Department of Biology, Saint Louis University, 3507 Laclede Avenue, Saint Louis, MO 63103, USA.
Virol J. 2011 Dec 20;8:549. doi: 10.1186/1743-422X-8-549.
Human infants are frequently hospitalized due to infection with the paramyxovirus respiratory syncytial virus (RSV). However, very little is known about the neonatal response to paramyxoviral infection. Here, a neonatal model of paramyxoviral infection is developed using the mouse pathogen Sendai virus (SeV).
Adult mice infected with SeV developed a predominantly neutrophilic inflammatory cell influx and a concomitant reduction in lung function, as determined by oxygen saturation. In contrast, neonates with SeV had significantly reduced inflammation and normal lung function. Surprisingly, infected neonates had similar viral loads as adult mice. A reduced neutrophil influx in the neonates may be due in part to reduced expression of both CXCL2 and intracellular adhesion molecule-1 (ICAM-1). Expression of IFN-γ and TNF-α increased in a dose-dependent manner in adult lungs, but neonates did not increase expression of either of these cytokines, even at the highest doses. Importantly, the expression of the RIG-I-like receptors (RLRs) was delayed in the neonatal mice, which might have contributed to their reduced inflammation and differential cytokine expression.
Neonatal mice developed similar SeV titers and cleared the virus with similar efficiency despite developing a dramatically lower degree of pulmonary inflammation compared to adults. This suggests that inflammation in the lung may not be required to control viral replication. Future studies will be needed to determine any effect the reduced inflammation may have on the development of a protective memory response in neonates.
由于感染副粘病毒呼吸道合胞病毒（RSV），人类婴儿经常住院。然而，对于新生儿对副粘病毒感染的反应知之甚少。在这里，使用小鼠病原体仙台病毒（SeV）开发了副粘病毒感染的新生儿模型。
感染 SeV 的成年小鼠表现出以中性粒细胞为主的炎症细胞浸润，同时肺功能下降，通过氧饱和度来确定。相比之下，感染 SeV 的新生儿炎症明显减少，肺功能正常。令人惊讶的是，感染的新生儿与成年小鼠具有相似的病毒载量。新生儿中中性粒细胞浸润减少的部分原因可能是 CXCL2 和细胞间黏附分子-1（ICAM-1）的表达均降低。IFN-γ和 TNF-α在成年肺中呈剂量依赖性增加，但新生儿即使在最高剂量下也不会增加这两种细胞因子的表达。重要的是，新生儿中的 RIG-I 样受体（RLRs）表达延迟，这可能导致其炎症减少和细胞因子表达差异。
尽管与成年人相比，新生儿肺部的炎症程度明显降低，但新生小鼠仍能产生类似的 SeV 滴度，并以相似的效率清除病毒。这表明肺部炎症可能不是控制病毒复制所必需的。需要进一步的研究来确定减少的炎症可能对新生儿保护性记忆反应的发展产生的任何影响。
