficient human-to-human transmission, it spread globally. **Analysis of Incorrect Options:** * **H2N2:** While H2N2 caused the 1957 Asian Flu pandemic, it is not the *only* answer. However, in the context of this specific question format, H1N1 is the most frequently tested and clinically relevant prototype for pandemics. (Note: If this were a "Multiple Correct" style, H2N2 would also be a candidate, but H1N1 remains the primary answer). * **H5N1:** Known as **Avian Influenza (Bird Flu)**. While it has a high mortality rate in humans, it has **not** caused a pandemic because it lacks the ability for sustained human-to-human transmission. * **H9N1:** This is a subtype of avian influenza that occasionally infects humans but has never caused a pandemic or widespread outbreaks. **High-Yield Clinical Pearls for NEET-PG:** * **Antigenic Shift:** Major change (reassortment); causes **Pandemics**. Seen only in Influenza A. * **Antigenic Drift:** Minor change (point mutations); causes **Epidemics**. Seen in both Influenza A and B. * **Drug of Choice:** Oseltamivir (Neuraminidase inhibitor) is the treatment for both seasonal and pandemic H1N1. * **Pandemic Years to Remember:** 1918 (H1N1), 1957 (H2N2), 1968 (H3N2), and 2009 (H1N1).

Q: Segmented genome is found in all of the following viruses except?

Rhabdovirus. ### Explanation The concept of a **segmented genome** is a high-yield topic in virology. Viruses with segmented genomes can undergo **genetic reassortment** (antigenic shift), leading to the emergence of new strains and potential pandemics. **1. Why Rhabdovirus is the Correct Answer:** Rhabdoviruses (e.g., Rabies virus) possess a **non-segmented, single-stranded, negative-sense RNA genome**. Their genetic material is a continuous linear molecule, meaning they cannot undergo reassortment. Morphologically, they are characterized by a distinct bullet-shaped appearance. **2. Analysis of Incorrect Options:** To remember segmented viruses, use the mnemonic **"BOAR"**: * **B - Bunyavirus (Option C):** Contains **3 segments** (Large, Medium, Small). Examples include Hantavirus and Crimean-Congo hemorrhagic fever virus. * **O - Orthomyxovirus (Option A):** Includes **Influenza virus**, which has **8 segments** (Influenza A and B) or 7 segments (Influenza C). This segmentation is the basis for antigenic shift. * **A - Arenavirus:** Contains **2 segments** (Large and Small). Examples include Lassa fever virus. * **R - Reovirus (Option B):** The only double-stranded RNA virus in this list, containing **10–12 segments**. Rotavirus (a member of this family) typically has 11 segments. **Clinical Pearls for NEET-PG:** * **Antigenic Shift:** Occurs only in segmented viruses (primarily Influenza A) due to reassortment of segments. * **Antigenic Drift:** Occurs in all viruses due to point mutations. * **Reovirus:** Remember it as "Double-Double" (Double-stranded and Double-layered capsid). * **Rabies (Rhabdovirus):** Look for **Negri bodies** (intracytoplasmic inclusions) in Purkinje cells of the cerebellum or pyramidal cells of the hippocampus.

Q: What is the highest risk factor for perinatal transmission when a mother is positive for a specific marker?

HBeAg. **Explanation:** The risk of vertical transmission of Hepatitis B Virus (HBV) from mother to child is primarily determined by the mother's viral load and replicative status. **Why HBeAg is the Correct Answer:** **HBeAg (Hepatitis B e-antigen)** is a marker of **active viral replication** and high infectivity. If a pregnant woman is positive for both HBsAg and HBeAg, the risk of vertical transmission to the newborn is approximately **70% to 90%** in the absence of immunoprophylaxis. Conversely, if the mother is HBsAg positive but HBeAg negative (and anti-HBe positive), the transmission risk drops significantly to about 10% to 40%. **Analysis of Incorrect Options:** * **HBsAg (Hepatitis B surface antigen):** While this indicates that the mother is a carrier or has an active infection, it does not specify the level of infectivity as accurately as HBeAg does. * **IgM anti-HBc (not HBsAg):** This indicates an acute infection but is not the primary determinant of transmission risk compared to the e-antigen status. * **IgG anti-HBs:** This represents **immunity** (either from past infection or vaccination). A mother with these antibodies cannot transmit the virus to the fetus; rather, she provides protective passive immunity. **High-Yield Clinical Pearls for NEET-PG:** * **Most common timing:** Most vertical transmission occurs **during delivery** (peripartum) through exposure to maternal blood and vaginal secretions. * **Prevention:** To prevent transmission, the newborn must receive both the **HBV Vaccine** and **Hepatitis B Immunoglobulin (HBIG)** within 12 hours of birth. This reduces the risk by >90%. * **Chronic Status:** Infants infected at birth have a **90% risk** of developing chronic Hepatitis B, compared to only a 5-10% risk if infected during adulthood.

Q: Which of the following viruses appears to be involved in the pathogenesis of Kaposi's sarcoma?

Human Herpes Virus 8. ### Explanation **Correct Answer: C. Human Herpes Virus 8 (HHV-8)** **Pathogenesis:** Kaposi’s Sarcoma (KS) is a vascular neoplasm caused by **Human Herpes Virus 8 (HHV-8)**, also known as **Kaposi Sarcoma-associated Herpesvirus (KSHV)** [1]. HHV-8 infects vascular and lymphatic endothelial cells. The virus carries genes that mimic host cellular genes (like v-cyclin and v-IL6), which promote cell proliferation, inhibit apoptosis, and induce angiogenesis (via VEGF). It is most commonly seen in the context of HIV/AIDS (Epidemic KS), but also occurs in elderly Mediterranean men (Classic KS), organ transplant recipients (Iatrogenic KS), and endemic regions of Africa [1]. **Analysis of Incorrect Options:** * **A. Human Herpes Virus 3 (Varicella-Zoster Virus):** Causes chickenpox (primary infection) and shingles (reactivation). It is not oncogenic. * **B. Human Herpes Virus 1 (Herpes Simplex Virus-1):** Primarily causes orolabial herpes (cold sores) and sporadic encephalitis. * **D. Human Herpes Virus 4 (Epstein-Barr Virus):** While EBV is oncogenic, it is associated with Burkitt lymphoma, Nasopharyngeal carcinoma, and Hodgkin lymphoma, but not Kaposi’s sarcoma [1]. **High-Yield NEET-PG Pearls:** * **Histology:** Look for **spindle-shaped cells**, slit-like vascular spaces, and extravasated RBCs with hemosiderin-laden macrophages. * **Marker:** **LANA-1** (Latency-Associated Nuclear Antigen) is a highly specific immunohistochemical marker for HHV-8 in tissue sections. * **Clinical Presentation:** Characterized by purple, red, or brown skin plaques or nodules, often involving the lower extremities, mucous membranes, or viscera [1]. * **Association:** HHV-8 is also implicated in **Primary Effusion Lymphoma (PEL)** and **Multicentric Castleman Disease**. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 261-262.

Question 1

What is true about prions?

Accepted Answer

Heat labile

Answer

Associated with Cruetzfeldt-Jacob disease

Answer

Sensitive to proteases

Answer

Infectious proteinaceous particles

Question 2

An 8-year-old boy presents with behavioral changes, intellectual deterioration, and "laziness." Over several months, he develops increasing clumsiness and periodic, involuntary, jerky movements every 3 to 6 seconds. Visual deterioration is apparent on visual field testing, and optic atrophy is evident on funduscopic examination. Cerebrospinal fluid studies show oligoclonal bands of IgG on electrophoresis but no significant pleocytosis. The electroencephalogram reveals periodic discharges synchronous with the myoclonus. Computed tomography (CT) of the head demonstrates low-density white matter lesions and cerebral atrophy. The boy dies at age 10. Prior infection with which of the following agents was most likely related to this patient's condition?

Accepted Answer

Measles virus

Answer

Mumps virus

Answer

Papillomavirus

Answer

Poliovirus

Question 3

A 30-year-old patient presented with a 10-day history of jaundice. Liver function tests showed a bilirubin of 10 mg/dl, SGOT/SGPT of 1100/1450, and serum alkaline phosphatase of 240 IU. The patient was positive for HBsAg. What is the confirmatory test to establish an acute Hepatitis B infection?

Accepted Answer

IgM anti-HBc antibody

Answer

HBeAg

Answer

HBV DNA by PCR

Answer

Anti-HBc antibody

Question 4

A viral organism was isolated from a painful blister on the lip of a teenage girl. The agent was found to have double-stranded, linear DNA and was enveloped. The patient had a similar sore approximately 2 months ago. Which of the following is the most likely causative organism?

Accepted Answer

Herpes simplex type 1 virus

Answer

Adenovirus

Answer

Coxsackie virus

Answer

Herpes zoster virus

Question 5

A male patient is HBsAg positive, HBeAg negative, and anti-HBe antibody positive. HBV DNA copies are 100,000/ml, and SGOT and SGPT are elevated to 6 times the upper limit of normal. What is the likely diagnosis?

Accepted Answer

HBV precore mutant

Answer

HBV surface mutant

Answer

Wild HBsAg

Answer

Inactive HBV carrier

Question 6

Hepatitis C virus resembles which of the following virus groups?

Accepted Answer

Flaviviruses

Answer

Picornaviruses

Answer

Herpesviruses

Answer

Hepadnaviruses

Question 7

Which influenza strain has caused a pandemic?

Accepted Answer

H1N1

Answer

H2N2

Answer

H5N1

Answer

H9N1

Question 8

Segmented genome is found in all of the following viruses except?

Accepted Answer

Rhabdovirus

Answer

Influenza virus

Answer

Reovirus

Answer

Bunyavirus

Question 9

What is the highest risk factor for perinatal transmission when a mother is positive for a specific marker?

Accepted Answer

HBeAg

Answer

HBsAg

Answer

IgM anti HBsAg

Answer

IgG anti HBsAg

Question 10

Which of the following viruses appears to be involved in the pathogenesis of Kaposi's sarcoma?

Accepted Answer

Human Herpes Virus 8

Answer

Human Herpes Virus 3

Answer

Human Herpes Virus 1

Answer

Human Herpes Virus 4

Virology — MCQs

Virology — MCQs

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