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Give me 10 CmV virus microbiology MCQ based on pyqs of neet pg and inicet

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CMV cytomegalovirus microbiology NEET PG INICET MCQ previous year questions

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I now have comprehensive information from the medical library. Let me compile the 10 high-quality NEET PG / INICET-style CMV MCQs:

10 CMV Microbiology MCQs - NEET PG / INICET Pattern

Q1. CMV belongs to which subfamily of herpesviruses?
  • A) Alphaherpesvirinae
  • B) Betaherpesvirinae
  • C) Gammaherpesvirinae
  • D) Deltaherpesvirinae
✅ Answer: B) Betaherpesvirinae
Explanation: CMV (Human Herpesvirus 5) is a beta-herpesvirus. The three subfamilies of Herpesviridae are: Alpha (HSV-1, HSV-2, VZV), Beta (CMV, HHV-6, HHV-7), and Gamma (EBV, HHV-8). CMV has the largest genome among all human herpesviruses (~240 kbp of double-stranded DNA. (Sherris & Ryan's Medical Microbiology, 8th Ed.)
Q2. The characteristic histopathological finding in CMV infection is:
  • A) Cowdry type A inclusion bodies
  • B) "Owl eye" intranuclear inclusions with perinuclear cytoplasmic inclusions
  • C) Negri bodies
  • D) Guarnieri bodies
✅ Answer: B) "Owl eye" intranuclear inclusions with perinuclear cytoplasmic inclusions
Explanation: CMV is named for its cytopathic effect - it produces characteristic "owl's eye" large intranuclear inclusions AND smaller perinuclear cytoplasmic inclusions, along with cell enlargement (cytomegaly). This combination is unique to CMV among herpesviruses. The cells are NOT multinucleated (unlike HSV/VZV). (Sherris & Ryan's Medical Microbiology, 8th Ed.; Quick Compendium of Clinical Pathology)
Q3. CMV preferentially grows in which cell type in tissue culture?
  • A) Epithelial cells
  • B) Lymphocytes
  • C) Fibroblasts
  • D) Macrophages
✅ Answer: C) Fibroblasts
Explanation: Although CMV replicates in a variety of cell types in vivo (including endothelial cells, dendritic cells, epithelial cells), in tissue culture it grows preferentially in human fibroblasts. This is a classic NEET PG fact - the replication cycle in fibroblasts is also notably slow (days vs. hours for alpha-herpesviruses). (Harrison's Principles of Internal Medicine 22E)
Q4. The gene responsible for phosphorylating ganciclovir to its active monophosphate form in CMV is:
  • A) Thymidine kinase (TK)
  • B) UL97 kinase
  • C) UL83 (pp65)
  • D) DNA polymerase (UL30)
✅ Answer: B) UL97 kinase
Explanation: Unlike HSV/VZV where thymidine kinase activates acyclovir, CMV encodes a viral kinase (UL97) that efficiently monophosphorylates ganciclovir. Mutations in UL97 are the most common cause of ganciclovir resistance in CMV. UL83 encodes pp65 (phosphoprotein 65), the matrix protein used in the pp65 antigenemia assay for CMV diagnosis. (Sherris & Ryan's Medical Microbiology, 8th Ed.)
Q5. The most common cause of congenital viral infection in the United States / most common viral cause of congenital sensorineural hearing loss (SNHL) is:
  • A) Rubella
  • B) Herpes Simplex Virus
  • C) Cytomegalovirus
  • D) Toxoplasma gondii
✅ Answer: C) Cytomegalovirus
Explanation: CMV is the most common cause of congenital viral infection (affecting ~0.67% of all births globally) and is the leading viral cause of congenital SNHL. Up to 90% of infected infants are asymptomatic at birth, yet 10-15% of these asymptomatic infants can later develop hearing loss or neurodevelopmental delay. Congenital rubella has been largely eliminated by vaccination. (Harrison's Principles of Internal Medicine 22E; K.J. Lee's Essential Otolaryngology)
Q6. A neonate presents with hepatosplenomegaly, jaundice, petechial rash, microcephaly, and thrombocytopenia. CMV is suspected. Which sample is best for confirming congenital CMV infection in the first 3 weeks of life?
  • A) Serum IgM
  • B) Urine PCR or saliva PCR
  • C) Shell vial culture of blood
  • D) CSF antibody titres
✅ Answer: B) Urine PCR or saliva PCR
Explanation: Congenital CMV must be confirmed within the first 3 weeks of life. Urine PCR (or saliva PCR) is the gold standard - CMV is shed in urine and saliva in high titers. After 3 weeks, a positive PCR cannot distinguish congenital from perinatally acquired infection. IgM serology has poor specificity (false positives, cross-reactions). Shell vial culture is sensitive but slower and less practical. (Red Book 2021; Harriet Lane Handbook 23rd Ed.)
Q7. In an HIV-positive patient with CD4 count <50 cells/mm³, which CMV end-organ disease is most common?
  • A) CMV pneumonitis
  • B) CMV colitis
  • C) CMV retinitis
  • D) CMV encephalitis
✅ Answer: C) CMV retinitis
Explanation: CMV retinitis is the most common serious opportunistic ocular infection in advanced AIDS (CD4 <50 cells/mm³). It was a leading cause of blindness in the pre-HAART era. Presenting features include floaters, scotomas, and "brushfire" retinal lesions. CMV colitis is more common in transplant recipients. Ganciclovir/valganciclovir is the treatment of choice. (Harrison's Principles of Internal Medicine 22E)
Q8. In solid organ transplantation, which donor-recipient CMV serostatus combination carries the HIGHEST risk of CMV disease?
  • A) Donor negative / Recipient negative (D-/R-)
  • B) Donor positive / Recipient positive (D+/R+)
  • C) Donor positive / Recipient negative (D+/R-)
  • D) Donor negative / Recipient positive (D-/R+)
✅ Answer: C) Donor positive / Recipient negative (D+/R-)
Explanation: D+/R- (seronegative recipient receiving an organ from a seropositive donor) is the highest-risk combination in solid organ transplantation (SOT) - up to 50% of such recipients may develop CMV viremia after prophylaxis stops. The virus is transmitted via the graft. Contrast this with HCT where D-/R+ is highest risk, because the seropositive recipient harbors latent CMV. (Harrison's Principles of Internal Medicine 22E)
Q9. The drug used for PROPHYLAXIS of CMV after allogeneic hematopoietic cell transplantation (HCT), which has a novel mechanism (terminase complex inhibitor), is:
  • A) Ganciclovir
  • B) Valganciclovir
  • C) Foscarnet
  • D) Letermovir
✅ Answer: D) Letermovir
Explanation: Letermovir is a CMV terminase complex inhibitor (acts on pUL51, pUL56, pUL89 proteins) with a mechanism distinct from DNA polymerase inhibitors. It is approved for CMV prophylaxis after allo-HCT (used for 100 days post-transplant). Importantly, letermovir does NOT cover HSV/VZV, so acyclovir/valaciclovir must be added separately. Valganciclovir is used for SOT prophylaxis. (Harrison's Principles of Internal Medicine 22E)
Q10. The older laboratory method for monitoring CMV viremia - now largely replaced by PCR - was:
  • A) Shell vial culture
  • B) pp65 antigenemia assay
  • C) ELISA for IgM
  • D) Complement fixation test
✅ Answer: B) pp65 antigenemia assay
Explanation: The pp65 (UL83) antigenemia assay detected CMV lower matrix phosphoprotein pp65 in peripheral blood leukocytes using monoclonal antibodies, and was the standard quantitative test for CMV viremia in the 1990s-2000s. It has now been replaced by quantitative PCR (qPCR), which detects CMV DNA in whole blood or plasma and is expressed in international units/mL (IU/mL), allowing standardized comparisons. PCR is faster, more sensitive, and more objective. (Harrison's Principles of Internal Medicine 22E; Sherris & Ryan's Medical Microbiology, 8th Ed.)

Quick Revision Summary for NEET PG / INICET

High-Yield FactKey Point
ClassificationBeta-herpesvirus (HHV-5), largest HHV genome (~240 kbp)
HistologyOwl-eye intranuclear + perinuclear cytoplasmic inclusions
Cell cultureGrows in fibroblasts (slow replication)
KinaseUL97 phosphorylates ganciclovir (not TK like HSV)
CongenitalMost common viral cause of SNHL; confirm with urine/saliva PCR <3 weeks
AIDSCMV retinitis at CD4 <50 cells/mm³
SOT riskD+/R- = highest risk
HCT prophylaxisLetermovir (terminase inhibitor) for 100 days
CMV diagnosis nowqPCR (replaced pp65 antigenemia)
TreatmentGanciclovir / Valganciclovir (first line); Foscarnet, Cidofovir (resistant cases)

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