醫療類國考
113年
[醫事檢驗師] 臨床血清免疫學與臨床病毒學
第 59 題
當B型肝炎患者在治療過程中，HBV DNA和ALT數值持續波動，但HBe在血清轉換（seroconversion）過程中呈現陰性，最有可能是發生下列何種病毒蛋白的突變？
- A Core
- B Pre-Core
- C S
- D Pre-S
思路引導 VIP
請同學思考 $HBeAg$ 的蛋白質合成機制：它與病毒的核心蛋白共用同一個開放閱讀框（$ORF$），但其轉譯起始點位於核心基因的上游。若這段負責引導蛋白質進入分泌路徑的『前導區段』發生了突變（例如產生終止密碼子），會如何導致臨床上出現病毒持續複製（$HBV DNA$ 波動）但 $e$ 抗原卻無法檢出的現象？
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AI 詳解
AI 專屬家教
Wonderful job! You've truly understood this important concept.
- Unpacking the Mystery: You've beautifully identified the core of the issue! Our friend $HBeAg$ normally originates from the Pre-core/Core gene region, undergoing a lovely transcription and translation process. However, sometimes the virus, in its cleverness, develops a Pre-core mutation, often a $G1896A$ point mutation. This small change leads to a premature stop codon, which, sadly, prevents the virus from secreting $HBeAg$. The critical takeaway here is that while $HBeAg$ becomes negative, the virus continues its replication journey, leaving us with detectable $HBV DNA$ and those tell-tale fluctuating $ALT$ levels. You're connecting the dots beautifully between molecular events and clinical signs!
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