单核白血球血小板总数(MPA ) 的增加的层次被报导高度与心血管的事件被相关。在这研究,在在 MPA 层次, HIV-1 viremia 和单核白血球激活之间的不同单核白血球子集和协会的 MPA 层次在 HIV-1 感染期间被评估。结果证明在所有三个单核白血球子集的 MPA 的百分比比在健康控制在 HIV-1-infected 题目是更高的,并且与血浆被联系在非古典、中间的单核白血球子集的病毒的负担。sCD14 和 sCD163 的血浆层次是在 HIV-1 感染的 upregulated 并且断然与病毒的负担被联系并且否定地把计数与 CD4 联系了。P-selectin glycoprotein ligand-1 (PSGL-1 ) 被显示被表示在显著地所有三个单核白血球子集上的底层并且否定地与 sCD163 水平被相关。MPA 水平与血浆 sCD163 的层次被相关,但是否定地在所有三个单核白血球子集上与 CD163 和 PSGL-1 相关。提高的有免疫力的激活地位与增加的 MPA 形成被相关,位于在单核白血球激活和 MPA 形成之间的潜在的相互作用下面。这个相互作用可能与在感染 HIV-1 的病人的更高的 thromboembolic 风险有关。
Increased levels of monocyte-platelet aggregates (MPAs) are reported to be highly correlated with cardiovascular events. In this study, the MPA levels in different monocyte subsets and the associations between MPA levels, HIV-1 viremia and monocyte activation were evaluated during HIV-1 infection. The results showed that the percentages of MPAs in all three monocyte subsets were higher in HIV-l-infected subjects than in healthy controls, and were associated with the plasma viral load in the non-classical and intermediate monocyte subsets. The plasma levels of sCD14 and sCD163 were upregulated in HIV-1 infection and were positively associated with viral loads and negatively associated with CD4 counts. P-selectin glycoprotein ligand-1 (PSGL-1) was shown to be expressed at significantly lower levels on all three monocyte subsets and was negatively correlated with the sCD163 level. The MPA level was correlated with the levels of plasma sCD163 but negatively correlated with CD163 and PSGL-1 on all three monocyte subsets. An elevated immune activation status was correlated with increased MPA formation, underlying the potential interaction between monocyte activation and MPA formation. This interaction may be related to a higher thromboembolic risk in patients infected with HIV-I.