PMC:7103735 / 1700-4636 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7103735","sourcedb":"PMC","sourceid":"7103735","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7103735","text":"Coronaviruses (CoVs) are found in various animals including aves and mammals. They can be divided into four genera named Alphacoronavirus, Betacoronavirus, Gammacoronavirus, and Deltacoronavirus [1]. The 2019 novel CoV (SARS-CoV-2) is the newest addition to human CoVs (HCoVs) that also include 229E, OC43, HKU1, NL63, severe acute respiratory syndrome (SARS) CoV, and Middle East respiratory syndrome (MERS) CoV. Whereas 229E and NL63 belong to Alphacoronavirus, others are members in the genus of Betacoronavirus. All of them are positive-stranded RNA viruses containing a polycistronic genome of ∼30 kb in size, coding for multiple non-structural proteins (ORF1a and ORF1b, processed into multiple nsp proteins) at the 5′-end plus multiple structural (S, E, M, and N) and lineage-specific accessory proteins (such as ORF3a, ORF3b, ORF6, ORF7a, ORF7b, ORF8a, ORF8b, and ORF9b in SARS-CoV) at the 3′-end (Figure 1). SARS-CoV and MERS-CoV are highly pathogenic and can cause severe diseases presented as acute respiratory distress syndrome (ARDS). Although the other four community-acquired HCoVs are a common cause of common cold only, they are thought to cause pandemics and major outbreaks of probably more severe respiratory diseases when they initially crossed species barriers to infect humans decades and centuries ago. All seven HCoVs have a zoonotic origin from bats, rodents, or domestic animals. Their reservoir hosts are selected through evolution. As a result of this selection and mutual adaptation for a long period of time, they usually become non-pathogenic or cause very mild diseases in their native reservoir hosts. However, when an animal CoV such as SARS-CoV-2 enters a new host such as humans, the severity of the disease is significantly increased at the start of a new round of adaptation. The outcome of infection is governed largely by the interplay between virus and host antiviral defence. Through years of co-evolution, this tug-of-war ultimately reaches a tie or a balance under which virus and host co-exist peacefully or even in mutual benefit. Understanding the host restriction factors and the viral countermeasures will shed significant new light on viral pathogenesis and antiviral development. Although it remains to be elucidated how SARS-CoV-2 interacts with host antiviral immunity, lessons can be learned from other HCoVs and human pathogenic viruses in other families including the human immunodeficiency viruses (HIVs). In this review, we focus on some of the key questions surrounding SARS-CoV-2 and its interplay with the host.\nFigure 1. Genome organization of HCoVs. Schematic diagram of seven known HCoVs is shown (not in scale). The genes encoding structural proteins spike (S), envelope (E), membrane (M), and nucleocapsid (N) are in green. The gene encoding haemagglutinin-esterase (HE) in lineage A of betacoronaviruses is in orange. 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