AIDS Weekly Plus
National Institute of Allergy and Infectious Diseases (NIAID) Details Research in HIV/AIDS
February 25, 2013
2013 FEB 25 (NewsRx) -- By a News Reporter-Staff News Editor at AIDS Weekly -- Investigators discuss new findings in Immune System Diseases and Conditions. According to news reporting out of Bethesda, Maryland, by NewsRx editors, research stated, "We recently reported that human immunodeficiency virus type 1 (HIV-1) carrying PTAP and LYPX(n)L L domains ceased budding when the nucleocapsid (NC) domain was mutated, suggesting a role for NC in HIV-1 release. Here we investigated whether NC involvement in virus release is a property specific to HIV-1 or a general requirement of retroviruses."
Our news journalists obtained a quote from the research from the National Institute of Allergy and Infectious Diseases (NIAID), "Specifically, we examined a possible role for NC in the budding of retroviruses relying on divergent L domains and structurally homologous NC domains that harbor diverse protein sequences. We found that NC is critical for the release of viruses utilizing the PTAP motif whether it functions within its native Gag in simian immunodeficiency virus cpzGAB2 (SIVcpzGAB2) or SIVsmmE543 or when it is transplanted into the heterologous Gag protein of equine infectious anemia virus (EIAV). In both cases, virus release was severely diminished even though NC mutant Gag proteins retained the ability to assemble spherical particles. Moreover, budding-defective NC mutants, which displayed particles tethered to the plasma membrane, were triggered to release virus when access to the cell endocytic sorting complex required for transport pathway was restored (i.e., in trans expression of Nedd4.2s). We also examined the role of NC in the budding of EIAV, a retrovirus relying exclusively on the (L)YPX(n)L-type L domain. We found that EIAV late budding defects were rescued by overexpression of the isolated Alix Bro1 domain (Bro1). Bro1-mediated rescue of EIAV release required the wild-type NC. EIAV NC mutants lost interactions with Bro1 and failed to produce viruses despite retaining the ability to self-assemble."
According to the news editors, the research concluded: "Together, our studies establish a role for NC in the budding of retroviruses harboring divergent L domains and evolutionarily diverse NC sequences, suggesting the utilization of a common conserved mechanism and/or cellular factor rather than a specific motif."
For more information on this research see: Budding of retroviruses utilizing divergent L domains requires nucleocapsid. The Journal of Virology, 2012;86(8):4182-93 (see also Immune System Diseases and Conditions).
Our news journalists report that additional information may be obtained by contacting N.F. Bello, Laboratory of Molecular Microbiology, Virus Budding Unit, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, United States.
Keywords for this news article include: Virion, Bethesda, Maryland, HIV/AIDS, Virology, gag Genes, RNA Viruses, Viral Genes, Nucleocapsid, Retroviridae, United States, HIV Infections, Genetic Phenomena, Genome Components, Genetic Structures, Vertebrate Viruses, Primate Lentiviruses, North and Central America, Human Immunodeficiency Virus.
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