Virology — MCQs

Virology Indian Medical PG Practice Questions and MCQs

Question 531: What is the usual incubation period for hepatitis B virus infection?

A. 1-2 days
B. 1-2 weeks
C. 1-6 months (Correct Answer)
D. 1 year

Explanation: **Explanation:** Hepatitis B Virus (HBV) is a DNA virus characterized by a **long and variable incubation period**, typically ranging from **30 to 180 days (1–6 months)**, with an average of about 60–90 days. This prolonged period is due to the virus's slow replication cycle and the time required for the host's immune system to mount a cell-mediated response against the hepatocytes, which causes the clinical symptoms. **Analysis of Options:** * **Option A (1-2 days):** This is characteristic of respiratory viruses (like Influenza) or bacterial gastroenteritis (like *Vibrio cholerae*). * **Option B (1-2 weeks):** This is typical for Hepatitis A (which has a total range of 2–6 weeks) or Arboviruses like Dengue. * **Option C (1-6 months):** **Correct.** HBV and HCV both share this long incubation window. * **Option D (1 year):** While some chronic infections or slow viruses (like Prions or Rabies in rare cases) can have incubation periods of a year or more, it is not the "usual" presentation for acute HBV. **NEET-PG High-Yield Pearls:** * **Hepatitis Incubation Periods:** * **HAV:** 2–6 weeks (Short) * **HBV:** 1–6 months (Long) * **HCV:** 2 weeks – 6 months (Variable) * **HEV:** 2–8 weeks (Similar to HAV) * **First Marker to Appear:** HBsAg is the first detectable serological marker, appearing even before the onset of symptoms (during the incubation period). * **Window Period:** The interval between the disappearance of HBsAg and the appearance of Anti-HBs. During this time, **Anti-HBc IgM** is the only diagnostic marker.

Question 532: What are the target binding sites of HIV?

A. gp 120, gp 41 (Correct Answer)
B. gp 120, p24
C. gp 120
D. p24, p40

Explanation: **Explanation:** The entry of HIV into a host cell is a multi-step process mediated by the **envelope glycoproteins (env gene products)**, which serve as the primary target binding sites. 1. **gp120 (Surface Glycoprotein):** This is responsible for the initial **attachment**. It binds specifically to the **CD4 receptor** on T-helper cells, macrophages, and dendritic cells. Following this, it undergoes a conformational change to bind to co-receptors (**CCR5** or **CXCR4**). 2. **gp41 (Transmembrane Glycoprotein):** Once gp120 is anchored, gp41 mediates the **fusion** of the viral envelope with the host cell membrane, allowing the viral capsid to enter the cytoplasm. **Analysis of Incorrect Options:** * **Option B & D (p24):** p24 is the **capsid protein** (encoded by the *gag* gene). While it is a major serological marker for early diagnosis (p24 antigenemia), it is an internal structural protein and does not participate in the initial binding or fusion with the host cell. * **Option C (gp120 only):** While gp120 is the primary attachment protein, it cannot complete the entry process alone. The "target binding sites" collectively involve both the attachment (gp120) and the fusion (gp41) subunits of the envelope complex. * **Option D (p40):** This is not a standard diagnostic or structural protein associated with HIV entry. **NEET-PG High-Yield Pearls:** * **Enfuvirtide:** A fusion inhibitor drug that specifically targets and binds to **gp41**. * **Maraviroc:** A drug that acts as a **CCR5 antagonist**, preventing the gp120-co-receptor interaction. * **Tropism:** M-tropic strains (early infection) use **CCR5**; T-tropic strains (late infection) use **CXCR4**. * **Homozygous CCR5-Δ32 mutation:** Confers resistance to HIV infection.

Question 533: Syncytium formation is the typical cytopathic effect (CPE) produced by which virus?

A. BK virus
B. JC virus
C. SV 40 virus
D. Measles virus (Correct Answer)

Explanation: **Explanation:** The correct answer is **Measles virus**. Syncytium formation (also known as multinucleated giant cell formation) is a hallmark cytopathic effect (CPE) of certain enveloped viruses. **Why Measles is Correct:** Measles virus, a member of the *Paramyxoviridae* family, possesses a specialized **Fusion (F) protein** on its envelope. This protein allows the viral envelope to fuse with the host cell membrane. During replication, the F-protein is expressed on the surface of the infected cell, causing it to fuse with neighboring uninfected cells. This results in a large, cytoplasmic mass containing multiple nuclei, known as a **syncytium**. In clinical practice, these are identified in lymphoid tissue as **Warthin-Finkeldey giant cells**. **Analysis of Incorrect Options:** * **BK virus, JC virus, and SV 40 virus:** These are all members of the *Polyomaviridae* family. Polyomaviruses are small, non-enveloped DNA viruses. Because they lack a fusion protein and an envelope, they do not induce cell-to-cell fusion (syncytia). Instead, their typical CPE involves **intranuclear inclusions** (e.g., "decoy cells" in urine for BK virus). **High-Yield Clinical Pearls for NEET-PG:** * **Other Syncytia-forming viruses:** Remember the mnemonic **"MR. H"** — **M**easles, **R**SV (Respiratory Syncytial Virus), and **H**IV/Herpes Simplex Virus. * **Warthin-Finkeldey Cells:** Pathognomonic multinucleated giant cells found in the tonsils/lymph nodes of Measles patients. * **Koplik Spots:** The prodromal enanthem of Measles; look for "grains of salt on a red base" opposite the lower molars. * **Tzanck Smear:** Used to identify syncytia (multinucleated giant cells) in HSV or VZV infections.

Question 534: The 'slapped cheek' sign is characteristic of which viral infection?

A. Parvovirus B19 (Correct Answer)
B. JC virus
C. Rotavirus
D. Mumps virus

Explanation: **Explanation:** The **'slapped cheek' appearance** (erythema infectiosum or Fifth disease) is the classic clinical hallmark of **Parvovirus B19** infection. **1. Why Parvovirus B19 is correct:** Parvovirus B19 is a small, non-enveloped, single-stranded DNA virus. It specifically targets and replicates in **erythroid progenitor cells** by binding to the **P-antigen** (globoside). The characteristic rash occurs in two phases: initially, an erythematous eruption on the malar eminences (slapped cheek), followed 1–4 days later by a symmetric, **lace-like (reticular) maculopapular rash** on the trunk and extremities. The rash is immune-mediated and typically appears after the viremic phase has resolved. **2. Why other options are incorrect:** * **JC Virus:** A polyomavirus that causes **Progressive Multifocal Leukoencephalopathy (PML)**, a demyelinating CNS disease in immunocompromised patients; it does not cause a rash. * **Rotavirus:** The leading cause of severe **gastroenteritis** (diarrhea and vomiting) in infants and young children; it has no cutaneous manifestations. * **Mumps Virus:** A paramyxovirus characterized by **nonsuppurative parotitis** (painful swelling of salivary glands), orchitis, and aseptic meningitis. **Clinical Pearls for NEET-PG:** * **Aplastic Crisis:** Parvovirus B19 can cause a life-threatening cessation of erythropoiesis in patients with high red cell turnover (e.g., **Sickle Cell Anemia**, Hereditary Spherocytosis). * **Hydrops Fetalis:** Infection during pregnancy can lead to severe fetal anemia, high-output cardiac failure, and fetal death. * **Arthropathy:** In adults, it often presents as symmetrical small joint arthritis resembling Rheumatoid Arthritis. * **Diagnosis:** Detection of **IgM antibodies** or PCR for viral DNA.

Question 535: Man is the primary host for which poxvirus?

A. Monkey pox
B. Orf
C. Tanapox
D. Molluscum contagiosum (Correct Answer)

Explanation: ### Explanation **Correct Answer: D. Molluscum contagiosum** **1. Why it is correct:** Poxviruses are generally **zoonotic**, meaning they primarily circulate in animals and only incidentally infect humans. **Molluscum contagiosum virus (MCV)** is the notable exception. It is an **obligate human pathogen** with no known animal reservoir. Humans are the primary and only natural hosts. It is transmitted via direct skin-to-skin contact, fomites, or sexual contact, leading to characteristic umbilicated papules. **2. Why the other options are incorrect:** * **A. Monkeypox:** The primary hosts are **rodents** (such as squirrels and Gambian pouched rats) and non-human primates in Central and West Africa. Human infection is accidental. * **B. Orf:** This is a parapoxvirus whose primary hosts are **sheep and goats**. It causes "contagious pustular dermatitis" in animals; humans (usually shearers or veterinarians) are accidental hosts. * **C. Tanapox:** This is a yatapoxvirus endemic to the Tana River valley in Kenya. The primary hosts are **monkeys**, and it is transmitted to humans via arthropod bites or direct contact. **3. High-Yield Clinical Pearls for NEET-PG:** * **Smallpox (Variola):** Like Molluscum, Variola also had humans as the only host, which is why global eradication was possible. * **Histopathology of Molluscum:** Look for **Henderson-Patterson bodies** (large, eosinophilic intracytoplasmic inclusion bodies) in the epidermis. * **Clinical Presentation:** Small, pearly, flesh-colored, **dome-shaped papules with central umbilication**. In HIV/immunocompromised patients, lesions can be giant or disseminated. * **Poxvirus General Feature:** They are the largest DNA viruses and are unique because they **replicate entirely in the cytoplasm** (carrying their own DNA-dependent RNA polymerase).

Question 536: Kaposi's sarcoma is caused by which of the following agents?

A. Human Immunodeficiency Virus (HIV)
B. Human Papillomavirus (HPV)
C. Human Herpesvirus 8 (HHV8) (Correct Answer)
D. Cytomegalovirus (CMV)

Explanation: **Explanation:** **Kaposi’s Sarcoma (KS)** is a multicentric angioproliferative tumor of endothelial origin. The correct answer is **Human Herpesvirus 8 (HHV8)**, also known as Kaposi’s Sarcoma-associated Herpesvirus (KSHV). 1. **Why HHV8 is correct:** HHV8 is a gamma-herpesvirus that infects vascular and lymphatic endothelial cells. It carries oncogenes (like the v-cyclin and v-FLIP) that dysregulate the cell cycle and inhibit apoptosis. While KS is most commonly seen in AIDS patients, the virus is the direct oncogenic driver across all four clinical variants (Classic, Endemic/African, Iatrogenic, and AIDS-associated). 2. **Why the other options are incorrect:** * **HIV:** While HIV-induced immunosuppression significantly increases the risk and severity of KS, HIV itself does not cause the tumor. It acts as a cofactor. * **HPV:** Human Papillomavirus is associated with squamous cell carcinomas (cervical, anal, oropharyngeal) and warts, not vascular tumors. * **CMV (HHV5):** Although CMV is common in immunocompromised patients and can cause retinitis or colitis, it is not the causative agent of KS. **High-Yield Clinical Pearls for NEET-PG:** * **Histology:** Look for "slit-like vascular spaces" containing extravasated RBCs and spindle-shaped cells. * **Clinical Presentation:** Characterized by violaceous (purple) macules, plaques, or nodules on the skin, mucous membranes, or viscera. * **Transmission:** Primarily via saliva (non-sexual) and sexual contact. * **Treatment:** Highly Active Antiretroviral Therapy (HAART) often leads to regression in AIDS-associated KS by restoring immune function.

Question 537: A sexually active 17-year-old male presents with small, white papules with a central depression on his penis. There is no discharge or pain on urination. What is the virus most likely causing these lesions?

A. Adenovirus
B. Coxsackievirus A
C. HPV type 6
D. Molluscipoxvirus (Correct Answer)

Explanation: ### Explanation **Correct Answer: D. Molluscipoxvirus** The clinical presentation of small, white, pearly papules with a **central depression (umbilication)** is the hallmark of **Molluscum Contagiosum**, caused by the **Molluscipoxvirus** (a member of the Poxviridae family). In adolescents and adults, it is frequently transmitted sexually, presenting on the genitals, lower abdomen, or inner thighs. The lesions are typically asymptomatic (painless and non-pruritic) and contain a curd-like core consisting of infected keratinocytes. **Analysis of Incorrect Options:** * **A. Adenovirus:** Typically causes respiratory infections, conjunctivitis (pink eye), or hemorrhagic cystitis, but does not present with umbilicated skin papules. * **B. Coxsackievirus A:** Known for causing **Hand-Foot-and-Mouth Disease** (vesicular eruptions on the palms, soles, and oral mucosa) or Herpangina, not chronic umbilicated genital papules. * **C. HPV type 6:** Causes **Condyloma acuminatum** (genital warts). These are typically cauliflower-like, fleshy, or filiform growths, lacking the central umbilication characteristic of Molluscum. **NEET-PG High-Yield Pearls:** * **Histopathology:** Look for **Henderson-Patterson bodies** (large, eosinophilic intracytoplasmic inclusion bodies) within the epidermis. * **Virology:** Molluscipoxvirus is a **dsDNA virus** that replicates in the **cytoplasm** (unique for DNA viruses). * **Clinical Association:** In adults, extensive or giant molluscum lesions should prompt an investigation for **HIV/immunodeficiency**. * **Transmission:** Occurs via direct contact or fomites (e.g., towels, gym equipment).

Question 538: Which of the following is true about hepatitis A, except?

A. It is difficult to culture
B. It belongs to enterovirus
C. Vaccines are available
D. Chronicity is the hallmark of the disease (Correct Answer)

Explanation: **Explanation:** Hepatitis A Virus (HAV) is a leading cause of acute viral hepatitis worldwide. The hallmark of HAV infection is that it **never causes chronic infection**. It is an acute, self-limiting disease that does not lead to a carrier state, chronic hepatitis, or cirrhosis. **Analysis of Options:** * **Option D (Correct):** This is the false statement. Unlike Hepatitis B and C, HAV does not progress to chronicity. Once the acute phase resolves, the patient develops lifelong immunity. * **Option A:** HAV is notoriously **difficult to culture** in the laboratory. While it can be grown in certain primate cell lines (like fetal rhesus monkey kidney cells), it does not produce a cytopathic effect (CPE), making primary isolation impractical for diagnosis. * **Option B:** HAV is a non-enveloped, positive-sense RNA virus. It was formerly classified as **Enterovirus 72** but is now placed in its own genus, *Hepatovirus*, within the *Picornaviridae* family. * **Option C:** Both **Inactivated (killed)** and **Live-attenuated** vaccines are available. In India, the inactivated vaccine (e.g., Havrix) is commonly used, administered in two doses. **High-Yield Clinical Pearls for NEET-PG:** * **Transmission:** Fecal-oral route (most common). * **Incubation Period:** Short (average 2–4 weeks). * **Diagnosis:** Detection of **IgM anti-HAV** is the gold standard for acute infection. IgG indicates past infection or vaccination. * **Complication:** While it doesn't cause chronicity, it can rarely cause **Fulminant Hepatic Failure**, especially in adults or those with pre-existing liver disease. * **Shellfish:** Consumption of raw/undercooked shellfish is a classic risk factor mentioned in clinical vignettes.

Question 539: Which HBV gene codes for HBe Ag?

A. PreC+C (Correct Answer)
B. S
C. X
D. C

Explanation: **Explanation:** The Hepatitis B Virus (HBV) genome is a circular, partially double-stranded DNA molecule with four overlapping Open Reading Frames (ORFs). The **C (Core) gene** contains two initiation codons: the **Pre-core** and the **Core** regions. 1. **Why PreC+C is correct:** When translation starts from the **Pre-core (PreC)** region, a precursor protein is formed. This protein undergoes proteolytic processing and is secreted into the blood as **HBeAg** (Hepatitis B e-antigen). HBeAg serves as a marker of active viral replication and high infectivity. 2. **Why Option D (C) is incorrect:** If translation starts only from the **Core** region (skipping the Pre-core sequence), the resulting protein is the **HBcAg** (Hepatitis B core antigen). Unlike HBeAg, HBcAg is a structural protein that assembles into the viral nucleocapsid and is *not* secreted into the blood. 3. **Why Option B (S) is incorrect:** The **S gene** (Pre-S1, Pre-S2, and S) codes for the surface proteins, collectively known as **HBsAg**. 4. **Why Option C (X) is incorrect:** The **X gene** codes for the **HBx protein**, a transcriptional transactivator involved in viral replication and the pathogenesis of hepatocellular carcinoma (HCC). **High-Yield Clinical Pearls for NEET-PG:** * **HBeAg:** Indicates high replication and high vertical transmission risk. * **Pre-core Mutants:** Some HBV strains have a mutation in the Pre-core region that prevents HBeAg production. These patients will be **HBeAg negative but have high HBV DNA levels** and active liver disease. * **P Gene:** The largest gene, coding for DNA Polymerase (Reverse Transcriptase). * **Window Period:** The time between the disappearance of HBsAg and the appearance of Anti-HBs; **Anti-HBc IgM** is the only diagnostic marker during this phase.

Question 540: HBV replication is indicated by all of the following, except:

A. HBV DNA
B. DNA polymerase
C. HBe Ag
D. HBs Ag (Correct Answer)

Explanation: **Explanation:** The presence of **HBsAg (Hepatitis B Surface Antigen)** indicates that an individual is currently infected with the Hepatitis B virus (either acute or chronic). However, it is **not** a direct marker of active viral replication. HBsAg is produced in massive excess by the host liver cells and can persist in the blood even when the virus is not actively multiplying. **Why the other options indicate replication:** * **HBV DNA:** This is the most sensitive and specific quantitative marker of viral replication. Its presence in the serum directly reflects the viral load. * **DNA Polymerase:** As an enzyme required for synthesizing new viral genomes, its activity is a direct biochemical indicator that the virus is actively replicating. * **HBeAg (Hepatitis B 'e' Antigen):** This is a soluble protein secreted during active viral replication. Its presence signifies high infectivity and a high rate of viral multiplication. **Clinical Pearls for NEET-PG:** * **Window Period:** The interval where HBsAg becomes negative and Anti-HBs has not yet appeared. During this time, **Anti-HBc IgM** is the only serological marker of acute infection. * **Seroconversion:** The shift from HBeAg to Anti-HBe usually indicates a transition from a high-replication state to a low-replication (latent) state. * **Pre-core Mutants:** In some patients, HBV DNA remains high despite being HBeAg negative due to a mutation in the pre-core region; these patients are still actively replicating. * **HBsAg persistence** for >6 months defines **Chronic Hepatitis B**.

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