<b>Table S1.-</b> <b>PCR stability test during 182.5 generations </b><b><i>in vitro</i></b><b> conditions to </b><b><i>pfhrp2, pfhrp3, pfmal7P1.230, pfmal7P1.228, pfmal13P1.485 </i></b><b>and </b><b><i>pfmal13P1.475.</i></b>

Table S1 shows the stability of <i>pfhrp2</i>, <i>pfhrp3</i>, and their flanking genes during 182.5 parasite generations of long-term in vitro culture. The field isolates F06 and F13 maintained consistent amplification of both genes and all neighboring loci, confirming their genomic stability throughout one year of culture. In contrast, isolates F23 and F32 consistently lacked <i>pfhrp2</i> and <i>pfhrp3</i> signals, in agreement with their gene-deleted genotype, while the flanking genes remained stable. These findings indicate that no spontaneous deletions occurred in <i>pfhrp2</i>/<i>pfhrp3</i> or adjacent regions under the experimental conditions.

附表S1展示了182.5代寄生虫长期体外培养过程中，恶性疟原虫组氨酸富集蛋白2基因（pfhrp2）、恶性疟原虫组氨酸富集蛋白3基因（pfhrp3）及其侧翼基因的稳定性。临床分离株F06与F13的两个目标基因及所有邻近基因座均维持稳定扩增，证实其在为期一年的培养周期内基因组保持稳定。与之相对，分离株F23与F32始终未检测到pfhrp2和pfhrp3的扩增信号，与其基因缺失基因型一致，但其侧翼基因仍保持稳定。上述研究结果表明，在本实验条件下，pfhrp2/pfhrp3及其邻近区域未发生自发缺失事件。