Distribution of Equid herpesvirus‐1 (EHV‐1) in respiratory tract associated lymphoid tissue: implications for cellular immunity

Kydd, Julia H.; Smith, K. C.; Hannant, D.; Livesay, Georgia; Mumford, J. A.

doi:10.1111/j.2042-3306.1994.tb04052.x

Cited by 107 publications

(81 citation statements)

References 14 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…This is the first clear definition of the cells which are specifically harbouring latent EHV-1 in the horse. While both lymphocytes and monocytes were identified as infectious in acute infections by Scott et al (1983) and Kydd et al (1994), our evidence indicates that T cells are a predominant site for latency, which is consistent with the detection of latency-associated transcripts (LATs) in leukocytes (Chester et al, 1997). The rapid appearance (at 6-12 h) of the reactivated virus is consistent with this being a primary event, and not a secondary cycle from monocytes infected during the acute phase.…”

Section: Discussionsupporting

confidence: 66%

“…Following this acute respiratory infection there is a leukocyteassociated viraemia (Scott et al, 1983) and leukopenia (Bumgardner et al, 1982 ;Allen & Bryans, 1986). During the viraemia EHV-1 has been isolated for up to 3 weeks postinfection from peripheral blood mononuclear cells, predominantly from T lymphocytes and to a lesser extent monocytes (Bumgardner et al, 1982 ;Kydd et al, 1994). This cell-associated viraemia in an acute infection has been shown to be a prerequisite for abortion and paresis by initiating replication of EHV-1 in endothelial cells in the pregnant uterus and CNS (Patel et al, 1982 ;Edington et al, 1986Edington et al, , 1991.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

In vitro reactivation of latent equid herpesvirus-1 from CD5+/CD8+ leukocytes indirectly by IL-2 or chorionic gonadotrophin.

Smith

Iqbal²,

Purewal³

et al. 1998

Journal of General Virology

View full text Add to dashboard Cite

Section: Discussionsupporting

confidence: 66%

Section: Introductionmentioning

confidence: 99%

In vitro reactivation of latent equid herpesvirus-1 from CD5+/CD8+ leukocytes indirectly by IL-2 or chorionic gonadotrophin.

Smith

Iqbal²,

Purewal³

et al. 1998

Journal of General Virology

View full text Add to dashboard Cite

“…In accordance with the findings reported by Soboll-Hussey et al Conclusions. Due to the cell-associated viremia that is central to the in vivo infection process of EHV-1, cell-mediated immunity is considered critical in EHV-1 protection (21,22,31). As with most viral infections, a Th1-polarized immune response associated with high levels of EHV-1-specific IFN-␥ production likely contributes to protection against disease.…”

Section: Equine Herpesvirus 1 Protective Correlatesmentioning

confidence: 99%

Immunological Correlates of Vaccination and Infection for Equine Herpesvirus 1

Goodman

Wimer

Dubovi

et al. 2012

Clin Vaccine Immunol

View full text Add to dashboard Cite

Equine herpesvirus 1 (EHV-1) induces a variety of disease manifestations, including respiratory disease, abortions, and myeloencephalopathy. Several vaccines are commercially available but could not previously be distinguished by serologic testing from infection with EHV-1 (or the closely related EHV-4). Currently available vaccines are not reliably protective against the severe manifestations of the disease, including fatal myeloencephalopathy. We determined immunological parameters that can differentiate vaccinated from previously infected animals by comparing humoral and cellular EHV-1-specific responses in clinically healthy horses 10 months after vaccination. Forty-seven horses with known histories of vaccination and infection were studied, including a group of horses that survived a severe neurological outbreak 5 years prior to vaccination. Results of serum virus neutralization (SN), serum IgG isotyping, and cytokine profiling of lymphocyte subsets were compared. IgG4/7 levels strongly correlated with virus neutralization (P < 0.0001). IgG1/3 and SN values distinguished vaccinated/outbreak-exposed (vacc/outbreak) horses from vaccinated horses (P < 0.05). EHV-1-specific gamma interferon (IFN-␥)-producing CD4 ؉ (but not CD8 ؉ ) T-cell numbers were also increased in vacc/outbreak horses, which distinguished them from vaccinated horses (P < 0.01). IFN-␣ secretion was similar between all groups and independent of previous exposure or vaccination. Our data suggest that IgG isotype responses to EHV-1 are more diverse under field conditions than is revealed by experimental studies and that the current modified-live virus (MLV) vaccine induces a more restricted IgG isotype response than does natural exposure to EHV-1. Since these parameters can be assessed in a high-throughput manner, they may prove useful in screening future vaccine candidates and assessing levels of protection.

show abstract

“…Although both viruses cause respiratory disease, only infection with EHV-1 results in epidemic abortion, perinatal mortality, and neurological disorders that differ in severity but often result in complete paralysis (4,21). The pathogenicity of EHV-1 is ascribed to the capacity of the virus to rapidly reach lymphoid tissues associated with the upper respiratory tract and to infect mononuclear cells that ultimately enter the bloodstream and lead to cell-associated viremia (41,78). As a result, EHV-1 can spread throughout the body by infected peripheral blood mononuclear cells (PBMC).…”

mentioning

confidence: 99%

Glycoproteins D of Equine Herpesvirus Type 1 (EHV-1) and EHV-4 Determine Cellular Tropism Independently of Integrins

Azab

Osterrieder

2012

J Virol

View full text Add to dashboard Cite

Equine herpesvirus type 1 (EHV-1) and EHV-4 are genetically and antigenically very similar, but their pathogenic potentials are strikingly different. The differences in pathogenicity between both viruses seem to be reflected in cellular host range: EHV-1 can readily be propagated in many cell types of multiple species, while EHV-4 entry and replication appear to be restricted mainly to equine cells. The clear difference in cellular tropism may well be associated with differences in the gene products involved in virus entry and/or spread from cell to cell. Here we show that (i) most of the EHV-1 permissive cell lines became resistant to EHV-1 expressing EHV-4 glycoprotein D (gD4) and the opposite was observed for EHV-4 harboring EHV-1 gD (gD1). (ii) The absence of integrins did not inhibit entry into and replication of EHV-1 in CHO-K1 or peripheral blood mononuclear cells (PBMC). Furthermore, integrin-negative K562 cells did not acquire the ability to bind to gD1 when ␣V␤3 integrin was overexpressed. (iii) PBMC could be infected with similar efficiencies by both EHV-1 and EHV-4 in vitro. (iv) In contrast to results for equine fibroblasts and cells of endothelial or epithelial origin, we were unable to block entry of EHV-1 or EHV-4 into PBMC with antibodies directed against major histocompatibility complex class I (MHC-I), a result that indicates that these viruses utilize a different receptor(s) to infect PBMC. Cumulatively, we provide evidence that efficient EHV-1 and EHV-4 entry is dependent mainly on gD, which can bind to multiple cell surface receptors, and that gD has a defining role with respect to cellular host range of EHV-1 and EHV-4.

show abstract

Distribution of Equid herpesvirus‐1 (EHV‐1) in respiratory tract associated lymphoid tissue: implications for cellular immunity

Cited by 107 publications

References 14 publications

In vitro reactivation of latent equid herpesvirus-1 from CD5+/CD8+ leukocytes indirectly by IL-2 or chorionic gonadotrophin.

In vitro reactivation of latent equid herpesvirus-1 from CD5+/CD8+ leukocytes indirectly by IL-2 or chorionic gonadotrophin.

Immunological Correlates of Vaccination and Infection for Equine Herpesvirus 1

Glycoproteins D of Equine Herpesvirus Type 1 (EHV-1) and EHV-4 Determine Cellular Tropism Independently of Integrins

Contact Info

Product

Resources

About