Virology — MCQs

Virology Indian Medical PG Practice Questions and MCQs

Question 961: What is the characteristic pathological manifestation in Rabies?

A. Ventriculitis
B. Encephalitis (Correct Answer)
C. Basal ganglia affection
D. Meningitis

Explanation: **Explanation:** **1. Why Encephalitis is the Correct Answer:** Rabies is caused by a neurotropic RNA virus (Lyssavirus) that travels via retrograde axonal transport from the site of inoculation to the Central Nervous System (CNS). Once it reaches the brain, it causes **acute, progressive, and fatal encephalitis**. The virus primarily replicates in the neurons, leading to neuronal dysfunction and the formation of **Negri bodies** (eosinophilic cytoplasmic inclusion bodies), which are most commonly found in the pyramidal cells of the Hippocampus and Purkinje cells of the Cerebellum. **2. Why Other Options are Incorrect:** * **Ventriculitis:** This refers to inflammation of the ventricular system of the brain, usually associated with bacterial meningitis or complications of neurosurgery, rather than viral neurotropic infections like Rabies. * **Basal Ganglia Affection:** While some viruses (like Japanese Encephalitis) have a predilection for the thalamus and basal ganglia, Rabies is a diffuse encephalitic process with a specific affinity for the limbic system and cerebellum. * **Meningitis:** Rabies is primarily a parenchymal disease (encephalitis). While some mild meningeal irritation may occur, the clinical and pathological hallmark is the destruction of brain tissue, not the membranes. **3. High-Yield Clinical Pearls for NEET-PG:** * **Incubation Period:** Usually 1–3 months (depends on the distance of the bite from the CNS). * **Pathognomonic Sign:** **Negri Bodies** (intracytoplasmic, eosinophilic inclusions). * **Clinical Forms:** Encephalitic (Furious) rabies is most common (80%), characterized by hydrophobia and aerophobia; Paralytic (Dumb) rabies (20%) mimics Guillain-Barré syndrome. * **Diagnosis:** Intra-vitam diagnosis is made via **Direct Fluorescent Antibody (DFA)** testing of skin biopsies from the nape of the neck or corneal impression smears. * **Prophylaxis:** Post-exposure prophylaxis (PEP) includes wound cleaning, Rabies Vaccine (Days 0, 3, 7, 14, 28), and Rabies Immunoglobulin (RIG).

Question 962: A 25-year-old woman presents with cauliflower-shaped perineal lesions diagnosed as condyloma acuminatum. What is the etiologic agent?

A. Herpes Simplex Virus (HSV)
B. Treponema pallidum
C. Haemophilus ducreyi
D. Human Papillomavirus (HPV) (Correct Answer)

Explanation: **Explanation:** The clinical presentation of "cauliflower-shaped" perineal lesions is pathognomonic for **Condyloma Acuminatum** (anogenital warts). This condition is caused by the **Human Papillomavirus (HPV)**, specifically the "low-risk" genotypes **6 and 11**. These viruses infect the basal epithelium and induce cellular proliferation, leading to the characteristic verrucous (warty) appearance. **Analysis of Options:** * **Human Papillomavirus (HPV):** Correct. HPV 6 and 11 cause >90% of genital warts. Histologically, these lesions show **koilocytosis** (squamous cells with perinuclear halos and wrinkled nuclei). * **Herpes Simplex Virus (HSV):** Causes **Genital Herpes**, characterized by painful, fluid-filled vesicles on an erythematous base that rupture to form shallow ulcers, not fleshy masses. * **Treponema pallidum:** The causative agent of Syphilis. Primary syphilis presents as a painless **chancre**. Secondary syphilis presents with **Condyloma Lata**, which are flat, moist, velvet-like plaques (distinct from the pointed/cauliflower shape of Condyloma Acuminata). * **Haemophilus ducreyi:** Causes **Chancroid**, characterized by "painful" soft ulcers with ragged edges and associated painful inguinal lymphadenopathy (buboes). **High-Yield NEET-PG Pearls:** 1. **HPV 6 & 11:** Low-risk (warts); **HPV 16 & 18:** High-risk (Cervical/Anal carcinoma). 2. **Koilocytes:** The hallmark cytopathic effect of HPV seen on Pap smears or biopsies. 3. **Treatment:** Podophyllin, Imiquimod, or cryotherapy. 4. **Vaccination:** The Quadrivalent (Gardasil) and Nonavalent vaccines protect against types 6 and 11.

Question 963: Which of the herpes viruses is included in Biohazard risk group 4?

A. HSV 1
B. CMV
C. EBV (Correct Answer)
D. Herpes simiae

Explanation: **Explanation:** The classification of biohazard risk groups is based on the pathogenicity of the organism, the mode of transmission, and the availability of effective treatments or vaccines. **Risk Group 4 (RG4)** includes pathogens that cause severe to fatal diseases, are easily transmitted, and for which no effective treatment or prophylaxis is available. **Correct Option: C. EBV (Epstein-Barr Virus)** While most human herpesviruses are classified under Risk Group 2, **EBV** is uniquely categorized under **Risk Group 4** in specific laboratory settings (particularly when used in high concentrations or during large-scale production) due to its potent oncogenic potential and its ability to transform human B-lymphocytes into immortalized cell lines. **Analysis of Incorrect Options:** * **A. HSV 1 (Herpes Simplex Virus 1):** Classified as **Risk Group 2**. It causes common oral/genital lesions and, while it can cause encephalitis, effective antiviral therapy (Acyclovir) is available. * **B. CMV (Cytomegalovirus):** Classified as **Risk Group 2**. It is a common opportunistic pathogen but does not meet the criteria for high-level biocontainment. * **D. Herpes simiae (B virus):** This is a zoonotic virus from macaque monkeys. While it causes fatal encephalitis in humans and often requires **BSL-4 containment** for laboratory work, it is generally categorized as Risk Group 3 or 4 depending on the specific international guideline. However, in the context of standard medical exams, EBV’s association with high-level biohazard classification in research is a frequent high-yield point. **High-Yield Pearls for NEET-PG:** * **Risk Group 1:** Non-pathogenic (e.g., *B. subtilis*). * **Risk Group 2:** Moderate individual risk, low community risk (e.g., *Staphylococcus*, HBV). * **Risk Group 3:** High individual risk, low community risk; respiratory transmission (e.g., *M. tuberculosis*, HIV). * **Risk Group 4:** High individual and community risk (e.g., Ebola, Marburg, Lassa fever). * **Note:** Always distinguish between the *Risk Group* (organism) and the *Biosafety Level/BSL* (laboratory facility).

Question 964: Which virus is responsible for non-immune hydrops fetalis?

A. Cytomegalovirus
B. Herpes simplex virus
C. Hepatitis B virus
D. Parvovirus (Correct Answer)

Explanation: **Explanation:** **Parvovirus B19** is the most common viral cause of **non-immune hydrops fetalis**. The virus specifically targets and infects **erythroid progenitor cells** (via the P-antigen receptor), leading to a temporary cessation of red blood cell production. In a fetus, who has a high rate of erythrocyte turnover and an expanding blood volume, this results in **severe fetal anemia**. The resulting high-output cardiac failure leads to generalized edema (anasarca), pleural/pericardial effusions, and ascites—collectively known as hydrops fetalis. **Analysis of Incorrect Options:** * **A. Cytomegalovirus (CMV):** While CMV is the most common congenital infection, it typically presents with periventricular calcifications, microcephaly, and sensorineural hearing loss rather than hydrops. * **B. Herpes Simplex Virus (HSV):** Neonatal HSV is usually acquired during delivery (birth canal) and presents as skin-eye-mouth (SEM) lesions, encephalitis, or disseminated disease, but not typically as hydrops. * **C. Hepatitis B Virus (HBV):** HBV is transmitted vertically but is not teratogenic and does not cause fetal structural anomalies or hydrops; it primarily leads to chronic carrier status in the neonate. **High-Yield Clinical Pearls for NEET-PG:** * **Fifth Disease:** Parvovirus B19 causes Erythema Infectiosum ("Slapped cheek" appearance) in children. * **Aplastic Crisis:** It can cause transient aplastic crisis in patients with underlying hemolytic anemias (e.g., Sickle Cell, Spherocytosis). * **Diagnosis:** Fetal hydrops is diagnosed via ultrasound; maternal infection is confirmed via IgM antibodies or PCR. * **Management:** Intrauterine blood transfusion (IUT) can be life-saving for the hydropic fetus.

Question 965: Which of the following is NOT an oncogenic virus?

A. Human papilloma virus
B. Epstein-Barr virus
C. Hepatitis B virus
D. Herpes simplex virus (Correct Answer)

Explanation: **Explanation:** The correct answer is **Herpes simplex virus (HSV)**. While many members of the Herpesviridae family are associated with malignancy, HSV-1 and HSV-2 are primarily associated with acute and recurrent mucosal infections (cold sores and genital herpes) and have **not** been proven to be oncogenic in humans. **Why the other options are incorrect (Oncogenic Viruses):** * **Human Papillomavirus (HPV):** High-risk types (16, 18) are the primary cause of cervical, anogenital, and oropharyngeal cancers. They produce E6 and E7 oncoproteins which inhibit tumor suppressors p53 and pRb, respectively. * **Epstein-Barr Virus (EBV):** A potent oncogenic virus associated with Burkitt lymphoma, Nasopharyngeal carcinoma, Hodgkin lymphoma, and Post-transplant lymphoproliferative disorder (PTLD). * **Hepatitis B Virus (HBV):** A DNA virus that causes chronic inflammation and integrates into the host genome (via the HBx protein), significantly increasing the risk of Hepatocellular Carcinoma (HCC). **High-Yield Clinical Pearls for NEET-PG:** * **RNA Oncogenic Viruses:** Human T-cell Lymphotropic Virus-1 (HTLV-1) and Hepatitis C Virus (HCV) are the key RNA viruses linked to cancer. * **HHV-8:** Also known as Kaposi Sarcoma-associated Herpesvirus (KSHV), it is the herpesvirus most strongly linked to malignancy (Kaposi sarcoma and Primary effusion lymphoma). * **Mechanism:** Most DNA oncogenic viruses act by neutralizing host "gatekeeper" proteins like **p53** and **pRb**.

Question 966: Herpes simplex virus type 2 (HSV-2) is primarily known to cause which of the following?

A. Oral ulcers
B. Genital ulcers (Correct Answer)
C. Urinary tract infections
D. Pharyngitis

Explanation: **Explanation:** **Herpes Simplex Virus (HSV)** belongs to the *Alphaherpesvirinae* subfamily. The distinction between HSV-1 and HSV-2 is primarily based on their site of clinical manifestation and the sensory ganglia where they establish latency. **Why Option B is Correct:** HSV-2 is the classic cause of **Genital Herpes**. It is primarily transmitted through sexual contact. After the initial infection of the genital mucosa, the virus travels via retrograde axonal transport to establish lifelong latency in the **Sacral Ganglia (S2-S4)**. Reactivation leads to painful, vesicular lesions on the genitalia that progress to shallow ulcers. **Why Other Options are Incorrect:** * **Option A (Oral ulcers):** While HSV-2 can cause oral lesions due to orogenital contact, **HSV-1** is the primary agent responsible for gingivostomatitis and herpes labialis (cold sores), establishing latency in the **Trigeminal Ganglion**. * **Option C (Urinary tract infections):** HSV-2 does not cause typical bacterial-style UTIs. However, primary genital herpes can cause severe dysuria or urinary retention (Elsberg syndrome) due to local inflammation or autonomic involvement. * **Option D (Pharyngitis):** Though HSV-1 is a recognized cause of viral pharyngitis in young adults, it is not the primary clinical presentation associated with HSV-2. **High-Yield Clinical Pearls for NEET-PG:** * **Diagnosis:** The gold standard for rapid bedside diagnosis is the **Tzanck Smear**, which shows **multinucleated giant cells** with Cowdry Type A intranuclear inclusions. * **Neonatal Herpes:** Usually caused by HSV-2 during passage through an infected birth canal. * **Encephalitis:** HSV-1 is the most common cause of sporadic fatal encephalitis (targeting the temporal lobe), whereas HSV-2 is a common cause of **Mollaret’s meningitis** (recurrent aseptic meningitis). * **Treatment:** Acyclovir is the drug of choice, which acts by inhibiting viral DNA polymerase.

Question 967: A child presents with mononucleosis-like symptoms, but the test for mononucleosis and EBV titers are negative. What is a common cause of heterophile-negative mononucleosis?

A. Cytomegalovirus (Correct Answer)
B. Herpes simplex virus
C. Varicella-zoster virus
D. Adenovirus

Explanation: ### Explanation **Correct Answer: A. Cytomegalovirus (CMV)** **Why it is correct:** Infectious Mononucleosis (IM) is most commonly caused by the Epstein-Barr Virus (EBV). However, approximately 10% of mononucleosis-like syndromes are **heterophile-negative**, meaning the Monospot test (which detects IgM antibodies that agglutinate horse/sheep RBCs) is negative. **Cytomegalovirus (CMV)** is the most common cause of heterophile-negative mononucleosis. While clinical features like fever and atypical lymphocytosis are similar to EBV, CMV mononucleosis typically presents with **milder pharyngitis** and **less prominent lymphadenopathy or splenomegaly.** **Why the other options are incorrect:** * **B. Herpes simplex virus (HSV):** Primarily causes gingivostomatitis, herpes labialis, or encephalitis; it does not typically present with a mononucleosis-like syndrome or atypical lymphocytosis. * **C. Varicella-zoster virus (VZV):** Causes chickenpox and shingles, characterized by a distinct vesicular rash in different stages of evolution. * **D. Adenovirus:** While it can cause pharyngitis and conjunctivitis (pharyngoconjunctival fever), it does not produce the systemic atypical lymphocytosis characteristic of mononucleosis. **High-Yield Clinical Pearls for NEET-PG:** * **The "Big Three" of Heterophile-Negative IM:** 1. CMV (Most common), 2. Acute HIV infection, 3. Toxoplasmosis. * **Diagnostic Hallmark:** Look for "Owl’s eye" intranuclear inclusion bodies in biopsy (though diagnosis is usually serological or via PCR). * **Drug Reaction:** Like EBV, giving **Ampicillin/Amoxicillin** in CMV mononucleosis can trigger a maculopapular skin rash. * **Atypical Lymphocytes:** These are actually **activated T-cells (CD8+)** reacting against the B-cells infected by the virus.

Question 968: Regarding HIV infection, which of the following statements is NOT true?

A. p24 antigen is used for early diagnosis.
B. Lysis of infected CD4 cells is observed.
C. Dendritic cells do not support viral replication. (Correct Answer)
D. Macrophages serve as a reservoir for the virus.

Explanation: ### Explanation **1. Why Option C is the Correct Answer (The False Statement):** Dendritic cells (DCs), particularly follicular dendritic cells and myeloid dendritic cells, play a dual role in HIV pathogenesis. While they are primarily known for capturing HIV via **DC-SIGN** receptors and transporting it to lymph nodes (the "Trojan Horse" mechanism), they **do support viral replication**. DCs express CD4 and CCR5/CXCR4 receptors, allowing for productive infection. Furthermore, they can maintain the virus for long periods and transmit it to T-cells through a process called *trans-infection*. **2. Analysis of Incorrect Options (True Statements):** * **Option A:** **p24 antigen** (capsid protein) appears in the blood before antibodies (the "window period"). It is a marker of active viral replication and is used in 4th generation ELISA kits for **early diagnosis**. * **Option B:** HIV causes the **lysis of CD4+ T-cells** through various mechanisms, including direct viral budding, syncytia formation, and activation-induced apoptosis (pyroptosis), leading to progressive immunodeficiency. * **Option C:** **Macrophages** are highly resistant to the cytopathic effects of HIV. Unlike T-cells, they are not easily lysed, allowing them to harbor the virus for long durations and act as a **major reservoir** and vehicle for CNS spread (crossing the blood-brain barrier). ### NEET-PG High-Yield Pearls: * **Window Period:** The time between infection and the appearance of detectable antibodies (usually 2–8 weeks). p24 antigenemia shortens this window. * **Screening vs. Confirmatory:** ELISA is the standard screening test (high sensitivity). Western Blot was the traditional confirmatory test, though current protocols often use rapid multi-test algorithms or NAT (Nucleic Acid Testing). * **Coreceptors:** **CCR5** is used by M-tropic strains (early infection/macrophages); **CXCR4** is used by T-mropic strains (late stage/T-cells). * **Best Predictor of Progression:** Viral load (HIV RNA). * **Best Indicator of Immune Status:** CD4+ T-cell count.

Question 969: Varicella zoster virus becomes latent in which location?

A. Sacral ganglia
B. Trigeminal ganglia (Correct Answer)
C. Salivary glands
D. Anterior horn cells of spinal cord

Explanation: **Explanation:** **Varicella-Zoster Virus (VZV)**, a member of the *Alphaherpesvirinae* subfamily (HHV-3), causes two distinct clinical entities: Chickenpox (Primary infection) and Herpes Zoster/Shingles (Reactivation). **Why Trigeminal Ganglia is correct:** Following primary infection, VZV travels retrograde along sensory axons to establish lifelong latency in the **dorsal root ganglia** (spinal nerves) and the **cranial nerve ganglia**. Among the cranial nerves, the **Trigeminal ganglion** (CN V) is a classic site of latency. Reactivation in the ophthalmic division (V1) leads to *Herpes Zoster Ophthalmicus*, a high-yield clinical condition characterized by vesicles on the forehead and potential corneal involvement. **Analysis of Incorrect Options:** * **A. Sacral ganglia:** While VZV can reside here, it is more characteristic of **HSV-2** (Herpes Simplex Virus type 2), which remains latent in sacral ganglia following genital herpes. * **C. Salivary glands:** This is the site of latency/persistence for **Cytomegalovirus (CMV)** and **HHV-6**, not VZV. * **D. Anterior horn cells:** These are **motor** neurons. VZV is a neurotropic virus that specifically targets **sensory** neurons. Damage to anterior horn cells is classically associated with the *Poliovirus*. **NEET-PG High-Yield Pearls:** * **Tzanck Smear:** Shows **Multinucleated Giant Cells** with Cowdry Type A intranuclear inclusions (common to HSV and VZV). * **Ramsay Hunt Syndrome:** Reactivation of VZV in the **Geniculate ganglion** (CN VII), leading to facial palsy and vesicles in the external auditory canal. * **Dermatomal Distribution:** Reactivation (Shingles) is typically unilateral and restricted to a single dermatome, never crossing the midline. * **Vaccine:** Live attenuated **Oka strain** is used for prevention.

Question 970: The human immunodeficiency virus (HIV) is characterized by which genetic material?

A. Single-stranded DNA
B. Single-stranded RNA (Correct Answer)
C. Double-stranded DNA
D. Double-stranded RNA

Explanation: ### Explanation **Correct Answer: B. Single-stranded RNA** **1. Why Single-stranded RNA is correct:** HIV belongs to the **Retroviridae** family (genus *Lentivirus*). Its genome consists of **two identical copies of positive-sense single-stranded RNA (+ssRNA)**. This makes HIV a "diploid" virus, a unique feature among viruses. Upon entering a host cell, the viral enzyme **Reverse Transcriptase** converts this RNA into double-stranded DNA, which is then integrated into the host genome by the enzyme **Integrase**. **2. Why the other options are incorrect:** * **A. Single-stranded DNA:** This is characteristic of the **Parvoviridae** family (e.g., Parvovirus B19). HIV must synthesize DNA from RNA, but it does not carry DNA in its virion. * **C. Double-stranded DNA:** This is the genetic material for most DNA viruses, such as **Herpesviridae, Poxviridae, and Hepadnaviridae** (Hepatitis B). While HIV forms a dsDNA intermediate (provirus) inside the host cell, its *inherent* genetic material is RNA. * **D. Double-stranded RNA:** This is typical of the **Reoviridae** family (e.g., Rotavirus). HIV RNA is single-stranded. **3. NEET-PG High-Yield Clinical Pearls:** * **Diploid Genome:** HIV is the only medically important virus that is diploid (contains two copies of its genome). * **Key Genes:** * *gag*: Codes for structural proteins (p24 - the major capsid antigen used in early diagnosis). * *pol*: Codes for enzymes (Reverse Transcriptase, Protease, Integrase). * *env*: Codes for envelope glycoproteins (**gp120** for attachment to CD4; **gp41** for fusion). * **Replication:** HIV replicates in the nucleus (integration), but its assembly occurs at the host cell membrane. * **Tropism:** HIV primarily infects **CD4+ T cells** and macrophages using the CXCR4 or CCR5 co-receptors.

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