Alpharetrovirus Envelope-Receptor Interactions

病毒包膜 脂质双层融合 病毒进入 融合机制 细胞生物学 糖蛋白 细胞质 疱疹病毒糖蛋白B 细胞内 生物 受体 细胞融合 病毒膜 化学 病毒 生物物理学 病毒学 病毒复制 生物化学 细胞
作者
Richard Barnard,John A. T. Young
出处
期刊:Current Topics in Microbiology and Immunology 卷期号:: 107-136 被引量:22
标识
DOI:10.1007/978-3-642-19012-4_3
摘要

Infection by all enveloped viruses occurs via the fusion of viral and cellular membranes and delivery of the viral nucleocapsid into the cell cytoplasm, after association of the virus with cognate receptors at the cell surface. This process is mediated by viral fusion proteins anchored in the viral envelope and can be defined based on the requirement for low pH to trigger membrane fusion. In viruses that utilize a pH-dependent entry mechanism, such as influenza virus, viral fusion is triggered by the acidic environment of intracellular organelles after uptake of the virus from the cell surface and trafficking to a low-pH compartment. In contrast, in viruses that utilize a pH-independent entry mechanism, such as most retroviruses, membrane fusion is triggered solely by the interaction of the envelope glycoprotein with cognate receptors, often at the cell surface. However, recent work has indicated that the alpharetrovirus, avian sarcoma and leukosis virus (ASLV), utilizes a novel entry mechanism that combines aspects of both pH-independent and pH-dependent entry. In ASLV infection, the interaction of the envelope glycoprotein (Env) with cognate receptors at the cell surface causes an initial conformational change that primes (activates) Env and renders it sensitive to subsequent low-pH triggering from an intracellular compartment. Thus unlike other pH-dependent viruses, ASLV Env is only sensitive to low-pH triggering following interaction with its cognate receptor. In this manuscript we review current research on ASLV Env-receptor interactions and focus on the specific molecular requirements of both the viral fusion protein and cognate receptors for ASLV entry. In addition, we review data pertaining to the novel two-step entry mechanism of ASLV entry and propose a model by which ASLV Env elicits membrane fusion.
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