title: Syncytium formation and HIV-1 replication are both accentuated by purified influenza and virus-associated neuraminidase.
abstract: The degree of sialylation has been shown previously to modulate the process of human immunodeficiency virus type-1 (HIV-1) infection by affecting the interaction between the virus and CD4-expressing target cells. In the present study, we investigated whether HIV-1 replication cycle was affected by neuraminidase (NA) derived from the human influenza (flu) virus. We first demonstrate that the level of HIV-1-mediated syncytium formation was greatly enhanced in the presence of purified flu NA. Pretreatment of established monocytic and lymphocytic cell lines as well as primary mononuclear cells with purified flu NA augmented also the process of virus infection. A comparable up-regulating effect was observed when using several strains of UV-inactivated whole flu virus, thereby suggesting that virus-anchored NA enzymes positively modulate the HIV-1 life cycle. Furthermore, flu NA-mediated positive effect on HIV-1 biology was abrogated with zanamivir, a specific flu NA inhibitor. Our results provide a new model allowing the investigation of the potential benefit of using NA inhibitors in the treatment of HIV-1-infected patients suffering from coinfection with NA-bearing pathogens.
authors.affiliation: Centre de Recherche en Infectiologie, Hôpital du Centre Hospitalier Universitaire de L'Université Laval, Québec G1V 4G2, Canada.
authors.forename: Jiangfeng
authors.initials: J
authors.lastname: Sun
authors.forename: Benoit
authors.initials: B
authors.lastname: Barbeau
authors.forename: Sachiko
authors.initials: S
authors.lastname: Sato
authors.forename: Guy
authors.initials: G
authors.lastname: Boivin
authors.forename: Nathalie
authors.initials: N
authors.lastname: Goyette
authors.forename: Michel J
authors.initials: MJ
authors.lastname: Tremblay
mesh_terms: D000998:Antiviral Agents / Q000494:pharmacology; D001665:Binding Sites; D015704:CD4 Antigens / Q000096:biosynthesis; D015496:CD4-Positive T-Lymphocytes / Q000378:metabolism / Q000821:virology; D002450:Cell Communication; D002460:Cell Line; D015726:Giant Cells / Q000378:metabolism* / Q000821:virology*; D006146:Guanidines; D015497:HIV-1 / Q000378:metabolism* / Q000502:physiology; D006801:Humans; D019169:Jurkat Cells; D008156:Luciferases / Q000378:metabolism; D008214:Lymphocytes / Q000378:metabolism; D009000:Monocytes / Q000378:metabolism; D009439:Neuraminidase / Q000378:metabolism*; D009975:Orthomyxoviridae / Q000201:enzymology* / Q000378:metabolism*; D010957:Plasmids / Q000378:metabolism; D011714:Pyrans; D011991:Receptors, Virus / Q000502:physiology; D012794:Sialic Acids / Q000494:pharmacology; D013997:Time Factors; D014466:Ultraviolet Rays; D015854:Up-Regulation; D053243:Zanamivir
chemical_list: D000998:Antiviral Agents; D015704:CD4 Antigens; D006146:Guanidines; D011714:Pyrans; D011991:Receptors, Virus; D012794:Sialic Acids; D008156:Luciferases; D009439:Neuraminidase; D053243:Zanamivir