PMC:7712180 / 24287-25937 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7712180","sourcedb":"PMC","sourceid":"7712180","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7712180","text":"In 1940, a new serotype of influenza viruses was isolated and designated type B. The first strain was named B/Lee/1940. Influenza B viruses have continued to cause respiratory disease in humans with antigenic change. Although HA and NA antigenic differences within influenza B viruses (IBVs) are not sufficient to separate antigenic subtypes, there were sufficient antigenic differences to classify IBVs into two lineages: (i) Victoria lineage B/Victoria/2/1987-like and (ii) Yamagata lineage B/Yamagata/16/1988-like viruses [170]. Consequently, morbidity and mortality-associated seasonal influenza is currently caused by the two lineages of IBVs and two subtypes of IAVs, 1968-derived H3N2 and 2009-derived H1N1 viruses. In contrast to IAVs, IBVs infect mainly humans, although there are sporadic reports of IBV infection in seals, pigs, horses, pheasants and dogs [65]. Similar to IAVs, IBVs have eight (-)ssRNA genome segments and possess receptor-binding and -destroying activities on different molecules, homo-trimeric HA and homo-tetrameric NA glycoproteins. Clinically approved NA inhibitors (NAIs), including zanamivir, oseltamivir, laninamivir and peramivir, are now used for treatment of infection with not only IAVs but also IBVs [171]. Several chemical compounds that have been developed as anti-influenza A NAs, including Neu5Ac2en mimetics for minimizing side effects on human Neu1-Neu4 enzymes [172,173] and NA covalent inhibitors for irreversible NA inhibition [174] and Psidium guajava Linn. (guava) tea [175] and povidone-iodine that possess anti-influenza A sialidase activities [176] might be able to inhibit influenza B 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