Is HIV coat the key to targeting cells?

July 1991
New Scientist;7/13/91, Vol. 131 Issue 1777, p23
Studies whether a small portion of HIV's protein coat seems to be crucial in determining which types of cell the virus infects. Explanation on how the different strains of HIV present in individuals' bodies mutate during the course of disease; Sequence of 20 amino acids in the V3 loop, a highly variable region in HIV's coat protein which is important in stimulating an immune response.


Related Articles

  • Cell cycle G2/M arrest through an S phase-dependent mechanism by HIV-1 viral protein R. Ge Li; Park, Hyeon U.; Dong Liang; Zhao, Richard Y. // Retrovirology;2010, Vol. 7, p59 

    Background: Cell cycle G2 arrest induced by HIV-1 Vpr is thought to benefit viral proliferation by providing an optimized cellular environment for viral replication and by skipping host immune responses. Even though Vpr-induced G2 arrest has been studied extensively, how Vpr triggers G2 arrest...

  • Integrating assays. Frederickson, Robert // Nature Biotechnology;Jun99, Vol. 17 Issue 6, p523 

    Reports on efforts of scientists to produce viral proteins from noninfectious HIV-derived vectors. Use of extracts from infected cells in the production of viral proteins.

  • A tough viral nut to crack. Pomerantz, Roger J. // Nature;8/8/2002, Vol. 418 Issue 6898, p594 

    Provides information on virion infectivity factor (Vif), an accessory protein in HIV-1 virus. Structure of viral accessory proteins; Other HIV-1 accessory proteins.

  • The regulation of primate immunodeficiency virus infectivity by Vif is cell species restricted: a role for Vif in determining virus host range and cross-species transmission. Simon, James H. M.; Miller, David L.; Fouchier, Ron A. M.; Soares, Marcelo A.; Peden, Keith W. C.; Malim, Michael H. // EMBO Journal;3/1/98, Vol. 17 Issue 5, p1259 

    The primate immunodeficiency virus Vif proteins are essential for replication in appropriate cultured cell systems and, presumably, for the establishment of productive infections in vivo. We describe experiments that define patterns of complementation between human and simian immunodeficiency...

  • Fold Recognition of the Human Immunodeficiency Virus Type 1 V3 Loop and flexibility of Its Crown Structure During the Course of Adaptation to a Host. Watabe, Teruaki; Kishino, Hirohisa; Okuhara, Yoshiyasu; Kitazoe, Yasuhiro // Genetics;Mar2006, Vol. 172 Issue 3, p1385 

    The third hypervariable (V3) region of the HIV-1 gp120 protein is responsible for many aspects of viral infectivity. The tertiary structure of the V3 loop seems to influence the coreceptor usage of the virus, which is an important determinant of HJV pathogenesis. Hence, the information about...

  • SIVSM/HIV-2 Vpx proteins promote retroviral escape from a proteasome-dependent restriction pathway present in human dendritic cells. Goujon, Caroline; Rivière, Lise; Jarrosson-Wuilleme, Loraine; Bernaud, Jeanine; Rigal, Dominique; Darlix, Jean-Luc; Cimarelli, Andrea // Retrovirology;2007, Vol. 4, p1 

    Background: Vpx is a non-structural protein coded by members of the SIVSM/HIV-2 lineage that is believed to have originated by duplication of the common vpr gene present in primate lentiviruses. Vpx is incorporated into virion particles and is thus present during the early steps of viral...

  • Tat's seductive side. Stevenson, Mario // Nature Medicine;Feb2003, Vol. 9 Issue 2, p163 

    Discusses the regulation by viral protein Tat of the expression of chemokines that promote lymphocyte and monocyte migration. Facilitation by Tat of HIV dissemination; Impact of Tat of gene expression; Biology of HIV and the activities of its gene products.

  • HIV: Antiviral action countered by Nef. Aiken, Christopher // Nature;10/8/2015, Vol. 526 Issue 7572, p202 

    Reviews are presented of the articles "HIV-1 Nef promotes infection by excluding SERINC5 from virion incorporation" by Annachiara Rosa, Ajit Chande, Serena Ziglio, and others, and "SERINC3 and SERINC5 restrict HIV-1 infectivity and are counteracted by Nef" by Yoshiko Usami, Yuanfei Wu and...

  • The Ebola Virus Glycoprotein and HIV-1 Vpu Employ Different Strategies to Counteract the Antiviral Factor Tetherin. Kühl, Annika; Banning, Carina; Marzi, Andrea; Votteler, Jörg; Steffen, Imke; Bertram, Stephanie; Glowacka, Ilona; Konrad, Andreas; Stürzl, Michael; Guo, Ju-Tao; Schubert, Ulrich; Feldmann, Heinz; Behrens, Georg; Schindler, Michael; Pöhlmann1, Stefan // Journal of Infectious Diseases;2011 Supplement 3, Vol. 204, pS850 

    The antiviral protein tetherin/BST2/CD317/HM1.24 restricts cellular egress of human immunodeficiency virus (HIV) and of particles mimicking the Ebola virus (EBOV), a hemorrhagic fever virus. The HIV-1 viral protein U (Vpu) and the EBOV-glycoprotein (EBOV-GP) both inhibit tetherin. Here, we...


Read the Article


Sorry, but this item is not currently available from your library.

Try another library?
Sign out of this library

Other Topics