ICV usually causes mild upper respiratory contamination but can cause lower respiratory contamination in children less than 2 years of age [178]. deaths from about 27 million cases of contamination as of 8 September 2020, has provoked worldwide investigations of CoVs. With the aim of developing efficient strategies for controlling computer virus outbreaks and recurrences of seasonal computer virus variants, here we overview the structures, diversities, host ranges and host receptors of all IVs and CoVs and critically evaluate current knowledge of receptor binding specificity of spike glycoproteins, which mediates contamination, of IVs and of zoonotic, pandemic and seasonal CoVs. (gr. 1)Single linear (+)ssRNA BatsRo(HKU10)-, Hi(HKU10)-, Rh(HKU2)-, Sc(512)-, Mi(1A, 1B, HKU8)- BatCoVUnknown [74] Other animalsFeCoV I & II (nonvirulent form of FCoV), CCoV, TGEV, PEDVGastroenteritisS1S1B (S1-CTD)(gr. 2)Single linear (+)ssRNA Other animalsMasked palm civet, raccoon doggie: SARS-CoV-like computer virus(gr.3)Single linear (+)ssRNA BirdsInfectious bronchitis computer virus (IBV2)Bronchitis, nephritis, reproductive problemsS1-NTDIBV: 2,3-linked sialic acids type 1 lactosamines(a new group)Single linear (+)ssRNA BirdsFalCoV, HouCoV, PiCoVUnknown [116] Other animalsPorCoV (PDCoV)Diarrhea in newborn pigletsS1pAPN in porcine alveolar macrophages but not necessary for infection of lung-derived fibroblast cells [77] Open in a separate windows 9-(Ra); Bat-SL-RmYN02: SARS-like CoV number 02 isolated from (Rm) in Chinas Yunnan (YN) province; BCoV: Purvalanol B bovine coronavirus; CCoV: canine coronavirus; CEACAM1: carcinoembryonic antigen-related cell adhesion molecule 1; ChRCoV: China Rattus coronavirus; CoV: coronavirus; CTD: C-terminal domain name; DC-SIGN: dendritic cell-specific ICAM-3 grabbing non-integrin; DC-SIGNR: DC-SIGN-related protein; EqCoV (ECoV): equine coronavirus; FalCoV: falcon coronavirus; FCoV: feline coronavirus; FeCoV I & II: feline coronavirus type I & II; FIPV: feline infectious peritonitis; GfCoV: guineafowl coronavirus; HCoV: human coronavirus; HE: hemagglutinin-esterase; Hi-: bat; HouCoV: houbara bustard coronavirus; Hp-: Chinese pipistrelle bat (bat; NCAM: neural cell adhesion molecule; Neo-: bat; PiCoV: pigeon coronavirus; PorCoV (PDCoV): Porcine deltacoronavirus; PRCoV: porcine respiratory coronavirus; RCoV: rat coronavirus; Rf-: bat; Ro-: bat; Rp-: bat; Sl-: bat; URTI: upper respiratory tract contamination. Of the three genera of IVs, alpha IVs (IAVs), beta IVs (IBVs) and gamma IVs (ICVs), that infect humans, eight segmented (?)ssRNA-containing IAVs (A/H3N2/68 and A/H1N1/09 variants) and IBVs (B/Yamagata and B/Victoria lineage-like viruses) with hemagglutinin (HA) spikes cause seasonal influenza epidemics that spread rapidly and cause moderate to severe or fatal illnesses. Seasonal influenza vaccines and anti-influenza drugs against IAVs and IBVs are available, but seasonal influenza still causes up to 5 million severe illnesses and up to 650,000 deaths each year [12]. Thus, epidemics of Purvalanol B IAVs and IBVs are important public health issues [12]. Seven segmented (?)ssRNA-containing ICVs with hemagglutinin-esterase-fusion (HEF) spikes usually cause mild upper respiratory disease but can cause lower respiratory disease in children and severe illness in infants [13]. Other seven segmented (?)ssRNA-containing IDVs with HEF spikes mainly infect cattle and cause respiratory illness [14]. These IDVs seem to have a zoonotic potential to infect humans, but whether they can cause illness in humans remains unknown [15]. Among all known influenza viruses, only IAVs are subtyped according to their HAs (H) and neuraminidase (NA or N) spikes BMP8A into H1CH18 and N1CN11. Several subtypes of IAVs, including H1N1, H3N2 and H5N1, have crossed the species barrier to infect a variety of birds and mammals including humans, indicating that they have zoonotic potential. IAVs not only mutate quickly but also prefer to reassort with other IAVs to form a new strain. Due to these properties, IAVs have caused four pandemics in the past 102 years [10,16]. These viruses continued to threat human health seasonally. However, the first recorded pandemic computer virus, A/H1N1/1918-derived computer virus, disappeared from human circulation after the appearance of the A/H2N2/1957 pandemic computer Purvalanol B virus made up of five gene segments (PB2, PA, NP, M and NS) from human A/H1N1/1918-derived computer virus. Similarly, A/H2N2/1957-derived computer virus disappeared after the appearance of A/H3N2/1968 pandemic computer virus made up of six gene segments (PB2, PA, NP, NA, M and NS) from human A/H2N2/1957-derived computer virus. In 1977, A/H1N1/1918-derived computer virus reemerged, probably due to accidental release from a laboratory, as a low-grade A/H1N1/1977 pandemic computer virus that primarily affected young immunologically na?ve people [17,18] who were born after the end of the H1 period (1957 and later). This resulted in two subtypes of IAVs circulating in humans, A/H1N1/1977-derived and A/H3N2/1968-derived viruses. After the appearance of the A/H1N1/2009 pandemic computer virus containing one human gene segment (PB1) from A/H3N2/1968-derived computer virus and three gene segments (H1, NP and NS) from classical swine A/H1N1 computer Purvalanol B virus believed to have been transmitted from.