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      Virus–host interaction in feline immunodeficiency virus (FIV) infection

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          Abstract

          Feline immunodeficiency virus (FIV) infection has been the focus of several studies because this virus exhibits genetic and pathogenic characteristics that are similar to those of the human immunodeficiency virus (HIV). FIV causes acquired immunodeficiency syndrome (AIDS) in cats, nevertheless, a large fraction of infected cats remain asymptomatic throughout life despite of persistent chronic infection. This slow disease progression may be due to the presence of factors that are involved in the natural resistance to infection and the immune response that is mounted by the animals, as well as due to the adaptation of the virus to the host. Therefore, the study of virus–host interaction is essential to the understanding of the different patterns of disease course and the virus persistence in the host, and to help with the development of effective vaccines and perhaps the cure of FIV and HIV infections.

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          Genetic restriction of HIV-1 infection and progression to AIDS by a deletion allele of the CKR5 structural gene. Hemophilia Growth and Development Study, Multicenter AIDS Cohort Study, Multicenter Hemophilia Cohort Study, San Francisco City Cohort, ALIVE Study.

          M. Dean, M. Carrington, C. Winkler … (1996)
          The chemokine receptor 5 (CKR5) protein serves as a secondary receptor on CD4(+) T lymphocytes for certain strains of human immunodeficiency virus-type 1 (HIV-1). The CKR5 structural gene was mapped to human chromosome 3p21, and a 32-base pair deletion allele (CKR5Delta32) was identified that is present at a frequency of approximately0.10 in the Caucasian population of the United States. An examination of 1955 patients included among six well-characterized acquired immunodeficiency syndrome (AIDS) cohort studies revealed that 17 deletion homozygotes occurred exclusively among 612 exposed HIV-1 antibody-negative individuals (2.8 percent) and not at all in 1343 HIV-1-infected individuals. The frequency of CKR5 deletion heterozygotes was significantly elevated in groups of individuals that had survived HIV-1 infection for more than 10 years, and, in some risk groups, twice as frequent as their occurrence in rapid progressors to AIDS. Survival analysis clearly shows that disease progression is slower in CKR5 deletion heterozygotes than in individuals homozygous for the normal CKR5 gene. The CKR5Delta32 deletion may act as a recessive restriction gene against HIV-1 infection and may exert a dominant phenotype of delaying progression to AIDS among infected individuals.
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            Natural versus adaptive regulatory T cells.

            Jeffrey Bluestone, Abul K Abbas (2003)
            The regulation of immune responses to self-antigens is a complex process that involves maintaining self-tolerance while retaining the capacity to mount robust immune responses against invading microorganisms. Over the past few years, many new insights into this process have been gained, leading to the re-emergence of the idea that regulatory T (T(Reg)) cells are a central mechanism of immune regulation. These insights have raised fundamental questions concerning what constitutes a T(Reg) cell, where they develop and what signals maintain T(Reg)-cell populations in a functional state. Here, we propose the existence of two subsets of CD4+ T(Reg) cells--natural and adaptive--that differ in terms of their development, specificity, mechanism of action and dependence on T-cell receptor and co-stimulatory signalling.
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              The HIV coreceptors CXCR4 and CCR5 are differentially expressed and regulated on human T lymphocytes.

              C. C. Bleul, L. Wu, J A Hoxie … (1997)
              The chemokine receptors CXCR4 and CCR5 function as coreceptors for HIV-1 entry into CD4+ cells. During the early stages of HIV infection, viral isolates tend to use CCR5 for viral entry, while later isolates tend to use CXCR4. The pattern of expression of these chemokine receptors on T cell subsets and their regulation has important implications for AIDS pathogenesis and lymphocyte recirculation. A mAb to CXCR4, 12G5, showed partial inhibition of chemotaxis and calcium influx induced by SDF-1, the natural ligand of CXCR4. 12G5 stained predominantly the naive, unactivated CD26(low) CD45RA+ CD45R0- T lymphocyte subset of peripheral blood lymphocytes. In contrast, a mAb specific for CCR5, 5C7, stained CD26(high) CD45RA(low) CD45R0+ T lymphocytes, a subset thought to represent previously activated/memory cells. CXCR4 expression was rapidly up-regulated on peripheral blood mononuclear cells during phytohemagglutinin stimulation and interleukin 2 priming, and responsiveness to SDF-1 increased simultaneously. CCR5 expression, however, showed only a gradual increase over 12 days of culture with interleukin 2, while T cell activation with phytohemagglutinin was ineffective. Taken together, the data suggest distinct functions for the two receptors and their ligands in the migration of lymphocyte subsets through lymphoid and nonlymphoid tissues. Furthermore, the largely reciprocal expression of CXCR4 and CCR5 among peripheral blood T cells implies distinct susceptibility of T cell subsets to viral entry by T cell line-tropic versus macrophage-tropic strains during the course of HIV infection.
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                Author and article information

                Contributors
                Sueli Akemi Taniwaki
                Andreza Soriano Figueiredo
                João Pessoa Araujo Jr.
                Journal
                Journal ID (nlm-ta): Comp Immunol Microbiol Infect Dis
                Journal ID (iso-abbrev): Comp. Immunol. Microbiol. Infect. Dis
                Title: Comparative Immunology, Microbiology and Infectious Diseases
                Publisher: Elsevier Ltd.
                ISSN (Print): 0147-9571
                ISSN (Electronic): 1878-1667
                Publication date PMC-release: 2 August 2013
                Publication date (Print): December 2013
                Publication date (Electronic): 2 August 2013
                Volume: 36
                Issue: 6
                Pages: 549-557
                Affiliations
                [a ]Department of Preventive Veterinary Medicine and Animal Health, School of Veterinary Medicine and Animal Science, University of São Paulo, São Paulo 05508-270, São Paulo, Brazil
                [b ]Laboratory of Viral Hepatitis, Oswaldo Cruz Institute (FIOCRUZ), Rio de Janeiro 21040-360, RJ, Brazil
                [c ]Department of Microbiology and Immunology, Biosciences Institute, Univ. Estadual Paulista (UNESP), Botucatu 18618-970, São Paulo, Brazil
                Author notes
                [* ]Corresponding author at: Laboratório de Virologia e Diagnóstico Molecular, Departamento de Microbiologia e Imunologia, Instituto de Biociências, Universidade Estadual Paulista (UNESP), Campus de Botucatu, Distrito de Rubião Jr. s/n, Botucatu 18618-970, São Paulo, Brazil. Tel.: +55 1438800422. jpessoa@ 123456ibb.unesp.br jp.cebola@ 123456gmail.com
                Article
                Publisher ID: S0147-9571(13)00055-6
                DOI: 10.1016/j.cimid.2013.07.001
                PMC ID: 7112627
                PubMed ID: 23910598
                SO-VID: 7bfaf508-8253-4e0f-b381-efb433293c80
                Copyright © Copyright © 2013 Elsevier Ltd. All rights reserved.
                License:

                Since January 2020 Elsevier has created a COVID-19 resource centre with free information in English and Mandarin on the novel coronavirus COVID-19. The COVID-19 resource centre is hosted on Elsevier Connect, the company's public news and information website. Elsevier hereby grants permission to make all its COVID-19-related research that is available on the COVID-19 resource centre - including this research content - immediately available in PubMed Central and other publicly funded repositories, such as the WHO COVID database with rights for unrestricted research re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for free by Elsevier for as long as the COVID-19 resource centre remains active.

                History
                Date received : 22 February 2013
                Date revision received : 28 June 2013
                Date accepted : 2 July 2013
                Categories
                Subject: Article

                ScienceOpen disciplines: Microbiology & Virology
                Keywords: feline immunodeficiency virus,immunopathogenesis,immune system dysfunction,natural resistence,cats
                Data availability:
                ScienceOpen disciplines: Microbiology & Virology
                Keywords: feline immunodeficiency virus, immunopathogenesis, immune system dysfunction, natural resistence, cats

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