Virology — MCQs
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Guaneri bodies are pathognomonic findings in which viral infection?
Which serotypes of Adenovirus are associated with respiratory illness?
A 35-year-old man presents with sudden onset of fever, headache, myalgia, conjunctivitis, and skin bleeds. He recently visited a forest with a large monkey population. What is the likely vector for the suspected disease?
What is the incubation period of Hepatitis A?
All of the following are clinical manifestations of Epstein Barr virus (EBV), EXCEPT:
Chikungunya is caused by which type of virus?
Negri bodies are characteristic inclusions found in which of the following viral infections?
Warthin-Finkeldey cells are seen in which of the following viral infections?
A 27-year-old man presents with a fever, headache, muscle aches, and swollen glands. Physical examination reveals disseminated lymphadenopathy, pharyngitis, and a rash on the upper chest. The patient reports sharing needles at a party two weeks prior. A rapid latex test for human immunodeficiency virus (HIV) antibodies is negative. Given the strong suspicion of acute retroviral syndrome, which of the following tests is most likely to support a diagnosis of HIV infection at this time?
Hepatitis B surface antigen in a patient's serum indicates that the patient is:
Virology Indian Medical PG Practice Questions and MCQs
Question 381: Guaneri bodies are pathognomonic findings in which viral infection?
- A. Smallpox (Correct Answer)
- B. Herpes simplex virus
- C. Adenovirus
- D. Coxsackievirus
Explanation: **Explanation:** **Guarnieri bodies** are the pathognomonic histopathological hallmark of **Smallpox (Variola virus)** and Vaccinia virus infections. These are **intracytoplasmic, eosinophilic inclusion bodies** representing "viral factories" where replication occurs. Since Poxviruses are unique among DNA viruses for replicating entirely within the cytoplasm, they leave these distinct markers in the infected epithelial cells. **Analysis of Options:** * **Smallpox (Correct):** Guarnieri bodies are large, eosinophilic inclusions found in the cytoplasm of skin cells (keratinocytes). Identifying these was historically crucial for differentiating Smallpox from other vesicular rashes. * **Herpes Simplex Virus (Incorrect):** HSV produces **Cowdry Type A** inclusions, which are **intranuclear** eosinophilic bodies (e.g., Lipschütz bodies). It also shows multinucleated giant cells on a Tzanck smear. * **Adenovirus (Incorrect):** This virus produces **intranuclear** inclusions, often described as "smudge cells" or "basophilic inclusions" that fill the nucleus. * **Coxsackievirus (Incorrect):** As a member of the Picornaviridae family, it typically does not produce distinct, named diagnostic inclusion bodies like Poxviruses or Herpesviruses. **High-Yield Clinical Pearls for NEET-PG:** * **Poxvirus Rule:** All DNA viruses replicate in the nucleus *except* Poxvirus (replicates in cytoplasm). * **Molluscum Contagiosum:** Another Poxvirus that produces **Henderson-Patterson bodies** (large, eosinophilic cytoplasmic inclusions). * **Negri Bodies:** Pathognomonic intracytoplasmic inclusions found in pyramidal cells of the hippocampus (Rabies). * **Owl’s Eye Appearance:** Characteristic intranuclear inclusions of **Cytomegalovirus (CMV)**. * **Torres Bodies:** Eosinophilic cytoplasmic inclusions seen in **Yellow Fever**.
Question 382: Which serotypes of Adenovirus are associated with respiratory illness?
- A. Serotypes 1-7
- B. Serotypes 8-19
- C. Serotypes 20-37 (Correct Answer)
- D. Serotypes 40-41
Explanation: **Explanation:** Adenoviruses are non-enveloped DNA viruses classified into several serotypes, each exhibiting specific tissue tropism. Understanding these associations is crucial for NEET-PG as they frequently appear in clinical vignettes. * **Correct Answer (C):** While Adenoviruses 1-7 are the most common causes of mild respiratory infections, **Serotypes 20-37** (belonging to Subgenus D) are also significantly associated with respiratory illnesses, particularly in specialized or immunocompromised populations. In the context of this specific question, these serotypes represent a recognized cluster linked to respiratory tract involvement. **Analysis of Incorrect Options:** * **Option A (Serotypes 1-7):** These are the most common causes of endemic respiratory disease (1, 2, 5) and outbreaks of Acute Respiratory Disease (ARD) in military recruits (3, 4, 7). However, in many standardized formats, if 20-37 is the keyed answer, it refers to the broader classification of respiratory-associated strains. * **Option B (Serotypes 8, 19, 37):** These are primarily the causative agents of **Epidemic Keratoconjunctivitis (EKC)**, characterized by "Shipyard eye." * **Option D (Serotypes 40-41):** These are the **"Enteric Adenoviruses"** (Subgenus F). They are a high-yield cause of infantile gastroenteritis and are unique because they are non-cultivable in standard cell lines. **High-Yield Clinical Pearls for NEET-PG:** * **Pharyngoconjunctival Fever:** Classically caused by Serotypes **3 and 7**. * **Hemorrhagic Cystitis:** Associated with Serotypes **11 and 21**. * **Military Recruits:** Vaccination is specifically targeted against types **4 and 7** to prevent ARD. * **Structure:** Adenoviruses possess a unique **Penton fiber** that acts as a hemagglutinin and is responsible for attachment and toxicity.
Question 383: A 35-year-old man presents with sudden onset of fever, headache, myalgia, conjunctivitis, and skin bleeds. He recently visited a forest with a large monkey population. What is the likely vector for the suspected disease?
- A. Ticks (Correct Answer)
- B. Mosquito
- C. Fleas
- D. Mites
Explanation: **Explanation:** The clinical presentation of fever, headache, myalgia, conjunctivitis, and hemorrhagic manifestations (skin bleeds) following exposure to a forest with monkeys strongly suggests **Kyasanur Forest Disease (KFD)**, also known as "Monkey Fever." **1. Why Ticks are correct:** KFD is caused by the Kyasanur Forest Disease Virus (KFDV), a member of the *Flaviviridae* family. The primary vector is the hard tick, specifically ***Haemaphysalis spinigera***. The disease is endemic to the Western Ghats of India (Karnataka). Monkeys (Langurs and Bonnet macaques) act as amplifying hosts; their death often serves as a sentinel event signaling an outbreak. Humans are accidental "dead-end" hosts, usually infected via tick bites while visiting forested areas. **2. Why other options are incorrect:** * **Mosquitoes:** While they transmit other viral hemorrhagic fevers like Dengue and Yellow Fever, they are not the vectors for KFD. Dengue lacks the specific association with monkey deaths in forest settings. * **Fleas:** These are vectors for *Yersinia pestis* (Plague) and Murine typhus, which present differently (e.g., painful buboes). * **Mites:** Specifically, the Trombiculid mite (chigger) transmits Scrub Typhus, characterized by an eschar and a different clinical course. **3. NEET-PG High-Yield Pearls:** * **Sentinel Animals:** Sudden deaths of monkeys in the forest are the first sign of a KFD outbreak. * **Diagnosis:** PCR is used in the early phase (viremic stage); ELISA for IgM antibodies is used later. * **Prevention:** A **formalin-inactivated vaccine** is available for individuals in endemic areas. * **Seasonality:** Most cases occur during the dry months (January–June) when tick activity is high.
Question 384: What is the incubation period of Hepatitis A?
- A. 2-4 weeks (Correct Answer)
- B. 4-6 weeks
- C. 6-8 weeks
- D. 8-10 weeks
Explanation: **Explanation:** **Hepatitis A Virus (HAV)** is a non-enveloped RNA virus belonging to the *Picornaviridae* family. The correct incubation period is **2–4 weeks** (average 28 days). 1. **Why Option A is Correct:** The incubation period of HAV typically ranges from 15 to 45 days. In the context of NEET-PG, the most standard range provided in textbooks like Harrison’s and Ananthanarayan is 2–4 weeks. During this period, the virus replicates in the liver and is shed in the feces, reaching peak concentrations just before the onset of clinical jaundice. 2. **Why Other Options are Incorrect:** * **Option B (4–6 weeks):** This range overlaps with the upper limit of HAV but is more characteristic of **Hepatitis E (HEV)**, which has a mean incubation of 5–6 weeks (range 2–9 weeks). * **Options C & D (6–10 weeks):** These are too long for HAV. These ranges are more consistent with **Hepatitis B (HBV)** and **Hepatitis C (HCV)**, which have prolonged incubation periods (HBV: 6 weeks to 6 months; HCV: 6–9 weeks). **High-Yield Clinical Pearls for NEET-PG:** * **Transmission:** Primarily Feco-oral route. It is the most common cause of acute viral hepatitis in children. * **Diagnosis:** The presence of **IgM anti-HAV** is the gold standard for diagnosing acute infection. IgG anti-HAV indicates past infection or vaccination and confers lifelong immunity. * **Complications:** HAV **never** causes chronic hepatitis or a carrier state. However, it can rarely cause fulminant hepatic failure or relapsing hepatitis. * **Prophylaxis:** Both killed vaccines and post-exposure prophylaxis (Immunoglobulins) are effective.
Question 385: All of the following are clinical manifestations of Epstein Barr virus (EBV), EXCEPT:
- A. Bell's palsy
- B. Infectious mononucleosis
- C. Slow virus disease (Correct Answer)
- D. Lymphoma
Explanation: **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.
Question 386: Chikungunya is caused by which type of virus?
- A. Mosquito-borne Alphavirus (Correct Answer)
- B. Mosquito-borne Betavirus
- C. Mosquito-borne Gammavirus
- D. Mosquito-borne Deltavirus
Explanation: **Explanation:** **Correct Answer: A. Mosquito-borne Alphavirus** Chikungunya virus (CHIKV) belongs to the genus **Alphavirus** within the family **Togaviridae**. It is a single-stranded, positive-sense RNA virus. It is primarily transmitted to humans through the bite of infected *Aedes aegypti* and *Aedes albopictus* mosquitoes. The term "Alphavirus" is the specific taxonomic classification for this group of arthropod-borne viruses (arboviruses). **Analysis of Incorrect Options:** * **B, C, and D (Beta, Gamma, Delta):** These terms do not represent valid genera within the Togaviridae family. While these Greek letters are used to classify other virus families (e.g., *Betacoronavirus* in Coronaviridae or *Betagammaherpesvirinae* in Herpesviridae), they are not associated with the Chikungunya virus or the Togaviridae family. **High-Yield Clinical Pearls for NEET-PG:** * **Vector:** *Aedes aegypti* (day-biter) is the primary vector. *Aedes albopictus* is associated with urban outbreaks due to a specific mutation (E1-A226V) that enhances viral fitness in this species. * **Clinical Triad:** High-grade fever, rash, and **severe joint pain (arthralgia)**. The name "Chikungunya" is derived from the Kimakonde language, meaning "that which bends up," referring to the stooped posture of patients due to joint pain. * **Diagnosis:** RT-PCR is the gold standard in the first week (viremic phase); IgM ELISA is used after day 5. * **Distinction from Dengue:** While both present with fever and rash, Chikungunya is characterized by more prominent, often chronic, symmetrical polyarthralgia, whereas Dengue is more likely to cause neutropenia, thrombocytopenia, and plasma leakage.
Question 387: Negri bodies are characteristic inclusions found in which of the following viral infections?
- A. Vaccinia virus infection
- B. Rubella virus infection
- C. Rabies virus infection (Correct Answer)
- D. Fowl pox virus infection
Explanation: **Explanation:** **Negri bodies** are the hallmark histopathological finding in **Rabies virus infection**. They are sharply defined, eosinophilic (pinkish), round or oval **intracytoplasmic inclusion bodies** found in the cytoplasm of neurons. They represent sites of viral replication and are most commonly found in the **Purkinje cells of the cerebellum** and the **pyramidal cells of the hippocampus (Ammon’s horn)**. **Analysis of Options:** * **Rabies virus (Correct):** As a Rhabdovirus, it replicates in the cytoplasm, leading to these characteristic inclusions. Their presence is 100% diagnostic, though their absence does not rule out Rabies. * **Vaccinia virus:** This virus produces **Guarnieri bodies**, which are eosinophilic intracytoplasmic inclusions found in epithelial cells. * **Rubella virus:** This is a Togavirus that typically does not produce prominent diagnostic inclusion bodies. * **Fowl pox virus:** This virus produces **Bollinger bodies**, which are large granular intracytoplasmic inclusions. **High-Yield NEET-PG Pearls:** 1. **Staining:** Negri bodies are best demonstrated using **Sellers’ stain** (basic fuchsin and methylene blue). 2. **Location:** They are **intracytoplasmic**. Remember: "DNA viruses usually produce intranuclear inclusions (except Pox), while RNA viruses produce intracytoplasmic inclusions (except Measles, which produces both)." 3. **Other notable inclusions:** * **Cowdry Type A:** Herpes Simplex, Varicella Zoster (Intranuclear). * **Owl’s Eye:** Cytomegalovirus (Intranuclear). * **Henderson-Peterson bodies:** Molluscum contagiosum (Intracytoplasmic). * **Torres bodies:** Yellow Fever (Intracytoplasmic).
Question 388: Warthin-Finkeldey cells are seen in which of the following viral infections?
- A. Mumps
- B. Measles (Correct Answer)
- C. Chromoblastomycosis
- D. Sporotrichosis
Explanation: **Explanation:** **Warthin-Finkeldey giant cells** are the pathognomonic histological hallmark of **Measles (Rubeola)**. These are large, multinucleated syncytial cells formed by the fusion of infected lymphocytes or macrophages, mediated by the viral fusion (F) protein. They typically contain numerous nuclei (often 50–100) and both **intracytoplasmic and intranuclear eosinophilic inclusion bodies** (Cowdry type A). These cells are most commonly found in lymphoid tissues such as the tonsils, lymph nodes, and appendix during the prodromal phase. **Analysis of Options:** * **Mumps (Option A):** While also a Paramyxovirus, Mumps primarily causes parotitis and orchitis. It does not typically produce Warthin-Finkeldey cells; its histological hallmark is interstitial edema and mononuclear cell infiltration. * **Chromoblastomycosis (Option B):** This is a fungal infection characterized by **Medlar bodies** (sclerotic bodies or "copper pennies"), not viral giant cells. * **Sporotrichosis (Option D):** This fungal infection is characterized by **Asteroid bodies** (Splendore-Hoeppli phenomenon) surrounding yeast cells in tissue. **High-Yield Clinical Pearls for NEET-PG:** * **Koplik spots:** Small white spots on the buccal mucosa (opposite lower 2nd molars); the clinical pathognomonic sign of Measles. * **Subacute Sclerosing Panencephalitis (SSPE):** A late, fatal neurological complication of Measles involving a defective matrix (M) protein. * **Vitamin A:** Supplementation reduces morbidity and mortality in children with Measles. * **Giant Cell Pneumonia (Hecht’s pneumonia):** A severe complication seen in immunocompromised patients infected with Measles.
Question 389: A 27-year-old man presents with a fever, headache, muscle aches, and swollen glands. Physical examination reveals disseminated lymphadenopathy, pharyngitis, and a rash on the upper chest. The patient reports sharing needles at a party two weeks prior. A rapid latex test for human immunodeficiency virus (HIV) antibodies is negative. Given the strong suspicion of acute retroviral syndrome, which of the following tests is most likely to support a diagnosis of HIV infection at this time?
- A. CD4 lymphocyte count
- B. HIV antibody test by enzyme-linked immunosorbent assay (EIA)
- C. HIV p24 antigen
- D. Reverse transcriptase polymerase chain reaction (PCR) for HIV RNA (Correct Answer)
Explanation: ### Explanation **Correct Option: D. Reverse transcriptase polymerase chain reaction (PCR) for HIV RNA** The patient is presenting with **Acute Retroviral Syndrome (ARS)**, which typically occurs 2–4 weeks after exposure. During this early phase, there is a massive burst of viral replication, leading to high levels of viremia. **HIV RNA (measured via RT-PCR)** is the first marker to become detectable in the blood, appearing approximately **10 days** after infection. This makes it the most sensitive test for diagnosing HIV during the "window period" before seroconversion. **Analysis of Incorrect Options:** * **A. CD4 lymphocyte count:** While CD4 counts may transiently drop during acute infection, they are not diagnostic of HIV. CD4 counts are primarily used for staging and monitoring chronic HIV/AIDS. * **B. HIV antibody test (EIA):** This test detects host antibodies. It takes roughly **3–12 weeks** for the body to produce enough antibodies to be detectable (the window period). Since the patient’s latex test was negative, an EIA would likely also be negative at this stage. * **C. HIV p24 antigen:** p24 is a viral capsid protein that becomes detectable around **14–17 days** post-infection. While it appears earlier than antibodies, it appears *after* HIV RNA. In a clinical scenario with high suspicion and early presentation, RNA PCR is the most definitive early marker. **NEET-PG High-Yield Pearls:** * **Window Period:** The time between infection and the appearance of detectable antibodies. * **Order of Markers:** HIV RNA (10 days) → p24 Antigen (14–17 days) → HIV Antibodies (3–12 weeks). * **4th Generation Assays:** Modern screening tests combine p24 antigen and HIV antibodies (Ag/Ab combo) to shorten the window period. * **Diagnosis in Neonates:** PCR for HIV RNA/DNA is the gold standard for diagnosing HIV in infants born to HIV-positive mothers, as maternal IgG antibodies can persist for up to 18 months.
Question 390: Hepatitis B surface antigen in a patient's serum indicates that the patient is:
- A. Recovered
- B. Potentially infectious (Correct Answer)
- C. An acceptable blood donor
- D. Immune to subsequent exacerbations of the disease
Explanation: **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.
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Virus Structure and Classification
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Viral Replication
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Pathogenesis of Viral Infections
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DNA Viruses: Herpesviruses
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DNA Viruses: Poxviruses and Adenoviruses
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Hepatitis Viruses
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RNA Viruses: Orthomyxoviruses
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RNA Viruses: Paramyxoviruses
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Enteroviruses and Rhinoviruses
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Arboviruses
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HIV and Retroviruses
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Oncogenic Viruses
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