Dermatology MCQ - Viral Infections - Malawi polyomavirus (human polyomavirus-10)
A 45-year-old woman with advanced HIV (CD4 count 80 cells/µL) presents with multiple, firm, violaceous nodules on her trunk and extremities. Biopsy reveals a diffuse proliferation of spindle-shaped cells forming slit-like vascular spaces, with extravasated red blood cells. Malawi polyomavirus (human polyomavirus-10)
9/4/20252 min read
A 45-year-old woman with advanced HIV (CD4 count 80 cells/µL) presents with multiple, firm, violaceous nodules on her trunk and extremities. Biopsy reveals a diffuse proliferation of spindle-shaped cells forming slit-like vascular spaces, with extravasated red blood cells. Immunohistochemistry is positive for HHV-8 (LNA-1). However, further molecular testing also detects Malawi polyomavirus (MWPyV) DNA within the lesions. Which of the following is the most accurate interpretation of the MWPyV finding in this context?
A) MWPyV is the primary oncogenic driver of this tumor
B) MWPyV is a bystander with no established pathogenic role
C) MWPyV causes a distinct trichodysplasia-like folliculitis
D) MWPyV integration into the host genome confirms malignancy
E) MWPyV requires immediate treatment with intravenous cidofovir
Correct Answer: B) MWPyV is a bystander with no established pathogenic role
Explanation
This patient has Kaposi sarcoma (KS), definitively diagnosed by histopathology and HHV-8 positivity. The detection of Malawi polyomavirus (MWPyV) is an incidental finding.
Key Facts about Malawi Polyomavirus (MWPyV):
Classification: MWPyV (also termed Human polyomavirus 10) is a relatively newly discovered polyomavirus.
Epidemiology: It has been detected in various human samples (skin, respiratory secretions, blood) but lacks a clear disease association.
Context in This Case:
The clinical, histologic, and IHC features are classic for HHV-8-driven Kaposi sarcoma.
MWPyV DNA has been found in KS lesions but is considered a bystander or passenger virus rather than a causative agent.
There is no evidence that MWPyV is oncogenic, integrates into host DNA, or contributes to KS pathogenesis.
Why Not the Other Options?
(A) Primary oncogenic driver: Only HHV-8 has a proven causal role in KS. MWPyV has no known oncogenic mechanisms.
(C) Trichodysplasia-like folliculitis: Trichodysplasia spinulosa is caused by TSPyV, not MWPyV.
(D) Genome integration confirming malignancy: MWPyV does not integrate into the host genome. Viral integration is a feature of MCPyV in Merkel cell carcinoma.
(E) Requires IV cidofovir: No indication for antivirals, as MWPyV is not pathogenic. Treatment should target the underlying KS (e.g., ART, chemotherapy).
Management Implications:
Treat the Kaposi sarcoma: Optimize ART for HIV, consider local (radiation) or systemic (liposomal doxorubicin) therapy.
Ignore MWPyV: No action is needed for this incidental finding.
Takeaway:
The discovery of novel polyomaviruses (like MWPyV) through advanced PCR techniques often reveals viral DNA in tissues without clinical significance. Correlation with histology and known pathogens (e.g., HHV-8) is essential to avoid misattribution.
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