52
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      The HIV-1 pandemic: does the selective sweep in chimpanzees mirror humankind’s future?

      review-article
      1 , , 1 , 2
      Retrovirology
      BioMed Central
      AIDS, Chimpanzee, HIV-1, HLA, Human, MHC, Repertoire reduction, SIVcpz, Zoonosis

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          An HIV-1 infection progresses in most human individuals sooner or later into AIDS, a devastating disease that kills more than a million people worldwide on an annual basis. Nonetheless, certain HIV-1-infected persons appear to act as long-term non-progressors, and elite control is associated with the presence of particular MHC class I allotypes such as HLA-B*27 or -B*57. The HIV-1 pandemic in humans arose from the cross-species transmission of SIV cpz originating from chimpanzees. Chimpanzees, however, appear to be relatively resistant to developing AIDS after HIV-1/SIV cpz infection. Mounting evidence illustrates that, in the distant past, chimpanzees experienced a selective sweep resulting in a severe reduction of their MHC class I repertoire. This was most likely caused by an HIV-1/SIV-like retrovirus, suggesting that chimpanzees may have experienced long-lasting host-virus relationships with SIV-like viruses. Hence, if natural selection is allowed to follow its course, prospects for the human population may look grim, thus underscoring the desperate need for an effective vaccine.

          Related collections

          Most cited references110

          • Record: found
          • Abstract: found
          • Article: not found

          HLA and HIV-1: heterozygote advantage and B*35-Cw*04 disadvantage.

          A selective advantage against infectious disease associated with increased heterozygosity at the human major histocompatibility complex [human leukocyte antigen (HLA) class I and class II] is believed to play a major role in maintaining the extraordinary allelic diversity of these genes. Maximum HLA heterozygosity of class I loci (A, B, and C) delayed acquired immunodeficiency syndrome (AIDS) onset among patients infected with human immunodeficiency virus-type 1 (HIV-1), whereas individuals who were homozygous for one or more loci progressed rapidly to AIDS and death. The HLA class I alleles B*35 and Cw*04 were consistently associated with rapid development of AIDS-defining conditions in Caucasians. The extended survival of 28 to 40 percent of HIV-1-infected Caucasian patients who avoided AIDS for ten or more years can be attributed to their being fully heterozygous at HLA class I loci, to their lacking the AIDS-associated alleles B*35 and Cw*04, or to both.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Peak SIV replication in resting memory CD4+ T cells depletes gut lamina propria CD4+ T cells.

            In early simian immunodeficiency virus (SIV) and human immunodeficiency virus-1 (HIV-1) infections, gut-associated lymphatic tissue (GALT), the largest component of the lymphoid organ system, is a principal site of both virus production and depletion of primarily lamina propria memory CD4+ T cells; that is, CD4-expressing T cells that previously encountered antigens and microbes and homed to the lamina propria of GALT. Here, we show that peak virus production in gut tissues of SIV-infected rhesus macaques coincides with peak numbers of infected memory CD4+ T cells. Surprisingly, most of the initially infected memory cells were not, as expected, activated but were instead immunophenotypically 'resting' cells that, unlike truly resting cells, but like the first cells mainly infected at other mucosal sites and peripheral lymph nodes, are capable of supporting virus production. In addition to inducing immune activation and thereby providing activated CD4+ T-cell targets to sustain infection, virus production also triggered an immunopathologically limiting Fas-Fas-ligand-mediated apoptotic pathway in lamina propria CD4+ T cells, resulting in their preferential ablation. Thus, SIV exploits a large, resident population of resting memory CD4+ T cells in GALT to produce peak levels of virus that directly (through lytic infection) and indirectly (through apoptosis of infected and uninfected cells) deplete CD4+ T cells in the effector arm of GALT. The scale of this CD4+ T-cell depletion has adverse effects on the immune system of the host, underscoring the importance of developing countermeasures to SIV that are effective before infection of GALT.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              DC-SIGN: escape mechanism for pathogens.

              Dendritic cells (DCs) are crucial in the defence against pathogens. Invading pathogens are recognized by Toll-like receptors (TLRs) and receptors such as C-type lectins expressed on the surface of DCs. However, it is becoming evident that some pathogens, including viruses, such as HIV-1, and non-viral pathogens, such as Mycobacterium tuberculosis, subvert DC functions to escape immune surveillance by targeting the C-type lectin DC-SIGN (DC-specific intercellular adhesion molecule-grabbing nonintegrin). Notably, these pathogens misuse DC-SIGN by distinct mechanisms that either circumvent antigen processing or alter TLR-mediated signalling, skewing T-cell responses. This implies that adaptation of pathogens to target DC-SIGN might support pathogen survival.
                Bookmark

                Author and article information

                Journal
                Retrovirology
                Retrovirology
                Retrovirology
                BioMed Central
                1742-4690
                2013
                24 May 2013
                : 10
                : 53
                Affiliations
                [1 ]Department of Comparative Genetics and Refinement, Biomedical Primate Research Centre, Lange Kleiweg 161, 2288 GJ Rijswijk, The Netherlands
                [2 ]Department of Theoretical Biology and Bioinformatics, Utrecht University, 3584 CH Utrecht, The Netherlands
                Article
                1742-4690-10-53
                10.1186/1742-4690-10-53
                3667106
                23705941
                6ef1fcaf-2134-40a7-aae4-6e6484411ada
                Copyright ©2013 de Groot and Bontrop; licensee BioMed Central Ltd.

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 6 December 2012
                : 4 April 2013
                Categories
                Review

                Microbiology & Virology
                aids,chimpanzee,hiv-1,hla,human,mhc,repertoire reduction,sivcpz,zoonosis
                Microbiology & Virology
                aids, chimpanzee, hiv-1, hla, human, mhc, repertoire reduction, sivcpz, zoonosis

                Comments

                Comment on this article