Natural reinfection with respiratory syncytial virus does not boost virus-specific T-cell immunity

Natural reinfection with respiratory syncytial virus does not boost virus-specific T-cell immunity
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DOI:
10.1203/00006450-200209000-00009
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发表时间:
2002-09-01
期刊:
影响因子:
3.6
通讯作者:
Kimpen, JLL
Kimpen, JLL
中科院分区:
医学3区
文献类型:
--
作者:
Bont, L;Versteegh, J;Kimpen, JLL

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为了确定自然再感染期间呼吸道合胞病毒(RSV)特定细胞介导的免疫的作用,我们研究了RSV特异性T细胞反应是否可以防止再感染,并且随后再感染是否会增强病毒特异性记忆。在因RSV支气管炎住院的55名婴儿中,在三个时间点时测量了外周血中RSV特异性淋巴增生性反应:入院时,入院后4周,在第二个冬季后1 Y后1 Y。记忆被定义为刺激指数(SI)> 2。在第二个冬季,在每种流鼻子的情况下都收集了鼻分泌物。如果免疫荧光或PCR为RSV,则可以诊断出重新感染。在原发性RSV感染入院时,在一个儿童中发现了病毒特异性记忆,而4周后44个婴儿(80%)患有记忆。在第二个冬季,在23名婴儿(43%)中发现了RSV的再感染。在第二季之后,发现了20名婴儿(38%)的记忆。第二个冬季季节后,有和没有再感染的婴儿之间没有SI的差异(2.3对2.1)。然而,在初次RSV感染后4周和第二个冬季后的SI测量之间发现了非常显着的相关性(r = 0.40,p = 0.001)。总之,RSV特异性的T细胞响应不能提供防止再感染的保护。此外,再感染并不能增强RSV特异性T细胞增殖。为了解释这两个发现,假设RSV特异性T细胞在重新感染后无法在体内扩展。
To determine the role of respiratory syncytial virus (RSV)specific cell-mediated immunity during natural reinfection, we investigated whether RSV-specific T-cell responses protect against reinfection and, subsequently, whether reinfection boosts virus-specific memory. In a cohort of 55 infants who were hospitalized for RSV bronchiolitis, RSV-specific lymphoproliferative responses in the peripheral blood were measured at three time-points: on admission, 4 wk after admission, and 1 y later, after the second winter season. Memory was defined as a stimulation index (SI) >2. During the second winter season, nasal secretions were collected in every case of a runny nose. Reinfection was diagnosed if immunofluorescence or PCR was positive for RSV. Virus-specific memory was found in one child on admission for primary RSV infection, whereas 4 wk later 44 infants (80%) had memory. Reinfection with RSV was found in 23 infants (43%) during the second winter season. After the second season, memory was found in 20 infants (38%). No differences in SI after the second winter season were found between infants with and without reinfection (2.3 versus 2.1). However, a highly significant correlation was found between SI measured 4 wk after primary RSV infection and SI after the second winter season (r = 0.40, p = 0.001). In conclusion, RSV-specific T-cell responses did not provide protection against reinfection. Moreover, reinfection did not boost RSV-specific T-cell proliferation. To explain both findings, it is hypothesized that RSV-specific T cells fail to expand in vivo upon reinfection.