Salha M-D, Cheynier R, Halwani R, McGrath H, Langaee T Y, Yassine Diab B, Fournier J, Parenteau M, Edgar J, Ko D, Sherring A, Bogdanovic D, Sekaly R-P, Rud E W
Department of Microbiology and Immunology, McGill University, Montreal, Canada PQ H3A 2B4.
Virology. 2008 Aug 1;377(2):239-47. doi: 10.1016/j.virol.2008.04.031.
Attempts to evaluate the protective effect of live attenuated SIV vaccine strains have yielded variable results depending on the route of immunization, the level of attenuation, the level of divergence between the vaccine candidate and the challenge. The protective mechanisms induced by these vaccines are still not well understood. In an effort to address whether the diversity of the CD4+ T cell repertoire in cynomolgus macaques plays a role in the immunological protection following SIVmacC8 infection, we have performed a longitudinal follow-up of the CD4 repertoire by heteroduplex tracking assay in macaques mock-infected or infected with either the attenuated SIVmacC8 or its homologous SIVmacJ5 and challenged with simian-human immunodeficiency virus (SHIV89.6P). Viral load and CD4 absolute counts were determined in these animals and the presence of SHIV89.6P virus in challenged animals was evaluated by PCR and serology. In all macaques that were protected against the challenging virus, we demonstrated a reduced diversity in the CD4+ TRBV repertoire and a few dominant CD4+ T cell clones during early primary infection. In contrast, CD4 TRBV repertoire in unprotected macaques remained highly diverse. Moreover, some of the CD4 T cell clones that were expanded during primary SIV infection re-emerged after challenge suggesting their role in protection against the challenging virus. These results underline the importance of maintaining the CD4 T cell repertoire developed during acute infection and point to the restriction of the CD4 response to the vaccine as a correlate of protection.
评估减毒活SIV疫苗株的保护效果的尝试产生了不同的结果,这取决于免疫途径、减毒水平、候选疫苗与攻击病毒之间的差异程度。这些疫苗诱导的保护机制仍未得到充分理解。为了探讨食蟹猴CD4+T细胞库的多样性是否在感染SIVmacC8后的免疫保护中发挥作用,我们通过异源双链追踪分析对模拟感染或感染减毒SIVmacC8或其同源SIVmacJ5并接受猿猴-人类免疫缺陷病毒(SHIV89.6P)攻击的猕猴的CD4库进行了纵向随访。测定了这些动物的病毒载量和CD4绝对计数,并通过PCR和血清学评估攻击动物中SHIV89.6P病毒的存在情况。在所有对攻击病毒具有保护作用的猕猴中,我们发现在初次感染早期,CD4+TRBV库的多样性降低,并且出现了一些占主导地位的CD4+T细胞克隆。相比之下,未受保护的猕猴的CD4 TRBV库仍然高度多样化。此外,一些在初次SIV感染期间扩增的CD4 T细胞克隆在攻击后重新出现,表明它们在抵抗攻击病毒方面发挥了作用。这些结果强调了维持急性感染期间形成的CD4 T细胞库的重要性,并指出将CD4对疫苗的反应限制作为保护的一个相关指标。