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Veterinary microbiology2006; 113(3-4); 265-273; doi: 10.1016/j.vetmic.2005.11.048

Absence of viral envelope proteins in equine herpesvirus 1-infected blood mononuclear cells during cell-associated viremia.

Abstract: In vitro studies demonstrated that most equine herpesvirus 1 (EHV-1)-infected peripheral blood mononuclear cells (PBMC) do not expose viral envelope proteins on their surface. This protects them against antibody-dependent lysis. We examined whether viral envelope proteins are also undetectable on infected PBMC during cell-associated viremia. Further, surface expression of major histocompatibility complex (MHC)-I was examined, since MHC-I assists in making infected cells recognizable for cytotoxic T-lymphocytes (CTL). Four ponies, previously exposed to EHV, and two ponies that had no contact with EHV before, were inoculated with EHV-1. PBMC were collected at different time points up to 28 days post inoculation. Ninety-eight percent of the infected PBMC did not show viral envelope proteins on their surface. Moreover, infected PBMC without surface expression only produced immediate early and, at least, one early protein, ICP22, but not late envelope proteins gB and gM. This indicates that surface expression of viral envelope proteins is absent, simply because the PBMC are in an early phase of infection. The percentage of infected PBMC showing surface expression of MHC-I was similar as observed in non-infected PBMC from the same ponies (80-100%). Therefore, inefficient recognition of EHV-1-infected PBMC by CTLs does not arise from absent surface expression of MHC-I.
Publication Date: 2006-01-18 PubMed ID: 16387454DOI: 10.1016/j.vetmic.2005.11.048Google Scholar: Lookup
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  • Journal Article

Summary

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The research article explores the interaction between equine herpesvirus 1 and peripheral blood mononuclear cells in horses, revealing that ample infected cells do not expose viral envelope proteins on their surface, thus safeguarding them against antibody-dependent lysis.

Understanding the Study and its Context

  • This study revolves around equine herpesvirus 1 (EHV-1), a virus that majorly infects horses. The researchers investigated this in vitro, meaning outside a living organism, typically in a lab petri dish or test tube.
  • The highlight was peripheral blood mononuclear cells (PBMC), a type of immune cell that includes lymphocytes (T cells, B cells, NK cells) and monocytes, which circulate in the blood.
  • Interestingly, these cells, when infected, tend to not expose any viral envelope proteins, making them unrecognized and refractory to destruction by antibody-dependent lysis, an immune response in which antibodies mark target cells for destruction.

The Experiment: Setup and Results

  • In this experiment, six ponies were utilized – four had been exposed to EHV-1 before and two had never been in contact with EHV-1.
  • All six ponies were then inoculated with EHV-1, and their PBMCs were collected at different intervals up to 28 days after inoculation. This process allowed the researchers to monitor the course of infection and how PBMCs responded.
  • Results showed that a whopping 98% of infected PBMCs did not reveal viral envelope proteins on their surface, thereby supporting the in vitro studies. The absence of these proteins indicates that the cells are in an early phase of virus infection.
  • The infected cells mostly produced immediate early and, certain early proteins, but not the late envelope proteins, further corroborating the above inference.

Finding the Role of Major Histocompatibility Complex (MHC-I)

  • The surface expression of MHC-I was also of interest in this study. This complex plays a crucial role in immune system function, primarily for enhancing the visibility of infected cells to cytotoxic T cells.
  • It was revealed that the infected cells demonstrated a similar extent of MHC-I surface expression to that of uninfected cells taken from the same ponies, thus showing that the inefficient recognition of infected cells by cytotoxic T cells does not arise from the absence of MHC-I surface expression.
  • This result proves pivotal in demonstrating that EHV-1 employs tactics that go beyond simply hindering MHC-I expression as a means of evading the immune response.

Cite This Article

APA
van der Meulen K, Caij B, Pensaert M, Nauwynck H. (2006). Absence of viral envelope proteins in equine herpesvirus 1-infected blood mononuclear cells during cell-associated viremia. Vet Microbiol, 113(3-4), 265-273. https://doi.org/10.1016/j.vetmic.2005.11.048

Publication

ISSN: 0378-1135
NlmUniqueID: 7705469
Country: Netherlands
Language: English
Volume: 113
Issue: 3-4
Pages: 265-273

Researcher Affiliations

van der Meulen, Karen
  • Laboratory of Virology, Faculty of Veterinary Medicine, Ghent University, Salisburylaan 133, 9820 Merelbeke, Belgium. karen.vandermeulen@ugent.be
Caij, Brigitte
    Pensaert, Maurice
      Nauwynck, Hans

        MeSH Terms

        • Animals
        • Cytotoxicity, Immunologic
        • Herpesviridae Infections / blood
        • Herpesviridae Infections / immunology
        • Herpesviridae Infections / veterinary
        • Herpesvirus 1, Equid / immunology
        • Histocompatibility Antigens Class I / immunology
        • Horse Diseases / blood
        • Horse Diseases / immunology
        • Horses
        • Leukocytes, Mononuclear / immunology
        • Leukocytes, Mononuclear / virology
        • Viral Envelope Proteins / immunology
        • Viremia / immunology
        • Viremia / veterinary
        • Viremia / virology

        Citations

        This article has been cited 8 times.
        1. Laval K, Poelaert KCK, Van Cleemput J, Zhao J, Vandekerckhove AP, Gryspeerdt AC, Garré B, van der Meulen K, Baghi HB, Dubale HN, Zarak I, Van Crombrugge E, Nauwynck HJ. The Pathogenesis and Immune Evasive Mechanisms of Equine Herpesvirus Type 1. Front Microbiol 2021;12:662686.
          doi: 10.3389/fmicb.2021.662686pubmed: 33746936google scholar: lookup
        2. Zarski LM, Weber PSD, Lee Y, Soboll Hussey G. Transcriptomic Profiling of Equine and Viral Genes in Peripheral Blood Mononuclear Cells in Horses during Equine Herpesvirus 1 Infection. Pathogens 2021 Jan 7;10(1).
          doi: 10.3390/pathogens10010043pubmed: 33430330google scholar: lookup
        3. Li Y, Wu Y, Wang M, Ma Y, Jia R, Chen S, Zhu D, Liu M, Yang Q, Zhao X, Zhang S, Huang J, Ou X, Mao S, Zhang L, Liu Y, Yu Y, Pan L, Tian B, Rehman MU, Chen X, Cheng A. Duplicate US1 Genes of Duck Enteritis Virus Encode a Non-essential Immediate Early Protein Localized to the Nucleus. Front Cell Infect Microbiol 2019;9:463.
          doi: 10.3389/fcimb.2019.00463pubmed: 32010642google scholar: lookup
        4. Van Cleemput J, Poelaert KCK, Laval K, Vanderheijden N, Dhaenens M, Daled S, Boyen F, Pasmans F, Nauwynck HJ. An Alphaherpesvirus Exploits Antimicrobial β-Defensins To Initiate Respiratory Tract Infection. J Virol 2020 Mar 31;94(8).
          doi: 10.1128/JVI.01676-19pubmed: 31996426google scholar: lookup
        5. Spiesschaert B, Goldenbogen B, Taferner S, Schade M, Mahmoud M, Klipp E, Osterrieder N, Azab W. Role of gB and pUS3 in Equine Herpesvirus 1 Transfer between Peripheral Blood Mononuclear Cells and Endothelial Cells: a Dynamic In Vitro Model. J Virol 2015 Dec;89(23):11899-908.
          doi: 10.1128/JVI.01809-15pubmed: 26378176google scholar: lookup
        6. Cornelissen E, Dewerchin HL, Van Hamme E, Nauwynck HJ. Absence of surface expression of feline infectious peritonitis virus (FIPV) antigens on infected cells isolated from cats with FIP. Vet Microbiol 2007 Mar 31;121(1-2):131-7.
          doi: 10.1016/j.vetmic.2006.11.026pubmed: 17188823google scholar: lookup
        7. van der Meulen K, Garré B, Croubels S, Nauwynck H. In vitro comparison of antiviral drugs against feline herpesvirus 1. BMC Vet Res 2006 Apr 26;2:13.
          doi: 10.1186/1746-6148-2-13pubmed: 16640781google scholar: lookup
        8. Pusterla N, Dorman DC, Burgess BA, Goehring L, Gross M, Osterrieder K, Soboll Hussey G, Lunn DP. Viremia and nasal shedding for the diagnosis of equine herpesvirus-1 infection in domesticated horses. J Vet Intern Med 2024 May-Jun;38(3):1765-1791.
          doi: 10.1111/jvim.16958pubmed: 38069548google scholar: lookup