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不同 HPV 长型异构体的表达作为规避适应性免疫的机制。

Expression of different L1 isoforms of papillomavirus as mechanism to circumvent adaptive immunity.

机构信息

Division of Viral Transformation Mechanisms, Research Program 'Infection, Inflammation and Cancer', German Cancer Research Center, Heidelberg, Germany.

Division of Functional Genome Analysis, Research Program 'Functional and Structural Genomics', German Cancer Research Center, Heidelberg, Germany.

出版信息

Elife. 2020 Aug 4;9:e57626. doi: 10.7554/eLife.57626.

DOI:10.7554/eLife.57626
PMID:32746966
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7402679/
Abstract

Although many high-risk mucosal and cutaneous human papillomaviruses (HPVs) theoretically have the potential to synthesize L1 isoforms differing in length, previous seroepidemiological studies only focused on the short L1 variants, co-assembling with L2 to infectious virions. Using the multimammate mouse as preclinical model, this is the first study demonstrating seroconversion against different L1 isoforms during the natural course of papillomavirus infection. Intriguingly, positivity with the cutaneous MnPV was accompanied by a strong seroresponse against a longer L1 isoform, but to our surprise, the raised antibodies were non-neutralizing. Only after a delay of around 4 months, protecting antibodies against the short L1 appeared, enabling the virus to successfully establish an infection. This argues for a novel humoral immune escape mechanism that may also have important implications on the interpretation of epidemiological data in terms of seropositivity and protection of PV infections in general.

摘要

尽管许多高风险的黏膜和皮肤型人乳头瘤病毒（HPV）理论上具有合成长度不同的 L1 同工型的潜力，但之前的血清流行病学研究仅关注短 L1 变体，与 L2 共同组装成感染性病毒颗粒。本研究首次使用多乳鼠作为临床前模型，证明了在自然感染 HPV 过程中针对不同 L1 同工型的血清转化。有趣的是，对皮肤型 MnPV 的阳性反应伴随着对较长 L1 同工型的强烈血清反应，但令我们惊讶的是，升高的抗体是非中和性的。只有在大约 4 个月的延迟后，针对短 L1 的保护性抗体才出现，使病毒能够成功建立感染。这表明存在一种新型的体液免疫逃逸机制，这可能对解释流行病学数据以及一般而言 HPV 感染的血清阳性率和保护具有重要意义。

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