Hasenkrug Kim J, Feldmann Friederike, Myers Lara, Santiago Mario L, Guo Kejun, Barrett Bradley S, Mickens Kaylee L, Carmody Aaron, Okumura Atsushi, Rao Deepashri, Collins Madison M, Messer Ronald J, Lovaglio Jamie, Shaia Carl, Rosenke Rebecca, van Doremalen Neeltje, Clancy Chad, Saturday Greg, Hanley Patrick, Smith Brian, Meade-White Kimberly, Shupert W Lesley, Hawman David W, Feldmann Heinz
Laboratory of Persistent Viral Diseases, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, MT, USA.
Rocky Mountain Veterinary Branch, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, MT, USA.
bioRxiv. 2021 Apr 4:2021.04.02.438262. doi: 10.1101/2021.04.02.438262.
Severe COVID-19 has been associated with T cell lymphopenia 1,2, but no causal effect of T cell deficiency on disease severity has been established. To investigate the specific role of T cells in recovery from SARS-CoV-2 infections we studied rhesus macaques that were depleted of either CD4+, CD8+ or both T cell subsets prior to infection. Peak virus loads were similar in all groups, but the resolution of virus in the T cell-depleted animals was slightly delayed compared to controls. The T cell-depleted groups developed virus-neutralizing antibody responses and also class-switched to IgG. When re-infected six weeks later, the T cell-depleted animals showed anamnestic immune responses characterized by rapid induction of high-titer virus-neutralizing antibodies, faster control of virus loads and reduced clinical signs. These results indicate that while T cells play a role in the recovery of rhesus macaques from acute SARS-CoV-2 infections, their depletion does not induce severe disease, and T cells do not account for the natural resistance of rhesus macaques to severe COVID-19. Neither primed CD4+ or CD8+ T cells appeared critical for immunoglobulin class switching, the development of immunological memory or protection from a second infection.
重症新型冠状病毒肺炎(COVID-19)与T细胞淋巴细胞减少有关[1,2],但尚未确定T细胞缺乏对疾病严重程度的因果影响。为了研究T细胞在从严重急性呼吸综合征冠状病毒2(SARS-CoV-2)感染中恢复过程中的具体作用,我们研究了在感染前耗竭CD4+、CD8+或这两种T细胞亚群的恒河猴。所有组的病毒载量峰值相似,但与对照组相比,T细胞耗竭动物体内病毒的清除略有延迟。T细胞耗竭组产生了病毒中和抗体反应,并且还发生了向IgG的类别转换。六周后再次感染时,T细胞耗竭动物表现出回忆性免疫反应,其特征是快速诱导高滴度病毒中和抗体、更快地控制病毒载量以及减轻临床症状。这些结果表明,虽然T细胞在恒河猴从急性SARS-CoV-2感染中恢复过程中发挥作用,但其耗竭不会诱发严重疾病,并且T细胞并非恒河猴对重症COVID-19天然抵抗力的原因。致敏的CD4+或CD8+ T细胞对于免疫球蛋白类别转换、免疫记忆的形成或预防再次感染似乎都不重要。