Virology Practice Questions

Q: Herpes viruses acquire their envelope from which cellular membrane?

Nuclear membrane. **Explanation:** The **Herpesviridae** family is unique among DNA viruses because of its specific replication and assembly process. Unlike most enveloped viruses that acquire their lipid bilayer from the plasma membrane, Herpes viruses undergo **primary budding through the inner nuclear membrane.** 1. **Why Option A is Correct:** After the viral DNA replicates and nucleocapsids are assembled inside the host cell nucleus, they must exit to the cytoplasm. The nucleocapsid buds through the inner nuclear membrane into the perinuclear space, acquiring its initial envelope. While this envelope undergoes a complex "de-envelopment and re-envelopment" process at the Golgi apparatus for final maturation, the **primary source** of the herpesvirus envelope is the **nuclear membrane**. 2. **Why Other Options are Incorrect:** * **Option B (Nucleolar membrane):** The nucleolus is a non-membrane-bound structure within the nucleus responsible for ribosome synthesis; it does not provide envelopes for viruses. * **Option C (Cytoplasmic/Plasma membrane):** Most other enveloped viruses (like Orthomyxoviruses or Retroviruses) acquire their envelope from the plasma membrane as they exit the cell. Herpes viruses are the classic exception to this rule. **NEET-PG High-Yield Pearls:** * **Tzanck Smear:** Look for multinucleated giant cells and **Cowdry Type A** intranuclear inclusion bodies (Lipschütz bodies) in HSV and VZV infections. * **Site of Latency:** HSV-1 (Trigeminal ganglion), HSV-2 (Sacral ganglion), VZV (Dorsal root ganglion), EBV (B-cells). * **Rule of Thumb:** All DNA viruses replicate in the nucleus **except Poxvirus** (replicates in the cytoplasm). All RNA viruses replicate in the cytoplasm **except Influenza and HIV/Retrovirus** (replicate in the nucleus).

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: 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 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).

Q: Which of the following is a known reservoir for the Ebola virus?

Ebola virus. **Explanation:** The **Ebola virus**, a member of the *Filoviridae* family, causes severe hemorrhagic fever. In the context of its natural life cycle, the primary reservoir is believed to be **fruit bats** (specifically genera *Hypsignathus monstrosus*, *Epomops franqueti*, and *Myonycteris torquata*). The virus is transmitted to humans through contact with infected bushmeat (monkeys, forest antelope) or directly via bat excreta. *Note: The question structure provided implies a self-referential identification; however, in a clinical sense, the "reservoir" refers to the ecological niche where the pathogen survives.* **Analysis of Options:** * **Option A (Japanese Encephalitis Virus):** This is a Flavivirus. Its natural reservoir is **pigs and water birds** (like herons and egrets), and it is transmitted to humans via the *Culex* mosquito. * **Option C (Zika Virus):** Another Flavivirus. While it primarily circulates between humans and *Aedes* mosquitoes, its sylvatic (jungle) reservoir involves **non-human primates**. * **Option D (Plasmodium falciparum):** This is a protozoan parasite, not a virus. Its primary reservoir and definitive host is the **female Anopheles mosquito**, while humans serve as intermediate hosts. **High-Yield Clinical Pearls for NEET-PG:** * **Transmission:** Human-to-human spread occurs through direct contact with **broken skin or mucous membranes** and bodily fluids (blood, vomit, feces). * **Pathogenesis:** Ebola causes "cytokine storm" and severe DIC (Disseminated Intravascular Coagulation). * **Diagnosis:** RT-PCR is the gold standard during the acute phase; ELISA for IgM/IgG is used later. * **Biosafety Level:** Ebola requires **BSL-4** containment, the highest level of laboratory security.

Question 1

Herpes viruses acquire their envelope from which cellular membrane?

Accepted Answer

Nuclear membrane

Answer

Nucleolar membrane

Answer

Cytoplasmic membrane

Answer

None of the above

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

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 5

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 6

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 7

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.

Question 8

What is true about Congenital Rubella Syndrome?

Accepted Answer

It can result in a chronic infection.

Answer

The virus can be isolated up to 6 months after birth.

Answer

The classic triad of CRS includes cataracts, cardiac defects, and hearing loss.

Answer

Congenital Rubella infection is most serious during the first trimester of pregnancy.

Question 9

Which of the following is a known reservoir for the Ebola virus?

Accepted Answer

Ebola virus

Answer

Japanese encephalitis virus

Answer

Zika virus

Answer

Plasmodium falciparum

Question 10

Which of the following statements about the virus described is/are true? The virus is enveloped, has club or petal shaped projections, and possesses a positive-sense single-stranded RNA genome with the largest genome among RNA viruses. Diseases caused by these viruses include SARS and MERS. The reservoir for SARS is horseshoe bats, with likely spread from palm civets and cats to humans. Symptoms of MERS appear within a day following contact with an infected patient. SARS is more severe than MERS. MERS infection is more severe in individuals with pre-existing illnesses like diabetes and heart diseases.

Accepted Answer

The statement regarding enveloped nature, projections, genome type, SARS/MERS causation, and MERS severity in those with pre-existing illness is true.

Answer

The statement regarding enveloped nature, projections, genome type, SARS/MERS causation, reservoir, and SARS severity is true.

Answer

The statement regarding enveloped nature, projections, genome type, SARS/MERS causation, and reservoir is true.

Answer

All the presented statements are true.

Virology — MCQs

Virology — MCQs

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