Infectious hepatitis type A and type E are caused by phylogenetically distinct single-stranded, positive-sense RNA viruses that were once considered to be non-enveloped. However, studies show that both are released nonlytically from hepatocytes as ‘quasi-enveloped’ virions cloaked in host membranes. These virion types predominate in the blood of infected individuals and mediate virus spread within the liver. They lack virally encoded proteins on their surface and are resistant to neutralizing anti-capsid antibodies induced by infection, yet they efficiently enter cells and initiate new rounds of virus replication. In this Review, we discuss the mechanisms by which specific peptide sequences in the capsids of these quasi-enveloped virions mediate their endosomal sorting complexes required for transport (ESCRT)-dependent release from hepatocytes through multivesicular endosomes, what is known about how they enter cells, and the impact of capsid quasi-envelopment on host immunity and pathogenesis.

A型和E型传染性肝炎是由系统发育上不同的单链、正义RNA病毒引起的，这些病毒曾经被认为是无包膜的。然而，研究表明，两者都以隐藏在宿主膜中的“准包膜”病毒体的形式从肝细胞中非裂解性释放。这些病毒体类型在感染者的血液中占主导地位，并介导病毒在肝脏内传播。它们的表面缺乏病毒编码的蛋白质，并且对感染引起的中和抗衣壳抗体有抵抗力，但它们能有效地进入细胞并启动新一轮的病毒复制。在这篇综述中，我们讨论了这些准包膜病毒粒子衣壳中的特定肽序列介导其内体分选复合物的机制，这些复合物是通过多囊泡内体从肝细胞中运输（ESCRT）依赖性释放所需的，以及它们如何进入细胞的已知信息，以及衣壳准包膜对宿主免疫和发病机制的影响。