Virology Practice Questions

Q: Renal involvement is seen in which of the following infections?

Polyoma virus. **Explanation:** The **Polyomaviridae** family, specifically the **BK and JC viruses**, are classic "nephrotropic" viruses. After a primary respiratory infection in childhood, these viruses remain latent in the **renal tubular epithelium**. In immunocompromised states (e.g., renal transplant recipients), the BK virus reactivates, leading to **BK virus-associated nephropathy (BKVAN)** and hemorrhagic cystitis. The JC virus, while primarily known for Progressive Multifocal Leukoencephalopathy (PML), also persists in the kidneys and is excreted in the urine. **Analysis of Options:** * **Polyoma virus (Correct):** It is the most direct answer because the kidney is its primary site of latency and clinical manifestation (BKVAN). * **Cytomegalovirus (CMV):** While CMV can be detected in urine and may cause systemic disease in transplant patients, it primarily targets the lungs (pneumonitis), retina (retinitis), and GI tract rather than being primarily defined by renal involvement. * **Human Papilloma virus (HPV):** HPV is strictly epitheliotropic, targeting the skin and mucosal surfaces (warts, cervical cancer). It does not involve the renal parenchyma. * **HIV:** While HIV can cause "HIV-Associated Nephropathy" (HIVAN), the virus itself infects CD4+ T cells and macrophages. The renal damage is a secondary complication of the systemic infection rather than the virus being primarily nephrotropic. **High-Yield Clinical Pearls for NEET-PG:** * **Decoy Cells:** Look for these in urine cytology; they are renal tubular cells with enlarged, basophilic intranuclear inclusions characteristic of Polyoma virus (BK virus). * **BK Virus:** "B" is for **B**ad **K**idney (Nephropathy/Ureteric stenosis). * **JC Virus:** "J" is for **J**unk **C**erebrum (PML). * **SV40:** A simian polyomavirus known for its potential oncogenic properties in laboratory settings.

Q: All the following viruses are known to cause Lymphomas except:

Japanese Encephalitis virus. **Explanation:** The correct answer is **Japanese Encephalitis Virus (JEV)** because it is a neurotropic virus belonging to the *Flaviviridae* family. It primarily causes acute encephalitis (inflammation of the brain parenchyma) and is not associated with oncogenesis or the development of malignancies like lymphoma. **Analysis of Options:** * **HTLV-I (Human T-cell Leukemia Virus-1):** This retrovirus is the definitive causative agent of **Adult T-cell Leukemia/Lymphoma (ATLL)**. It integrates into the host genome and utilizes the *Tax* protein to drive uncontrolled T-cell proliferation. * **EBV (Epstein-Barr Virus/HHV-4):** A highly oncogenic herpesvirus associated with several B-cell lymphomas, including **Burkitt Lymphoma** (starry-sky appearance), Hodgkin Lymphoma, and Diffuse Large B-cell Lymphoma (DLBCL), especially in immunocompromised patients. * **KSHV/HHV-8 (Kaposi Sarcoma-associated Herpesvirus):** Beyond causing Kaposi Sarcoma, this virus is the primary driver of **Primary Effusion Lymphoma (PEL)** and Multicentric Castleman Disease. **High-Yield NEET-PG Pearls:** * **Oncogenic DNA Viruses:** EBV, HHV-8, HBV, HPV (16, 18), and Merkel Cell Polyomavirus. * **Oncogenic RNA Viruses:** HTLV-1 and HCV (HCV is associated with B-cell Non-Hodgkin Lymphoma). * **JEV Key Fact:** It is transmitted by the *Culex tritaeniorhynchus* mosquito; the "amplifier host" is the pig. It is the most common cause of epidemic viral encephalitis in India. * **Burkitt Lymphoma Marker:** Associated with the **t(8;14)** translocation involving the *c-myc* gene.

Q: Condyloma acuminatum is caused by which types of HPV?

6, 11. **Explanation:** **Condyloma acuminatum**, commonly known as anogenital warts, is a sexually transmitted infection caused by the **Human Papillomavirus (HPV)**. **1. Why Option C is Correct:** HPV types **6 and 11** are classified as **"low-risk"** genotypes. They are responsible for approximately 90% of all cases of Condyloma acuminatum. These types cause benign epithelial proliferation (warts) but have a very low potential for malignant transformation into squamous cell carcinoma. **2. Analysis of Incorrect Options:** * **Option D (16, 18):** These are **"high-risk"** oncogenic types. While they can cause flat lesions, they are primarily associated with cervical intraepithelial neoplasia (CIN), cervical cancer, and other anogenital malignancies (vulvar, anal, and penile cancers). * **Option A (18, 31):** Both are high-risk types associated with malignancy rather than benign condylomas. * **Option B (17, 12):** These types are associated with **Epidermodysplasia verruciformis**, a rare genetic disorder characterized by an increased susceptibility to specific HPV strains and subsequent skin cancer. **3. NEET-PG High-Yield Pearls:** * **Clinical Appearance:** Flesh-colored, cauliflower-like growths in the perianal or genital region. * **Histopathology:** Characterized by **Koilocytes** (keratinocytes with perinuclear halo and wrinkled "raisinoid" nuclei). * **Treatment of Choice:** Podophyllotoxin, Imiquimod (immunomodulator), or destructive methods like cryotherapy and CO2 laser. * **Vaccination:** The quadrivalent vaccine (Gardasil) covers types 6, 11, 16, and 18, protecting against both warts and cervical cancer.

Q: What is the commonest hepatotropic virus that progresses to chronicity?

HCV. **Explanation:** The correct answer is **HCV (Hepatitis C Virus)**. The primary factor determining "chronicity" is the virus's ability to evade the host immune response and persist in the liver for more than six months. **Why HCV is the correct answer:** HCV has the highest rate of progression to chronic infection among all hepatotropic viruses. Approximately **75%–85%** of individuals infected with HCV fail to clear the virus acutely and develop chronic hepatitis [1]. This high rate of chronicity is largely due to the virus's high mutation rate (quasispecies), which allows it to stay ahead of the host’s immune system [1]. **Analysis of Incorrect Options:** * **HAV (Hepatitis A) & HEV (Hepatitis E):** These are transmitted via the fecal-oral route and typically cause acute, self-limiting illness. They **do not** progress to chronicity in immunocompetent individuals [2]. (Note: HEV can cause chronic infection specifically in organ transplant recipients or immunocompromised patients). * **HBV (Hepatitis B):** While HBV can become chronic, the rate depends heavily on the age of acquisition. In adults, only about **5%** of infections become chronic [1]. Although the absolute number of chronic HBV carriers is high globally, the *probability* of an individual infection progressing to chronicity is significantly lower than that of HCV [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Highest risk of chronicity:** HCV (up to 85%) [1]. * **Highest risk of Fulminant Hepatic Failure in pregnancy:** HEV. * **HBV Chronicity Risk:** 90% in neonates (vertical transmission), 20-30% in children, and <5% in adults [1]. * **HCV Screening:** Anti-HCV antibody is the screening test; HCV-RNA (PCR) is the gold standard for confirming active infection [1]. * **DNA vs. RNA:** HBV is the only DNA hepatotropic virus; all others (A, C, D, E) are RNA viruses.

Q: A patient, two months post-renal transplantation, presents with difficulty in breathing. X-ray shows bilateral diffuse interstitial pneumonia. What is the most probable etiologic agent?

Cytomegalovirus (CMV). ### **Explanation** **Correct Option: A. Cytomegalovirus (CMV)** Cytomegalovirus is the most common viral opportunistic infection in solid organ transplant (SOT) recipients, typically manifesting **1 to 6 months post-transplantation** (the period of maximal immunosuppression). In renal transplant patients, CMV classically presents as **interstitial pneumonia**, fever, and leukopenia. The radiological finding of bilateral diffuse interstitial infiltrates is a hallmark of CMV pneumonitis in this clinical context. **Analysis of Incorrect Options:** * **B. Histoplasma capsulatum:** While it can cause fungal pneumonia in immunocompromised hosts, it is geographically restricted (endemic areas) and usually presents with granulomatous lesions or mediastinal lymphadenopathy rather than diffuse interstitial pneumonia 2 months post-op. * **C. Candida species:** Candida is a common cause of oral thrush or candidemia in transplant patients, but it is a very rare cause of primary interstitial pneumonia. * **D. Pneumocystis jirovecii (PJP):** PJP presents similarly with diffuse interstitial infiltrates. However, due to the routine use of **Trimethoprim-Sulfamethoxazole (TMP-SMX) prophylaxis** in the first 6–12 months post-transplant, its incidence has significantly decreased, making CMV the more statistically probable answer in modern clinical scenarios. **High-Yield Clinical Pearls for NEET-PG:** * **Timeline:** CMV is the "King of the Middle Period" (1–6 months post-transplant). * **Diagnosis:** The gold standard for tissue diagnosis is the presence of **"Owl’s eye" inclusion bodies** (intranuclear inclusions with a clear halo). * **Treatment:** Intravenous **Ganciclovir** is the drug of choice for CMV pneumonitis; Valganciclovir is used for prophylaxis. * **Monitoring:** CMV viremia is monitored using quantitative PCR or the pp65 antigenemia assay.

Q: Regarding HIV, which of the following statements is not true?

It is a DNA retrovirus.. ### Explanation **1. Why Option A is the correct (False) statement:** HIV (Human Immunodeficiency Virus) is an **RNA virus**, not a DNA virus. Specifically, it belongs to the family *Retroviridae* and the genus *Lentivirus*. It contains two identical copies of single-stranded, positive-sense RNA (+ssRNA). While it produces a DNA intermediate during its life cycle, the virion itself carries RNA as its genetic material. **2. Analysis of other options:** * **Option B (True):** HIV contains the enzyme **Reverse Transcriptase** (RNA-dependent DNA polymerase). This enzyme is crucial for transcribing the viral RNA into complementary DNA (cDNA), which then integrates into the host genome. * **Option C (True):** While CD4+ T helper cells are the primary targets, HIV also infects other cells expressing the CD4 receptor and coreceptors (CCR5/CXCR4). These include **monocytes, macrophages, dendritic cells, and microglial cells** in the brain. * **Option D (True):** A hallmark of HIV progression to AIDS is the progressive depletion of CD4+ T cells. This occurs through direct viral lysis, syncytia formation, and apoptosis, leading to profound immunodeficiency at the late stage of the disease. ### NEET-PG High-Yield Pearls * **Structure:** HIV is an enveloped, icosahedral virus. The envelope contains spikes of **gp120** (for attachment) and **gp41** (for fusion). * **Key Genes:** * *gag*: Codes for structural proteins (p24 - the major capsid antigen used in early diagnosis). * *pol*: Codes for enzymes (Reverse Transcriptase, Integrase, Protease). * *env*: Codes for envelope glycoproteins (gp160, cleaved into gp120 and gp41). * **Screening vs. Confirmation:** ELISA is the standard screening test (high sensitivity), while **Western Blot** was traditionally the confirmatory test (high specificity), though current protocols often use 4th generation p24/antibody combination assays followed by nucleic acid testing (NAT).

Q: A 30-year-old patient presented with a 10-day history of jaundice. Liver function tests showed a bilirubin of 10 mg/dL, SGOT/SGPT of 1100/1450 IU/L, and serum alkaline phosphatase of 240 IU/L. The patient tested positive for HbsAg. What is the confirmatory test to establish acute hepatitis B infection?

IgM Anti-HBc antibody. ### **Explanation** The clinical presentation of jaundice with significantly elevated transaminases (SGOT/SGPT >1000 IU/L) and positive HBsAg indicates a diagnosis of Hepatitis B. However, HBsAg alone cannot distinguish between a **new acute infection** and a **chronic carrier state** experiencing a flare. **1. Why IgM Anti-HBc is the Correct Answer:** The **IgM antibody to Hepatitis B core antigen (IgM anti-HBc)** is the specific marker for **acute infection**. It appears shortly after HBsAg and remains positive for approximately 6 months. Crucially, it is the only marker present during the **"Window Period"** (the gap between the disappearance of HBsAg and the appearance of Anti-HBs). Its presence confirms that the infection was acquired recently. **2. Analysis of Incorrect Options:** * **HBeAg (Option B):** This is a marker of **active viral replication and high infectivity**. While often present in acute phases, it can also be positive in chronic hepatitis; it does not specifically define the "acute" stage. * **HBV DNA by PCR (Option C):** This measures viral load. While highly sensitive for diagnosing infection and monitoring treatment, it does not differentiate between acute and chronic phases. * **Anti-HBc antibody (Option D):** This refers to "Total" Anti-HBc (IgM + IgG). Since IgG persists for life, a total antibody test cannot distinguish between a current acute infection and a past/chronic infection. **3. NEET-PG High-Yield Pearls:** * **HBsAg:** First marker to appear in blood (1–12 weeks after exposure). * **Window Period Marker:** IgM Anti-HBc is the diagnostic marker of choice when HBsAg has cleared but Anti-HBs hasn't appeared yet. * **Chronic Infection:** Defined by the persistence of HBsAg for **>6 months**. * **Recovery/Immunity:** Marked by the appearance of **Anti-HBs** (also the only marker positive after vaccination).

Q: A 5-year-old boy presents with headache, fever, and vomiting. On examination, multiple small vesicles are present on the posterior pharyngeal wall. He is diagnosed with herpangina. What is herpangina caused by?

Enterovirus. **Explanation:** **Correct Answer: B. Enterovirus** Herpangina is a common childhood infection primarily caused by **Coxsackievirus Group A** (a genus within the **Enterovirus** family, Picornaviridae). The clinical hallmark is the sudden onset of fever, sore throat, and the appearance of small (1–2 mm) vesicular or ulcerative lesions specifically on the **posterior pharyngeal wall**, tonsils, and soft palate. Unlike gingivostomatitis (HSV-1), herpangina typically spares the buccal mucosa and gingiva. **Analysis of Incorrect Options:** * **A. Myxovirus:** This group includes Orthomyxoviruses (Influenza) and Paramyxoviruses (Measles, Mumps). These typically present with respiratory symptoms or parotitis, not posterior pharyngeal vesicles. * **C. Rhabdovirus:** The most notable member is the Rabies virus, which causes fatal encephalitis and hydrophobia, not localized vesicular pharyngitis. * **D. Rhinovirus:** While also a Picornavirus, Rhinoviruses are the primary cause of the common cold (upper respiratory tract infections) and do not typically cause vesicular eruptions. **High-Yield Clinical Pearls for NEET-PG:** * **Causative Agent:** Most commonly **Coxsackie A** (A1–A10, A16, A22). * **Hand-Foot-Mouth Disease (HFMD):** Also caused by Enteroviruses (Coxsackie A16 and Enterovirus 71). It differs from herpangina by the presence of a maculopapular or vesicular rash on the palms, soles, and buttocks. * **Seasonality:** Infections peak during summer and autumn months. * **Transmission:** Fecal-oral route and respiratory droplets. * **Management:** Treatment is purely supportive (hydration and analgesics) as the condition is self-limiting.

Q: Which of the following statements regarding Hepatitis E Virus (HEV) and Hepatitis D Virus (HDV) is FALSE?

HEV and HDV are DNA viruses.. ### Explanation **1. Why Option D is the Correct (False) Statement:** The fundamental classification of Hepatitis viruses is a high-yield NEET-PG topic. **Hepatitis E Virus (HEV)** and **Hepatitis D Virus (HDV)** are both **RNA viruses**. Specifically, HEV is a non-enveloped, single-stranded RNA virus (Hepeviridae), and HDV is a defective, single-stranded circular RNA virus (Deltavirus). In the mnemonic "Vowels are Bowels" (A and E), both are RNA viruses transmitted via the feco-oral route. Only Hepatitis B (HBV) is a DNA virus. **2. Analysis of Other Options:** * **Option A:** It is clinically possible for a patient to have multiple viral infections simultaneously, especially in high-risk groups (e.g., IV drug users or endemic areas), though they have different transmission routes (HEV is feco-oral; HDV is parenteral). * **Option B:** HDV infection occurs in two patterns: **Co-infection** (simultaneous with HBV) and **Superinfection** (HDV infecting a chronic HBV carrier). Superinfection is significantly more serious, often leading to rapid progression to cirrhosis or fulminant hepatic failure. * **Option C:** HDV is a **defective virus**. It requires the Hepatitis B Surface Antigen (HBsAg) to provide its outer envelope for assembly and transmission. Without an underlying HBV infection, HDV cannot propagate. **3. High-Yield Clinical Pearls for NEET-PG:** * **HEV & Pregnancy:** HEV carries a high mortality rate (up to 20%) in pregnant women, particularly in the third trimester, due to fulminant hepatic failure. * **HEV Genotypes:** Genotypes 1 and 2 are human-only (epidemic); Genotypes 3 and 4 are zoonotic (pork/deer meat). * **HDV Diagnosis:** The presence of **Anti-HDV IgM** indicates acute infection, while **HDV RNA** is the gold standard for active replication. * **Prevention:** The HBV vaccine indirectly prevents HDV infection because HDV cannot exist without HBV.

Q: In which cells does the Human Immunodeficiency Virus primarily replicate?

CD4 helper T cells. **Explanation:** The Human Immunodeficiency Virus (HIV) is a retrovirus that exhibits specific tropism for cells expressing the **CD4 molecule** on their surface. **1. Why CD4 helper T cells are correct:** The primary mechanism of HIV entry involves the binding of the viral envelope glycoprotein **gp120** to the **CD4 receptor** on the host cell. This interaction, along with co-receptors (**CCR5** on macrophages/early infection or **CXCR4** on T cells/late infection), triggers a conformational change in **gp41**, leading to membrane fusion and viral entry. CD4+ T helper cells are the principal targets because they express high densities of these receptors, making them the primary site for viral replication and subsequent depletion, which leads to AIDS. **2. Why the other options are incorrect:** * **CD8 T cells:** These are cytotoxic T cells that lack the CD4 receptor. While they play a role in the immune response *against* HIV, the virus cannot infect them directly. * **Natural Killer (NK) cells:** These are part of the innate immune system. Like CD8 cells, they do not express the CD4 receptor required for HIV entry. **High-Yield Clinical Pearls for NEET-PG:** * **Coreceptors:** **CCR5** is used by M-tropic strains (early stage); **CXCR4** is used by T-tropic strains (late stage). A mutation in the CCR5 gene (**CCR5-Δ32**) provides resistance to HIV infection. * **Other Target Cells:** Besides T cells, HIV infects **Macrophages, Dendritic cells, and Microglial cells** (the primary reservoir in the CNS), as these also express CD4. * **Markers:** The progression to AIDS is clinically defined when the CD4+ T cell count falls below **200 cells/mm³**.

Question 1

Renal involvement is seen in which of the following infections?

Accepted Answer

Polyoma virus

Answer

Cytomegalovirus

Answer

Human Papilloma virus

Answer

HIV

Question 2

All the following viruses are known to cause Lymphomas except:

Accepted Answer

Japanese Encephalitis virus

Answer

Human T cell leukemia Virus (HTLV-I)

Answer

Epstein Barr Virus (EBV)

Answer

KSHV/ HHV-8

Question 3

Condyloma acuminatum is caused by which types of HPV?

Accepted Answer

6, 11

Answer

18, 31

Answer

17, 12

Answer

16, 18

Question 4

What is the commonest hepatotropic virus that progresses to chronicity?

Accepted Answer

HCV

Answer

HEV

Answer

HAV

Answer

HBV

Question 5

A patient, two months post-renal transplantation, presents with difficulty in breathing. X-ray shows bilateral diffuse interstitial pneumonia. What is the most probable etiologic agent?

Accepted Answer

Cytomegalovirus (CMV)

Answer

Histoplasma capsulatum

Answer

Candida species

Answer

Pneumocystis jirovecii

Question 6

Regarding HIV, which of the following statements is not true?

Accepted Answer

It is a DNA retrovirus.

Answer

It contains Reverse Transcriptase.

Answer

It may infect host CD4 cells other than T lymphocytes.

Answer

It causes a reduction in host CD4 cells at a late stage of disease.

Question 7

A 30-year-old patient presented with a 10-day history of jaundice. Liver function tests showed a bilirubin of 10 mg/dL, SGOT/SGPT of 1100/1450 IU/L, and serum alkaline phosphatase of 240 IU/L. The patient tested positive for HbsAg. What is the confirmatory test to establish acute hepatitis B infection?

Accepted Answer

IgM Anti-HBc antibody

Answer

HbeAg

Answer

HBV DNA by PCR

Answer

Anti-HBc antibody

Question 8

A 5-year-old boy presents with headache, fever, and vomiting. On examination, multiple small vesicles are present on the posterior pharyngeal wall. He is diagnosed with herpangina. What is herpangina caused by?

Accepted Answer

Enterovirus

Answer

Myxovirus

Answer

Rhabdovirus

Answer

Rhinovirus

Question 9

Which of the following statements regarding Hepatitis E Virus (HEV) and Hepatitis D Virus (HDV) is FALSE?

Accepted Answer

HEV and HDV are DNA viruses.

Answer

Both HEV and HDV can infect simultaneously.

Answer

HDV causes a more serious infection due to superinfection.

Answer

HDV cannot infect in the absence of HBV.

Question 10

In which cells does the Human Immunodeficiency Virus primarily replicate?

Accepted Answer

CD4 helper T cells

Answer

CD8 T cells

Answer

Natural killer cells

Answer

None of the above

Virology — MCQs

Virology — MCQs

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