A　coronavirus　pandemic　caused　by　a　novel　coronavirus　(SARS-CoV-2)　has　spread　rapidly　worldwide　since　December　2019.　Improved　understanding　and　new　strategies　to　cope　with　novel　coronaviruses　are　urgently　needed.　Viruses　(especially　RNA　viruses)　encode　a　limited　number　and　size　(length　of　polypeptide　chain)　of　viral　proteins　and　must　interact　with　the　host　cell　components　to　control　(hijack)　the　host　cell　machinery.　To　achieve　this　goal,　the　extensive　mimicry　of　SLiMs　in　host　proteins　provides　an　effective　strategy.　However,　little　is　known　regarding　SLiMs　in　coronavirus　proteins　and　their　potential　targets　in　host　cells.　The　objective　of　this　study　is　to　uncover　SLiMs　in　coronavirus　proteins　that　are　present　within　host　cells.　These　SLiMs　have　a　high　possibility　of　interacting　with　host　intracellular　proteins　and　hijacking　the　host　cell　machinery　for　virus　replication　and　dissemination.　In　total,　1,479　SLiM　hits　were　identified　in　the　16　proteins　of　590　coronaviruses　infecting　humans.　Overall,　106　host　proteins　were　identified　that　may　interact　with　SLiMs　in　16　coronavirus　proteins.　These　SLiM-interacting　proteins　are　composed　of　many　intracellular　key　regulators,　such　as　receptors,　transcription　factors　and　kinases,　and　may　have　important　contributions　to　virus　replication,　immune　evasion　and　viral　pathogenesis.　A　total　of　209　pathways　containing　proteins　that　may　interact　with　SLiMs　in　coronavirus　proteins　were　identified.　This　study　uncovers　potential　mechanisms　by　which　coronaviruses　hijack　the　host　cell　machinery.　These　results　provide　potential　therapeutic　targets　for　viral　infections.