Virology Practice Questions

Q: An emerging viral pathogen causing pyelonephritis in kidney allograft recipients is:

Polyoma virus. **Explanation:** The correct answer is **Polyoma virus**, specifically the **BK virus (BKV)**. **1. Why Polyoma virus is correct:** The Polyomaviridae family includes the BK and JC viruses. BK virus is a significant opportunistic pathogen in immunocompromised individuals, particularly **renal transplant recipients**. Following primary infection in childhood (usually asymptomatic), the virus remains latent in the renal tubular epithelium. In the setting of potent immunosuppression post-transplant, the virus reactivates, leading to **BK virus-associated nephropathy (BKVAN)**. This clinically manifests as tubulointerstitial nephritis or pyelonephritis, often leading to allograft dysfunction or rejection. **2. Why other options are incorrect:** * **JC virus:** While also a Polyomavirus, JC virus primarily targets the CNS. It causes **Progressive Multifocal Leukoencephalopathy (PML)**, a demyelinating disease of the brain, rather than renal pathology. * **Marburg and Ebola viruses:** These are Filoviruses that cause severe **Viral Hemorrhagic Fevers (VHF)**. While they cause multi-organ failure, they are not associated with chronic allograft-related pyelonephritis or transplant-specific opportunistic infections. **3. NEET-PG High-Yield Pearls:** * **Diagnosis:** Look for **"Decoy cells"** (cells with large intranuclear inclusions) in urine cytology. Definitive diagnosis is via renal biopsy showing characteristic viral inclusions. * **Mnemonic:** **B**K virus affects the **B**ladder and **K**idney; **J**C virus affects the **J**unction (CNS). * **Management:** The primary treatment strategy for BKVAN is the reduction of immunosuppressive therapy.

Q: What is the primary receptor for Epstein-Barr virus (EBV)?

Complement receptor 2 (CR2). **Explanation:** The **Epstein-Barr Virus (EBV)**, a member of the *Herpesviridae* family (HHV-4), specifically targets B lymphocytes. The primary mechanism of entry involves the viral envelope glycoprotein **gp350/220** binding to the **Complement Receptor 2 (CR2)**, also known as **CD21**, located on the surface of B cells. This interaction is the classic example of viral tropism in medical microbiology. **Analysis of Options:** * **Option B (Correct):** CR2 (CD21) is the definitive receptor for EBV. It is normally involved in B-cell activation by binding to the C3d component of the complement system. EBV "mimics" this ligand to gain entry. * **Option A:** **CR1 (CD35)** is a receptor for C3b/C4b found on erythrocytes and leukocytes; it does not facilitate EBV entry. * **Option C & D:** **CD19 and CD20** are definitive B-cell markers used in clinical practice (e.g., Rituximab targets CD20), but they do not serve as the primary attachment point for EBV. **High-Yield Clinical Pearls for NEET-PG:** * **Receptor Synonym:** Always remember **CR2 = CD21**. A common mnemonic is *"EBV drinks at the Bar (B-cell) at age 21 (CD21)."* * **Secondary Receptor:** While CD21 is for attachment, EBV uses **MHC Class II** molecules as a co-receptor for membrane fusion. * **Atypical Lymphocytes:** In Infectious Mononucleosis, the "atypical cells" seen on a peripheral smear are **activated CD8+ T-cells** (Downey cells) reacting against the infected B-cells, not the infected B-cells themselves. * **Associated Malignancies:** EBV is strongly linked to Burkitt Lymphoma (t8;14), Nasopharyngeal Carcinoma, and Hodgkin Lymphoma.

Q: What is the serological pattern observed for acute Hepatitis B with active viral replication?

HBsAg, HBeAg, IgM Anti-HBc. **Explanation:** The serological diagnosis of Hepatitis B (HBV) depends on identifying specific antigens and antibodies that appear at different stages of the infection. **Why Option A is Correct:** In **Acute Hepatitis B**, the first marker to appear is **HBsAg** (Hepatitis B Surface Antigen), indicating active infection. The presence of **HBeAg** (Hepatitis B e-Antigen) is a hallmark of **active viral replication** and high infectivity. Crucially, the differentiation between acute and chronic infection relies on the core antibody: **IgM anti-HBc** is the definitive marker for acute infection (it is the only marker present during the "window period" when HBsAg and Anti-HBs are both negative). **Analysis of Incorrect Options:** * **Option B:** HBsAg with **IgG anti-HBc** indicates **Chronic Hepatitis B**. IgG replaces IgM after approximately 6 months. * **Option C:** HBeAg alone is never used for diagnosis; it is a supplemental marker for replication and must be interpreted alongside HBsAg. * **Option D:** HBsAg alone indicates infection but does not specify the stage (acute vs. chronic) or the status of viral replication. **High-Yield NEET-PG Pearls:** 1. **Window Period:** The interval between the disappearance of HBsAg and the appearance of Anti-HBs. The diagnostic marker here is **IgM anti-HBc**. 2. **Best marker for infectivity:** HBeAg (or HBV-DNA levels). 3. **Marker of Immunity:** **Anti-HBs** (following vaccination or recovery). 4. **Chronic Carrier:** Defined by the persistence of HBsAg for >6 months. 5. **First marker to appear:** HBsAg.

Q: What is the protein coat that covers the genetic material in a virus called?

Capsid. ### Explanation **Correct Answer: B. Capsid** **1. Why Capsid is Correct:** The **capsid** is the protective protein shell that surrounds and protects the viral nucleic acid (DNA or RNA). It is composed of repeating protein subunits. Its primary functions are to protect the viral genome from environmental damage (like nucleases) and to facilitate the attachment of the virus to host cell receptors in non-enveloped viruses. **2. Analysis of Incorrect Options:** * **A. Capsomere:** These are the individual morphological subunits that aggregate to form the capsid. A capsid is the complete structure, while capsomeres are its building blocks. * **C. Nucleocapsid:** This term refers to the **combined unit** of the viral genome (nucleic acid) plus the capsid. It is not just the protein coat itself but the entire internal complex. * **D. Envelope:** This is a lipid bilayer membrane derived from the host cell that surrounds the nucleocapsid in certain viruses (e.g., HIV, Influenza). Not all viruses have an envelope; those that don't are called "naked" viruses. **3. NEET-PG High-Yield Clinical Pearls:** * **Symmetry:** Capsids generally exhibit two types of symmetry: **Icosahedral** (e.g., Adenovirus, Poliovirus) or **Helical** (e.g., Rabies, Influenza). * **Antigenicity:** The capsid proteins are highly antigenic and are often the targets for the host's immune response (antibody production). * **Stability:** Non-enveloped (naked) viruses are generally more resistant to heat, detergents, and alcohols compared to enveloped viruses, which are easily inactivated by lipid solvents (like ether or bile salts). * **Rule of Thumb:** All viruses with helical symmetry are enveloped.

Q: Fecal-oral transmission occurs in which of the following?

Poliomyelitis. ### Explanation **Correct Answer: C. Poliomyelitis** **Mechanism of Transmission:** Poliovirus belongs to the **Picornaviridae** family (Genus: *Enterovirus*). The primary mode of transmission is the **fecal-oral route**, occurring through the ingestion of contaminated water or food. After ingestion, the virus replicates in the oropharynx and the Peyer’s patches of the small intestine before spreading to the regional lymph nodes and entering the bloodstream (primary viremia). This enteric cycle is fundamental to its spread, especially in areas with poor sanitation. **Analysis of Incorrect Options:** * **Hepatitis B (HBV) & Hepatitis C (HCV):** These are primarily **parenteral** viruses. Transmission occurs through infected blood/blood products, contaminated needles, sexual contact, or vertically (mother to child). They are not transmitted via the fecal-oral route. * **Rabies:** This is a zoonotic infection transmitted through the **saliva** of an infected animal, typically via a bite, scratch, or licks on broken skin/mucosa. It is not an enteric pathogen. **NEET-PG High-Yield Pearls:** * **Enteric Hepatitis Viruses:** Remember the mnemonic **"Vowels hit the Bowels"**—only Hepatitis **A** and **E** are transmitted via the fecal-oral route. * **Poliovirus Samples:** During the first week of infection, the virus can be isolated from the throat; however, it is excreted in the **feces** for several weeks, making stool the specimen of choice for diagnosis. * **Other Fecal-Oral Viruses:** Rotavirus, Norovirus, Astrovirus, and Echoviruses. * **Vaccination:** The Oral Polio Vaccine (OPV/Sabin) induces local **IgA immunity** in the gut, which directly interrupts fecal-oral transmission, unlike the Inactivated Polio Vaccine (IPV/Salk).

Q: During the asymptomatic latent phase of AIDS, the virus is actively proliferating and can be found in association with which of the following?

Follicular dendritic cells in lymph nodes. **Explanation:** The "asymptomatic" or clinical latency phase of HIV is a misnomer; while the patient is clinically stable, the virus is **actively replicating** within the lymphoid tissues. **Why Option B is Correct:** During this phase, the lymph nodes act as a major reservoir for the virus. HIV particles are trapped on the surface of **Follicular Dendritic Cells (FDCs)** in the germinal centers of lymph nodes. These FDCs are coated with HIV virions (bound via complement and Fc receptors), which then infect passing CD4+ T cells. This continuous interaction leads to the gradual depletion of CD4+ cells, eventually resulting in the breakdown of the follicular architecture and the onset of overt AIDS. **Why the other options are incorrect:** * **A. B lymphocytes:** While B-cell hyperplasia occurs due to polyclonal activation in HIV, B cells are not the primary site of viral proliferation or sequestration during latency. * **C. Ganglion cells:** These are associated with the latency of **Herpes Simplex Virus (HSV)** and **Varicella-Zoster Virus (VZV)**, not HIV. * **D. Oligodendrocytes:** These cells are the target of the **JC virus**, leading to Progressive Multifocal Leukoencephalopathy (PML) in AIDS patients, but they are not the site of HIV proliferation during clinical latency. **High-Yield Clinical Pearls for NEET-PG:** * **Primary Reservoir:** The "Latent Reservoir" of HIV is primarily **Resting Memory CD4+ T cells**, but the site of active proliferation during clinical latency is the **Lymph Node (FDCs)**. * **Viral Set Point:** The level of steady-state viremia at the end of the acute phase predicts the rate of progression to AIDS. * **Coreceptor Switch:** HIV typically uses **CCR5** (M-tropic) in early stages and may switch to **CXCR4** (T-tropic) in later stages.

Q: Which is the first antibody to appear in Hepatitis B infection?

IgM anti-HBc. ### Explanation **Correct Answer: B. IgM anti-HBc** In the natural course of a Hepatitis B Virus (HBV) infection, **IgM anti-HBc (Hepatitis B core antibody)** is the first antibody to appear in the serum. It typically becomes detectable shortly after HBsAg (the first marker overall) appears, but before the development of antibodies against surface or e-antigens. **Why it is the correct answer:** * **Window Period:** During the "window period," HBsAg has disappeared, but anti-HBs has not yet appeared. In this phase, **IgM anti-HBc** is the only reliable serological marker of an acute HBV infection. * **Marker of Acuity:** Its presence signifies acute infection or a recent flare of chronic HBV. **Why the other options are incorrect:** * **A & C (Anti-HBe):** These antibodies appear only after the disappearance of the HBeAg (Hepatitis B e-antigen). They signify a decrease in viral replication and lower infectivity, occurring much later than the core antibody. * **D (IgM anti-HBs):** This is a distractor. Anti-HBs is generally of the **IgG** class and appears during the recovery phase (after HBsAg disappears) or following vaccination. It provides protective immunity. --- ### High-Yield Clinical Pearls for NEET-PG: 1. **Sequence of Markers:** HBsAg (1st marker) → HBeAg → **IgM anti-HBc (1st antibody)** → Anti-HBe → Anti-HBs (Last marker). 2. **Window Period Marker:** IgM anti-HBc is the diagnostic marker of choice when HBsAg and Anti-HBs are both negative. 3. **Chronic Infection:** Defined by the persistence of **HBsAg for >6 months**. In chronic states, IgM anti-HBc is replaced by **IgG anti-HBc**. 4. **Vaccination vs. Natural Infection:** * **Vaccinated:** Only Anti-HBs is positive. * **Naturally Immune:** Both Anti-HBs and IgG anti-HBc are positive.

Q: Which of the following lymphomas is associated with HTLV-I virus infection?

Adult T-cell leukemia and lymphoma. **Explanation:** **Adult T-cell Leukemia/Lymphoma (ATLL)** is the correct answer because it is directly caused by the **Human T-lymphotropic virus type 1 (HTLV-1)**. HTLV-1 is a retrovirus that infects CD4+ T-cells. The viral **Tax protein** plays a critical role in oncogenesis by activating host cell genes involved in proliferation and inhibiting tumor suppressor genes (like p53), leading to the malignant transformation of T-cells. **Analysis of Incorrect Options:** * **Burkitt’s Lymphoma:** This is strongly associated with the **Epstein-Barr Virus (EBV)**, particularly the endemic form found in Africa, and involves a c-myc translocation t(8;14). * **B-cell Lymphoma:** While HTLV-1 affects T-cells, B-cell lymphomas are more commonly associated with EBV, HHV-8 (Primary Effusion Lymphoma), or Hepatitis C. * **Hodgkin’s Disease:** While EBV is found in about 40-50% of Hodgkin lymphoma cases (especially the Mixed Cellularity subtype), there is no established causal link with HTLV-1. **High-Yield NEET-PG Pearls:** * **Clinical Presentation:** ATLL often presents with aggressive lymphadenopathy, hepatosplenomegaly, lytic bone lesions, and **hypercalcemia**. * **Morphology:** A characteristic finding on peripheral blood smear is the presence of **"Flower cells"** (cloverleaf nuclei). * **Transmission:** HTLV-1 is transmitted via breastfeeding (most common), sexual contact, and blood transfusion. * **Endemic Areas:** It is most prevalent in Japan, the Caribbean, and parts of Central Africa.

Q: Which of the following is true regarding viral antibodies?

Antibodies are formed against viral surface proteins.. **Explanation:** **1. Why Option C is Correct:** The humoral immune response primarily targets the **viral surface proteins** (capsid proteins in non-enveloped viruses and glycoproteins in enveloped viruses). These surface antigens are the first to be recognized by B-lymphocytes. Antibodies against these proteins—specifically **neutralizing antibodies**—are clinically significant because they prevent the virus from attaching to and entering host cells, thereby conferring immunity. **2. Why Other Options are Incorrect:** * **Option A:** Interferons (IFN-α and IFN-β) are part of the **innate immune response** and are produced within hours of viral infection. Antibodies (adaptive immunity) take several days to weeks to develop. Therefore, **interferon appears before antibodies.** * **Option B:** Antibodies are generally formed against **proteins** (antigens). Viral nucleic acids (DNA/RNA) are sequestered inside the viral core and are not typically immunogenic during a natural infection unless they are recognized by intracellular receptors like TLRs. * **Option D:** While IgM appears early (within the first week), the **maximum antibody levels (peak titers)**, particularly IgG, are usually reached between **2 to 4 weeks** after the initial exposure, not within one week. **Clinical Pearls for NEET-PG:** * **Neutralizing Antibodies:** These are specific antibodies that bind to surface proteins and inhibit viral infectivity. * **Seroconversion:** The interval during which antibodies first become detectable in the blood. * **Diagnostic Marker:** IgM indicates an **acute/recent infection**, while IgG indicates a **past infection or chronic state**. * **Window Period:** The time between infection and the point where antibodies become detectable (e.g., in HIV).

Question 1

An emerging viral pathogen causing pyelonephritis in kidney allograft recipients is:

Accepted Answer

Polyoma virus

Answer

Marburg virus

Answer

JC virus

Answer

Ebola virus

Question 2

What is the primary receptor for Epstein-Barr virus (EBV)?

Accepted Answer

Complement receptor 2 (CR2)

Answer

Complement receptor 1 (CR1)

Answer

CD20

Answer

CD19

Question 3

What is the serological pattern observed for acute Hepatitis B with active viral replication?

Accepted Answer

HBsAg, HBeAg, IgM Anti-HBc

Answer

HBsAg, IgG Anti-HBc

Answer

HBeAg

Answer

HBsAg

Question 4

What is the protein coat that covers the genetic material in a virus called?

Accepted Answer

Capsid

Answer

Capsomere

Answer

Nucleocapsid

Answer

Envelope

Question 5

Which of the following statements is/are true regarding viral infections and their associated manifestations?

Accepted Answer

Epstein-Barr virus (EBV) causes lymphomatous lymphoma, Respiratory Syncytial Virus (RSV) causes bronchiolitis, and Erythema infectiosum is characterized by a 'slapped cheek' appearance.

Answer

Kaposi's sarcoma is caused by HHV-6, Epstein-Barr virus (EBV) causes lymphomatous lymphoma, and Respiratory Syncytial Virus (RSV) causes bronchiolitis.

Answer

Epstein-Barr virus (EBV) causes lymphomatous lymphoma and Respiratory Syncytial Virus (RSV) causes bronchiolitis.

Answer

Kaposi's sarcoma is caused by HHV-6 and Erythema infectiosum is characterized by a 'slapped cheek' appearance.

Question 6

Fecal-oral transmission occurs in which of the following?

Accepted Answer

Poliomyelitis

Answer

Hepatitis B Virus (HBV)

Answer

Hepatitis C Virus (HCV)

Answer

Rabies

Question 7

During the asymptomatic latent phase of AIDS, the virus is actively proliferating and can be found in association with which of the following?

Accepted Answer

Follicular dendritic cells in lymph nodes

Answer

B lymphocytes

Answer

Ganglion cells

Answer

Oligodendrocytes

Question 8

Which is the first antibody to appear in Hepatitis B infection?

Accepted Answer

IgM anti-HBc

Answer

IgM anti-HBe

Answer

IgG anti-HBe

Answer

IgM anti-HBs

Question 9

Which of the following lymphomas is associated with HTLV-I virus infection?

Accepted Answer

Adult T-cell leukemia and lymphoma

Answer

Burkitt's lymphoma

Answer

B-cell lymphoma

Answer

Hodgkin's disease

Question 10

Which of the following is true regarding viral antibodies?

Accepted Answer

Antibodies are formed against viral surface proteins.

Answer

Antibodies appear before interferon.

Answer

Antibodies are formed against viral nucleic acid.

Answer

Maximum antibody levels are seen within one week.

Virology — MCQs

Virology — MCQs

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