title: Comparative analysis of the fusion efficiency elicited by the envelope glycoprotein V1-V5 regions derived from human immunodeficiency virus type 1 transmitted perinatally.
abstract: Understanding the properties of viruses preferentially establishing infection during perinatal transmission of human immunodeficiency virus type 1 (HIV-1) is critical for the development of effective measures to prevent transmission. A previous study demonstrated that the newly transmitted viruses (in infants) of chronically infected mother-infant pairs (MIPs) were fitter in terms of growth, which was imparted by their envelope (Env) glycoprotein V1-V5 regions, than those in the corresponding chronically infected mothers. In order to investigate whether the higher fitness of transmitted viruses was conferred by their higher entry efficiency directed by the V1-V5 regions during perinatal transmission, the fusogenicity of Env containing V1-V5 regions derived from transmitted and non-tranmsmitted viruses of five chronically infected MIPs and two acutely infected MIPs was analysed using two different cell-cell fusion assays. The results showed that, in one chronically infected MIP, a higher fusion efficiency was induced by the infant Env V1-V5 compared with that of the corresponding mother. Moreover, the V4-V5 regions played an important role in discriminating the transmitted and non-transmitted viruses in this pair. However, neither a consistent pattern nor significant differences in fusogenicity mediated by the V1-V5 regions between maternal and infant variants was observed in the other MIPs. This study suggests that there is no consistent and significant correlation between viral fitness selection and entry efficiency directed by the V1-V5 regions during perinatal transmission. Other factors such as the route and timing of transmission may also be involved.
authors.affiliation: Key Laboratory of Molecular Microbiology and Biotechnology (Ministry of Education), Key Laboratory of Microbial Functional Genomics (Tianjin), College of Life Sciences, Nankai University, Tianjin, PR China.|Laboratory of Medical Molecular Virology, School of Medicine, Nankai University, Tianjin, PR China.
authors.forename: Hongyan
authors.initials: H
authors.lastname: Guo
authors.affiliation: Nebraska Center for Virology, School of Biological Sciences, University of Nebraska-Lincoln, Lincoln, NE 68508, USA.
authors.forename: Levon G
authors.initials: LG
authors.lastname: Abrahamyan
authors.affiliation: Laboratory of Medical Molecular Virology, School of Medicine, Nankai University, Tianjin, PR China.
authors.forename: Chang
authors.initials: C
authors.lastname: Liu
authors.affiliation: Nebraska Center for Virology, School of Biological Sciences, University of Nebraska-Lincoln, Lincoln, NE 68508, USA.
authors.forename: Mackenzie
authors.initials: M
authors.lastname: Waltke
authors.affiliation: Key Laboratory of Molecular Microbiology and Biotechnology (Ministry of Education), Key Laboratory of Microbial Functional Genomics (Tianjin), College of Life Sciences, Nankai University, Tianjin, PR China.
authors.forename: Yunqi
authors.initials: Y
authors.lastname: Geng
authors.affiliation: Key Laboratory of Molecular Microbiology and Biotechnology (Ministry of Education), Key Laboratory of Microbial Functional Genomics (Tianjin), College of Life Sciences, Nankai University, Tianjin, PR China.
authors.forename: Qimin
authors.initials: Q
authors.lastname: Chen
authors.affiliation: Nebraska Center for Virology, School of Biological Sciences, University of Nebraska-Lincoln, Lincoln, NE 68508, USA.
authors.forename: Charles
authors.initials: C
authors.lastname: Wood
authors.affiliation: Laboratory of Medical Molecular Virology, School of Medicine, Nankai University, Tianjin, PR China.
authors.forename: Xiaohong
authors.initials: X
authors.lastname: Kong
mesh_terms: D000328:Adult; D000595:Amino Acid Sequence; D001483:Base Sequence; D004279:DNA, Viral / Q000235:genetics; D005260:Female; D015699:HIV Envelope Protein gp120 / Q000235:genetics / Q000502:physiology; D015658:HIV Infections / Q000635:transmission* / Q000821:virology*; D015497:HIV-1 / Q000235:genetics / Q000472:pathogenicity* / Q000502:physiology*; D006801:Humans; D007231:Infant, Newborn; D018445:Infectious Disease Transmission, Vertical; D008297:Male; D008969:Molecular Sequence Data; D010446:Peptide Fragments / Q000235:genetics / Q000502:physiology; D011247:Pregnancy; D011251:Pregnancy Complications, Infectious / Q000821:virology*; D017386:Sequence Homology, Amino Acid; D014760:Viral Fusion Proteins / Q000235:genetics / Q000502:physiology; D053586:Virus Internalization; D055815:Young Adult; D054299:env Gene Products, Human Immunodeficiency Virus / Q000235:genetics / Q000502:physiology*
chemical_list: D004279:DNA, Viral; D015699:HIV Envelope Protein gp120; C059761:HIV envelope protein gp120 (135-148); C059762:HIV envelope protein gp120 (305-321); D010446:Peptide Fragments; D014760:Viral Fusion Proteins; D054299:env Gene Products, Human Immunodeficiency Virus