Virology — MCQs

Virology Indian Medical PG Practice Questions and MCQs

Question 191: Teratogenic effects are rare with which of the following infections?

A. Cytomegalovirus (CMV)
B. Rubella
C. Varicella
D. Human Immunodeficiency Virus (HIV) (Correct Answer)

Explanation: ### Explanation The correct answer is **Human Immunodeficiency Virus (HIV)**. **1. Why HIV is the correct answer:** While HIV is frequently transmitted from mother to child (Vertical Transmission) via the placenta, during delivery, or through breastfeeding, it is **not typically teratogenic**. HIV infection in utero does not cause structural malformations or a specific dysmorphic syndrome. Instead, it leads to pediatric HIV/AIDS, characterized by failure to thrive, recurrent infections, and CD4 depletion. **2. Why the other options are incorrect:** The other options are classic members of the **TORCH** group of infections, which are notorious for causing structural defects when acquired during pregnancy: * **Rubella:** Causes **Congenital Rubella Syndrome (CRS)**, characterized by the triad of cataracts, sensorineural deafness, and cardiac defects (PDA). It has the highest teratogenic potential if acquired in the first trimester. * **Cytomegalovirus (CMV):** The most common viral cause of congenital anomalies. It leads to microcephaly, periventricular calcifications, and sensorineural hearing loss. * **Varicella:** Infection during the first 20 weeks can lead to **Congenital Varicella Syndrome**, presenting with cicatricial skin scarring, limb hypoplasia, and chorioretinitis. **3. NEET-PG High-Yield Pearls:** * **Most common congenital infection:** CMV. * **Highest risk of malformation:** Rubella (especially if contracted <12 weeks gestation). * **HIV Management:** To prevent vertical transmission, the mother should be on HAART regardless of CD4 count, and the neonate should receive Zidovudine prophylaxis. * **Parvovirus B19:** Another important viral infection in pregnancy; it is not typically structural-teratogenic but causes **Hydrops Fetalis** due to severe fetal anemia.

Question 192: Which virus family does Hepatitis A virus belong to?

A. Flavivirus
B. Calicivirus
C. Hepadnaviridae (Correct Answer)
D. Defective virus

Explanation: ### Explanation **Correct Answer: C. Hepadnaviridae** The **Hepatitis B Virus (HBV)** is the only human hepatitis virus that belongs to the **Hepadnaviridae** family. The name is derived from "Hepa" (liver) and "dna" (DNA genome). It is a partially double-stranded circular DNA virus. It replicates via a unique mechanism involving **reverse transcriptase**, despite being a DNA virus. **Analysis of Incorrect Options:** * **A. Flavivirus:** This family includes **Hepatitis C Virus (HCV)**. Flaviviruses are enveloped, positive-sense single-stranded RNA (ssRNA) viruses. * **B. Calicivirus:** This family includes **Hepatitis E Virus (HEV)** (specifically the genus *Hepevirus*, though now often classified in its own family, *Hepeviridae*). Caliciviruses are non-enveloped, positive-sense ssRNA viruses. * **D. Defective virus:** This refers to **Hepatitis D Virus (HDV)**. It is considered a "subviral satellite" because it requires the surface antigen (HBsAg) of HBV to package its genome and infect other cells. **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic for Genomes:** All Hepatitis viruses are **RNA** viruses EXCEPT **Hepatitis B** (DNA). * **Transmission:** Hepatitis **A** and **E** are transmitted via the **fecal-oral** route (Vowels hit the Bowels). Hepatitis **B, C, and D** are transmitted parenterally. * **Chronic State:** Hepatitis A and E **never** cause chronic infection (exception: HEV in transplant recipients). HBV, HCV, and HDV are associated with chronic carrier states and Hepatocellular Carcinoma (HCC). * **Hepatitis A:** Belongs to the **Picornaviridae** family (Genus: *Hepatovirus*). It is a non-enveloped ssRNA virus.

Question 193: Influenza pandemics are primarily caused by which of the following mechanisms?

A. Antigenic shift (Correct Answer)
B. Antigenic drift
C. Different strains
D. All of the above

Explanation: **Explanation:** The primary mechanism behind influenza pandemics is **Antigenic Shift**. This occurs when two different strains of Influenza A virus infect the same host cell (usually in pigs or birds), leading to **genetic reassortment**. Because the influenza genome is **segmented** (8 segments), these segments can mix to create a completely new subtype with novel Hemagglutinin (H) or Neuraminidase (N) proteins (e.g., H1N1 shifting to H2N2). Since the global population has no pre-existing immunity to this new subtype, it spreads rapidly, causing a **pandemic**. **Analysis of Options:** * **Antigenic Drift (Option B):** This involves minor point mutations in the H or N genes. It leads to gradual changes, causing **seasonal epidemics** rather than pandemics. This is why the influenza vaccine must be updated annually. * **Different Strains (Option C):** While different strains exist, the mere presence of variety does not cause a pandemic; it is the sudden, major genetic shift between them that triggers global outbreaks. **High-Yield Clinical Pearls for NEET-PG:** * **Shift vs. Drift:** Remember: **S**hift = **S**udden (Pandemic); **D**rift = **D**radual (Epidemic). * **Virus Type:** Antigenic shift occurs **only in Influenza A** (due to its wide host range including animals). Influenza B only undergoes antigenic drift. * **Genome:** Influenza is a single-stranded, negative-sense RNA virus with a **segmented genome**, which is the prerequisite for reassortment. * **Drugs of Choice:** Oseltamivir (Neuraminidase inhibitor) is the standard treatment for both seasonal and pandemic strains.

Question 194: Which of the following is an important feature of AIDS?

A. Follicular tonsillitis
B. Lichen planus
C. Oral candidiasis (Correct Answer)
D. Hairy leukoplakia

Explanation: **Explanation:** **Oral candidiasis** (thrush) is the correct answer because it is one of the most common and early opportunistic infections seen in HIV-infected individuals. It typically occurs when the **CD4+ T-lymphocyte count falls below 200–500 cells/mm³**. In the context of AIDS, it serves as a clinical marker of disease progression and immune failure. While *Oropharyngeal candidiasis* is a common initial presentation, *Esophageal candidiasis* is classified as an **AIDS-defining illness**. **Analysis of Options:** * **A. Follicular tonsillitis:** This is typically a bacterial infection (most commonly *Streptococcus pyogenes*) seen in immunocompetent individuals. It is not a characteristic or diagnostic feature of HIV/AIDS. * **B. Lichen planus:** This is a chronic inflammatory condition affecting mucous membranes, often associated with Hepatitis C, but it is not a hallmark of AIDS. * **D. Hairy leukoplakia:** While Oral Hairy Leukoplakia (caused by EBV) is highly suggestive of HIV infection, **Oral Candidiasis** is considered a more "important" and frequent clinical feature used for staging and monitoring the severity of immunosuppression in global clinical guidelines. (Note: If the question asks for the *most common* or *earliest* sign, Candidiasis remains the primary clinical indicator). **NEET-PG High-Yield Pearls:** * **Most common fungal infection in AIDS:** Candidiasis. * **AIDS-defining fungal infections:** Esophageal candidiasis, Cryptococcosis (extrapulmonary), and Pneumocystis jirovecii pneumonia (PCP). * **CD4 Count Correlation:** * <500: Oral Candidiasis, Kaposi Sarcoma. * <200: PCP, Esophageal Candidiasis. * <100: Toxoplasmosis, Cryptococcosis. * <50: CMV retinitis, Mycobacterium avium complex (MAC).

Question 195: Late onset hemorrhagic cystitis after bone marrow transplantation is caused by which of the following?

A. Cyclophosphamide
B. Ifosfamide
C. Adenovirus (Correct Answer)
D. Cytomegalovirus

Explanation: **Explanation:** Hemorrhagic cystitis (HC) is a common complication following hematopoietic stem cell transplantation (HSCT). The etiology is typically divided into **early-onset** (within days) and **late-onset** (weeks to months post-transplant). **1. Why Adenovirus is correct:** Late-onset hemorrhagic cystitis is predominantly caused by viral infections due to prolonged immunosuppression. **Adenovirus (Serotypes 11 and 21)** is the most common viral cause. It typically occurs after engraftment (usually >2 weeks post-transplant). Another common viral culprit is the **BK Polyomavirus**, but Adenovirus remains a classic high-yield answer for this presentation in the context of HSCT. **2. Why the other options are incorrect:** * **Cyclophosphamide & Ifosfamide:** These are chemotherapeutic agents that cause **early-onset** hemorrhagic cystitis. They produce a toxic metabolite called **Acrolein**, which irritates the bladder urothelium. This is prevented by aggressive hydration and the administration of **MESNA**. * **Cytomegalovirus (CMV):** While CMV is a major cause of post-transplant morbidity (causing pneumonia, retinitis, or colitis), it is a very rare cause of hemorrhagic cystitis compared to Adenovirus and BK virus. **High-Yield Clinical Pearls for NEET-PG:** * **Early-onset HC (<7 days):** Chemical/Drug-induced (Cyclophosphamide/Ifosfamide). * **Late-onset HC (>7 days):** Viral-induced (Adenovirus, BK virus). * **Adenovirus Serotypes:** 11 and 21 are specifically associated with the urinary tract. * **Diagnosis:** Detection of viral DNA in urine or blood via PCR. * **Treatment:** Primarily supportive hydration; Cidofovir may be used in severe viral cases.

Question 196: Malnourished children are at increased risk for complications of measles, leading to greater morbidity and mortality. Which of the following vitamins should be administered to these children to reduce these risks?

A. Vitamin A (Correct Answer)
B. Vitamin B
C. Vitamin C
D. Vitamin D

Explanation: **Explanation:** **1. Why Vitamin A is the Correct Answer:** Measles virus significantly depletes Vitamin A stores in the body, leading to a state of "secondary deficiency." Vitamin A is essential for maintaining the integrity of epithelial surfaces (respiratory, intestinal, and ocular) and for the proper functioning of the immune system. In malnourished children, this deficiency impairs the body's ability to regenerate damaged mucosal barriers, leading to severe complications such as **blindness (keratomalacia)**, **severe pneumonia**, and **croup**. The World Health Organization (WHO) recommends Vitamin A supplementation for all children with acute measles. It has been clinically proven to reduce the severity of the disease, decrease the risk of secondary infections, and significantly lower the mortality rate. **2. Why Other Options are Incorrect:** * **Vitamin B:** While B-complex vitamins are essential for metabolism, they do not play a specific role in the pathogenesis or recovery of measles-related mucosal damage. * **Vitamin C:** Although an antioxidant that supports general immunity, there is no evidence that Vitamin C reduces the specific complications or mortality associated with measles. * **Vitamin D:** While important for bone health and general immune modulation, it is not the standard of care or the specific nutrient depleted during a measles infection. **3. High-Yield Clinical Pearls for NEET-PG:** * **Dosage:** Administer two doses, 24 hours apart: * < 6 months: 50,000 IU * 6–11 months: 100,000 IU * ≥ 12 months: 200,000 IU * **Koplik Spots:** Pathognomonic sign found on the buccal mucosa opposite the lower 2nd molars. * **SSPE (Subacute Sclerosing Panencephalitis):** The most dreaded late complication of measles, occurring years after the initial infection. * **Most Common Complication:** Otitis media. * **Most Common Cause of Death:** Pneumonia (Hecht’s Giant Cell Pneumonia).

Question 197: Which of the following statements regarding Hepatitis G virus is FALSE?

A. It is also called GB virus.
B. It is a blood-borne RNA virus.
C. It is mostly infected with Hepatitis C virus.
D. It responds to Lamivudine. (Correct Answer)

Explanation: **Explanation:** The Hepatitis G Virus (HGV), also known as **GB virus C (GBV-C)**, belongs to the *Flaviviridae* family. The correct answer is **D** because HGV is an **RNA virus**, and **Lamivudine** is a nucleoside reverse transcriptase inhibitor (NRTI) used primarily for DNA viruses like Hepatitis B (HBV) and retroviruses like HIV. It has no therapeutic efficacy against HGV. **Analysis of Options:** * **Option A (True):** HGV was independently discovered and named GB virus C. While they are slightly different isolates, they are considered the same virus species. * **Option B (True):** It is a positive-sense, single-stranded **RNA virus**. It is primarily transmitted through **blood and blood products**, similar to HBV and HCV. * **Option C (True):** HGV is frequently found as a **co-infection**, most commonly with **Hepatitis C virus (HCV)** (up to 10-20% of cases) and HIV, due to shared parenteral transmission routes. **High-Yield Clinical Pearls for NEET-PG:** * **Pathogenicity:** Unlike other hepatitis viruses, HGV is generally considered **non-pathogenic**. It does not cause significant liver disease, chronic hepatitis, or cirrhosis on its own. * **HIV Interaction:** Interestingly, co-infection with HGV in HIV-positive patients is associated with **slower progression to AIDS** and improved survival rates (HGV interferes with HIV entry/replication). * **Diagnosis:** Since it does not cause clinical disease, routine screening is not recommended. Diagnosis is made via **RT-PCR** for viral RNA. * **Treatment:** There is no specific treatment indicated for HGV; however, it may incidentally respond to **Interferon-alpha** (used for HCV), but never to Lamivudine.

Question 198: A 33-year-old nurse suffered a needle stick injury. The patient used illicit intravenous drugs. One month later, the nurse developed jaundice. Which of the following findings would implicate hepatitis B as the etiology?

A. Positive anti-hepatitis A antibody
B. Positive hepatitis B surface antigen (Correct Answer)
C. Positive anti-hepatitis B-core antibody
D. Positive anti-hepatitis B surface antibody

Explanation: ### Explanation **Correct Option: B. Positive hepatitis B surface antigen (HBsAg)** The clinical presentation of jaundice one month after a needle stick injury (a high-risk parenteral exposure) suggests acute viral hepatitis. **HBsAg** is the first serological marker to appear in the blood during an acute Hepatitis B infection, typically detectable 1 to 10 weeks after exposure and before the onset of clinical symptoms or jaundice. Its presence indicates an active infection (either acute or chronic). In this scenario, the timing and positive HBsAg confirm Hepatitis B as the etiology. **Analysis of Incorrect Options:** * **A. Positive anti-hepatitis A antibody:** Anti-HAV IgM indicates acute Hepatitis A, which is primarily transmitted via the fecal-oral route, not needle stick injuries. * **C. Positive anti-hepatitis B-core antibody (Anti-HBc):** While Anti-HBc IgM appears during acute infection, the question asks for a finding that *implicates* the virus. HBsAg is the definitive hallmark of active infection. Furthermore, Anti-HBc IgG alone would signify a past infection, not necessarily the cause of current jaundice. * **D. Positive anti-hepatitis B surface antibody (Anti-HBs):** This antibody indicates **immunity** (either from prior vaccination or recovery from a past infection). It is not present during the acute phase of the illness when the patient is jaundiced. **NEET-PG High-Yield Pearls:** * **HBsAg:** First marker to appear; indicates active infection. * **HBeAg:** Indicates high viral replication and high infectivity. * **Anti-HBc IgM:** The best marker for diagnosing acute HBV during the **"Window Period"** (the gap where HBsAg disappears but Anti-HBs hasn't appeared yet). * **Anti-HBs:** The only marker positive after successful HBV vaccination. * **Post-exposure prophylaxis (PEP):** For a needle stick in an unvaccinated individual, both HBV vaccine and Hepatitis B Immune Globulin (HBIG) should be administered.

Question 199: Which of the following is NOT a prion disease?

A. Bovine spongiform encephalopathy
B. Transmissible mink encephalopathy
C. Scrapie
D. Progressive multifocal leucoencephalopathy (Correct Answer)

Explanation: **Explanation:** The correct answer is **D. Progressive multifocal leucoencephalopathy (PML)**. The fundamental distinction lies in the causative agent. **Prion diseases** (Transmissible Spongiform Encephalopathies) are caused by **prions**, which are misfolded, infectious proteins (PrPSc) that lack nucleic acids. In contrast, **PML** is a viral disease caused by the **JC virus** (a double-stranded DNA Polyomavirus). PML occurs due to the reactivation of the JC virus in immunocompromised individuals (e.g., AIDS patients), leading to the destruction of oligodendrocytes and subsequent CNS demyelination. **Analysis of Incorrect Options:** * **Bovine Spongiform Encephalopathy (BSE):** Also known as "Mad Cow Disease," this is a classic prion disease in cattle that can be transmitted to humans as variant Creutzfeldt-Jakob Disease (vCJD). * **Transmissible Mink Encephalopathy (TME):** A rare, fatal neurodegenerative prion disease affecting farmed mink. * **Scrapie:** The prototypical prion disease found in sheep and goats, characterized by intense pruritus (leading animals to "scrape" against fences) and ataxia. **High-Yield Clinical Pearls for NEET-PG:** * **Prion Characteristics:** Resistant to standard sterilization (autoclaving at 121°C). They require **134°C for 1 hour** or immersion in **1N NaOH** for disinfection. * **Histopathology:** Prion diseases show "spongiform change" (vacuolation of neurons/gray matter) without any inflammatory response. * **Human Prion Diseases:** Include Kuru (associated with cannibalism), Creutzfeldt-Jakob Disease (CJD), Gerstmann-Sträussler-Scheinker syndrome (GSS), and Fatal Familial Insomnia (FFI). * **PML Hallmark:** On MRI, it presents as multifocal, non-enhancing white matter lesions without mass effect.

Question 200: Which of the following is also known as Australia antigen?

A. HBsAg (Correct Answer)
B. HBeAg
C. HBcAg
D. HBV DNA

Explanation: ### Explanation **Correct Answer: A. HBsAg** **Why HBsAg is the correct answer:** HBsAg (Hepatitis B surface antigen) is historically known as the **Australia antigen**. It was discovered in 1965 by **Baruch Blumberg** in the serum of an Australian Aboriginal person while he was studying serum protein polymorphisms. This discovery was pivotal as it led to the identification of the Hepatitis B virus (HBV). HBsAg is the first serological marker to appear in the blood after infection (even before symptoms) and its persistence beyond 6 months indicates chronic infection. **Analysis of Incorrect Options:** * **B. HBeAg (Envelope antigen):** This is a marker of **active viral replication** and high infectivity. It is a soluble protein secreted into the blood but was not the antigen discovered by Blumberg. * **C. HBcAg (Core antigen):** This is a particulate antigen found within the hepatocyte nuclei. It is **not detectable in serum** because it is sequestered within the HBsAg coat. * **D. HBV DNA:** This represents the viral load and is the most sensitive marker for viral replication, detected via PCR. **High-Yield Clinical Pearls for NEET-PG:** * **Window Period:** The interval during which HBsAg has disappeared but Anti-HBs has not yet appeared. The only marker present during this time is **Anti-HBc IgM**. * **Dane Particle:** The complete infectious virion of HBV (42 nm). * **Screening:** HBsAg is the standard marker used for screening blood donors for Hepatitis B. * **Ground Glass Hepatocytes:** The characteristic histopathological finding in chronic HBV infection, caused by the accumulation of HBsAg in the endoplasmic reticulum.

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