SARS-CoV, but not HCoV-NL63, utilizes cathepsins to infect cells: viral entry.

作者: I-Chueh Huang , Berend Jan Bosch , Wenhui Li , Michael Farzan , Peter M. Rottier

DOI: 10.1007/978-0-387-33012-9_60

关键词: ProteasesVirusCoronavirusCathepsin LVirologyViral entryFusion proteinBiologyCathepsinTissue tropism

摘要: Three genetic and serologic groups of coronaviruses have been described. Group 1 human coronavirus HCoV-229E utilizes aminopeptidase N (APN; CD13) as its cellular receptor, 2 whereas SARS-CoV, a group virus, uses angiotensin-converting enzyme (ACE2). 4 A recently identified novel coronavirus, HCoV-NL63, the SARS-CoV receptor ACE2, despite close similarity to other coronaviruses. Some S proteins are cleaved into domains by furin-like protease in virus-producing cells. The resulting S1 domain mediates binding, 7 Cterminal S2 fusion between viral membranes. This producer-cell processing protein is essential for infection HIV-1 influenza virus. Although can be their with proteins, HCoV-NL63 not processed producer Cathepsins diverse endosomal lysosomal proteases. role cathepsins reovirus well established. After receptor-mediated endocytosis, degradation outer capsid σ3 infection. Recently, it has demonstrated that mediated GP Zaire Ebola virus depends on cathepsin B. Here we show play an important In contrast, dependent activities. Thus variations proteases serve additional determinant tropism.

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