## Identifying the Incorrect Statement **Key Point:** The immediate-early (IE) genes encode regulatory proteins (ICP0, ICP4, ICP27), NOT DNA polymerase or thymidine kinase. DNA polymerase and thymidine kinase are encoded by early (E) genes, not IE genes. ### HSV Gene Expression Hierarchy | Gene Class | Timing | Key Products | Function | | --- | --- | --- | --- | | **Immediate-Early (IE)** | First | ICP0, ICP4, ICP27, ICP47 | Transactivators; shut down host protein synthesis | | **Early (E)** | Second | DNA polymerase, thymidine kinase, ribonucleotide reductase | Nucleotide metabolism; DNA replication | | **Late (L)** | Third | Structural proteins (VP5, VP19C, VP23, glycoproteins gB, gC, gD, gH, gJ) | Virion assembly and egress | **High-Yield:** The distinction between IE and E gene products is a classic NEET PG trap. IE genes encode *regulatory* proteins that activate downstream genes; E genes encode *enzymatic* proteins required for DNA synthesis. ### Why the Other Statements Are Correct - **Option 0 (83% homology):** HSV-1 and HSV-2 share ~83% nucleotide sequence identity, explaining their similar clinical presentations and cross-reactivity in serology. - **Option 1 (Latency in ganglia):** Sensory ganglia (trigeminal, sacral) are the classic latency sites; viral DNA persists as a non-integrated episome in neuronal nuclei, reactivating under stress, immunosuppression, or fever. - **Option 3 (Cell culture & CPE):** Vero cells are permissive; HSV produces characteristic ballooning degeneration and syncytia within 24–48 hours—a hallmark of herpesvirus infection. **Clinical Pearl:** Thymidine kinase deficiency in HSV mutants confers acyclovir resistance, a key mechanism of antiviral resistance in immunocompromised patients.
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