Han Haowei, Smythe Ciaran, Yousefian Faraz, Berman Brian
J Drugs Dermatol. 2023 Feb 1;22(2):182-189. doi: 10.36849/JDD.7230.
Molluscum contagiosum (MC) is an acute infection caused by the molluscum contagiosum virus (MCV) with a worldwide incidence of approximately 8,000 cases per 100,000 individuals annually. Greater than 90% of MC cases occur in the pediatric population, and affected adults are more likely to be younger or immunocompromised. MC has minimal inflammation initially; however, a strong inflammatory response can occur during resolution of the infection, termed the beginning of the end (BOTE). MC infections may last months to years, and it is hypothesized that persistent infections may be due to suppression of immunity by MCV proteins, thus affecting MC’s clinical progression.
We reviewed the current proposed mechanisms of MCV immune evasion and discuss potential therapeutic options for MC treatment.
A literature search was conducted using electronic databases (Pubmed, Google Scholar, Medline).
We compiled 18 original research articles and identified 11 proteins produced by MCV that are postulated to participate in evasion of host immunity through various molecular pathways. These proteins and/or their downstream pathways may be influenced by MC treatments in phase 3 development, including berdazimer gel 10.3% and VP-102 cantharidin, 0.7%.
MCV is distinctive in evading immune surveillance by inhibiting or dampening several immune pathways via the production of viral proteins. The result is decreasing local inflammatory response which contributes to the prolonged survival of MCV in the epidermis. Persistent MC can be a nuisance for some patients and treatment may be desired. Currently, no treatment has been approved by the US Food and Drug Administration (FDA). Two approaches in the pipeline may affect the immune avoidance mechanisms; nevertheless, their exact mechanisms between the potential therapeutics and viral proteins remain enigmatic. J Drugs Dermatol. 2023;22(2):182-189. doi:10.36849/JDD.7230.
传染性软疣（MC）是由传染性软疣病毒（MCV）引起的一种急性感染，全球发病率约为每年每10万人8000例。超过90%的MC病例发生在儿童群体中，受影响的成年人更可能是年轻人或免疫功能低下者。MC最初炎症反应轻微；然而，在感染消退过程中可能会出现强烈的炎症反应，称为“结束的开始”（BOTE）。MC感染可能持续数月至数年，据推测，持续感染可能是由于MCV蛋白抑制免疫，从而影响MC的临床进展。
我们回顾了当前提出的MCV免疫逃逸机制，并讨论MC治疗的潜在选择。
使用电子数据库（PubMed、谷歌学术、Medline）进行文献检索。
我们汇总了18篇原创研究文章，确定了MCV产生的11种蛋白质，推测这些蛋白质通过各种分子途径参与逃避宿主免疫。这些蛋白质和/或其下游途径可能受到处于3期开发阶段的MC治疗的影响，包括10.3%的贝达齐默凝胶和0.7%的VP-102斑蝥素。
MCV通过产生病毒蛋白抑制或减弱多种免疫途径来逃避免疫监视，这一点很独特。结果是局部炎症反应减弱，这有助于MCV在表皮中长期存活。持续性MC对一些患者来说可能是个麻烦，可能需要进行治疗。目前，美国食品药品监督管理局（FDA）尚未批准任何治疗方法。正在研发的两种方法可能会影响免疫逃避机制；然而，潜在治疗药物与病毒蛋白之间的确切机制仍不清楚。《药物皮肤病学杂志》。2023；22（2）：182 - 189。doi:10.36849/JDD.7230。
