Division of Pediatric Infectious Diseases, Department of Pediatrics, University of Minnesota, Minneapolis, Minnesota, United States of America.
Department of Pharmacology, University of Minnesota, Minneapolis, Minnesota, United States of America.
PLoS Pathog. 2024 Nov 4;20(11):e1012515. doi: 10.1371/journal.ppat.1012515. eCollection 2024 Nov.
Human cytomegalovirus (HCMV) is a ubiquitous herpesvirus and the leading cause of infectious disease related birth defects worldwide. How the immune response modulates the risk of intrauterine transmission of HCMV after maternal infection remains poorly understood. Maternal T cells likely play a critical role in preventing infection at the maternal-fetal interface and limiting spread across the placenta, but concerns exist that immune responses to infection may also cause placental dysfunction and adverse pregnancy outcomes. This study investigated the role of CD4+ and CD8+ T cells in a guinea pig model of primary cytomegalovirus infection. Monoclonal antibodies specific to guinea pig CD4 and CD8 were used to deplete T cells in non-pregnant and in pregnant guinea pigs after mid-gestation. CD4+ T cell depletion increased the severity of illness, caused significantly elevated viral loads, and increased the rate of congenital guinea pig cytomegalovirus (GPCMV) infection relative to animals treated with control antibody. CD8+ T cell depletion was comparably well tolerated and did not significantly affect the weight of infected guinea pigs or viral loads in their blood or tissue. However, significantly more viral genomes and transcripts were detected in the placenta and decidua of CD8+ T cell depleted dams post-infection. This study corroborates earlier findings made in nonhuman primates that maternal CD4+ T cells play a critical role in limiting the severity of primary CMV infection during pregnancy while also revealing that other innate and adaptive immune responses can compensate for an absent CD8+ T cell response in α-CD8-treated guinea pigs.
人巨细胞病毒(HCMV)是一种普遍存在的疱疹病毒,也是全球导致感染性疾病相关出生缺陷的主要原因。母体感染后免疫反应如何调节 HCMV 宫内传播的风险,目前仍知之甚少。母体 T 细胞可能在防止母体-胎儿界面感染和限制胎盘内传播方面发挥关键作用,但人们担心感染后的免疫反应也可能导致胎盘功能障碍和不良妊娠结局。本研究探讨了 CD4+和 CD8+T 细胞在豚鼠原发性巨细胞病毒感染模型中的作用。针对豚鼠 CD4 和 CD8 的单克隆抗体用于在妊娠中期后耗尽非妊娠和妊娠豚鼠的 T 细胞。与用对照抗体治疗的动物相比,CD4+T 细胞耗竭增加了疾病的严重程度,导致病毒载量显著升高,并增加了先天性豚鼠巨细胞病毒(GPCMV)感染的发生率。CD8+T 细胞耗竭耐受性相当好,并不显著影响感染豚鼠的体重或其血液或组织中的病毒载量。然而,在感染后,CD8+T 细胞耗竭的母鼠胎盘和蜕膜中检测到的病毒基因组和转录物明显更多。本研究证实了早先在非人类灵长类动物中发现的结果,即母体 CD4+T 细胞在限制妊娠期间原发性 CMV 感染的严重程度方面发挥关键作用,同时也表明其他先天和适应性免疫反应可以在 α-CD8 处理的豚鼠中弥补缺失的 CD8+T 细胞反应。